ORIGINAL_ARTICLE
External Dacryocystorhinostomy; Success Rate and Causes of Failure in Endoscopic and Pathologic Evaluations
Background and Objectives: External dacryocystorhinostomy (DCR) is the method of choice to treat nasolacrimal duct (NLD) obstruction and the other approaches are compared with it, with a failure rate of 4% to 13%. The current study aimed to assess the causes of failure in external DCR by postoperative endoscopic and pathological evaluation. Methods: The current retrospective cross sectional study followed-up113 patients with external DCR and silicone intubation for three months. Silicone tubes were removed after the third months. Failure was confirmed based on the clinical findings and irrigation test. Paranasal sinus computed tomography (CT) scanning, and endoscopic and pathological evaluations were performed in the failed cases. Results: Totally, 113 patients underwent external DCR. The patients included 71 females and 42 males. The mean age of the patients was 55.91 years; ranged from 18 to 86. Epiphora was the most common complaint before surgery (90.3%). Clinically, epiphora continued in 17 cases (15%), of which 94.11% had at least one sinus CT abnormality and 82.35% had at least one endoscopic abnormality. The most common endoscopic findings were deviated septum (70.6%), scar tissue (52.94%), concha bullosa (46.9%), septal adhesion (47.05%), enlarged middle turbinate (41.2%), and sump syndrome (11.7%). The failure was significantly associated with the chronicity of the initial symptoms (P-value=0.00). Pathologically, there were significant relationship amongst the failure rate, scar formation, and allergic rhinitis (P-values =0.00 and <0.05, respectively). Conclusion: Preoperative endonasal evaluation and consultation with an otolaryngologist can improve surgical outcomes and help to have a better conscious to intranasal abnormalities before external DCR surgery.
https://ijp.iranpath.org/article_24234_2c54d03d7e6ae8adc7f8703734b0abda.pdf
2017-07-01
189
194
10.30699/ijp.2017.24234
Lacrimal sac
Nasolacrimal Duct
Epiphora
Dacryocystorhinostomy
Hassan
Ghasemi
ghasemi518@yahoo.com
1
Dept of Ophthalmology, Medical School, Shahed University, Tehran, Iran
AUTHOR
Sajedeh
Asghari Asl
s_asghariasl@yahoo.com
2
Dept of Otolaryngology, Medical School, Shahed University, Tehran, Iran
AUTHOR
Mohammad Ebrahim
Yarmohammadi
meyarmohammadi@yahoo.com
3
Dept of Otolaryngology, Medical School, Shahed University, Tehran, Iran
LEAD_AUTHOR
Farhd
Jafari
jafarifarhaddr@yahoo.com
4
Dept of Otolaryngology, Medical School, Shahed University, Tehran, Iran
AUTHOR
Pupak
Izadi
pupakizadi@yahoo.com
5
Dept of Otolaryngology, Medical School, Shahed University, Tehran, Iran
AUTHOR
1. raujoFilho BC, Voegels RL, Butugan O, PinheiroNeto CD, Lessa MM. Endoscopic dacryocystrhinostomy. Braz J Otorhinolaryngol 2005 Nov;71(6):721-5.
1
2. Sibley D, Norris JH, Malhotra R. Management and outcomes of patients with epiphora referred to a specialist ophthalmic plastic unit. Clin Experiment Ophthalmol 2013 Apr;41(3):231-8.
2
3. Saha R, Sinha A, Phukan JP. Endoscopic versus external approach dacryocystorhinostomy: A comparative analysis. Niger Med J 2013 May;54(3):165-9.
3
4. Ozer S, Ozer PA. Endoscopic vs external dacryocystorhinostomy-comparison from the patients' aspect.Int J Ophthalmol 2014 Aug 18;7(4):689-96.
4
5. Mekonnen W, Adamu Y. Outcome of external dacryocystorhinostomy in Ethiopian patients. Ethiop Med J 2009 Jul;47(3):221-6.
5
6. Cokkeser Y, Evereklioglu C, Er H. Comparative external versus endoscopic dacryocystorhinostomy: results in 115 patients (130 eyes). Otolaryngol Head Neck Surg 2000 Oct;123(4):488-91.
6
7. Francisco FC, Carvalho AC, Francisco VF, Francisco MC, Neto GT. Evaluation of 1000 lacrimal ducts by dacryocystography. Br J Ophthalmol 2007 Jan;91(1):43-6.
7
8. Savino G, Battendieri R, Traina S, Corbo G, D'Amico G, Gari M, et al. External vs. endonasaldacryocystorhinostomy: has the current view changed? ActaOtorhinolaryngolItal 2014 Feb;34(1):29-35.
8
9. Ali MJ, Naik MN, Honavar SG. External dacryocystorhinostomy: Tips and tricks. Oman J Ophthalmol 2012 Sep;5(3):191-5.
9
10. Duggal P, Chakravorty S, Azad RK, Mohan C. An epidemiological study on patients undergoing dacryocystorhinostomy. Indian J Otolaryngol Head Neck Surg 2006 Oct;58(4):349-51.
10
11. Thornton SP. Nasolacrimal duct reconstruction with the nasolacrimal duct prosthesis: an alternative to standard dacryocystorhinostomy. Ann Ophthalmol 1977 Dec;9(12):1575-8, 1581.
11
12. El-Guindy A, Dorgham A, Ghoraba M. Endoscopic revision surgery for recurrent epiphora occurring after external dacryocystorhinostomy. Ann OtolRhinolLaryngol 2000 Apr;109(4):425-30.
12
13. Ben Simon GJ, Joseph J, Lee S, Schwarcz RM, McCann JD, Goldberg RA. External versus endoscopic dacryocystorhinostomy for acquired nasolacrimal duct obstruction in a tertiary referral center. Ophthalmology 2005 Aug;112(8):1463-8.
13
14. Choussy O, RetoutA, Marie JP, Cozlean A, Dehesdin D. Endoscopic revision of external dacryocystorhinostomy failure. Rhinology 2010 Mar;48(1):104-7.
14
15. Elmorsy SM, Fayk HM. Nasal endoscopic assessment of failure after external dacryocystorhinostomy. Orbit 2010 Aug;29(4):197-201.
15
16. Korkut AY, TekerAM, Ozsutcu M, Askiner O, Gedikli O. A comparison of endonasal with external dacryocystorhinostomy in revision cases.Eur Arch Otorhinolaryngol 2011 Mar;268(3):377-81.
16
17. Liang J, Hur K, Merbs SL, Lane AP. Surgical and anatomic considerations in endoscopic revision of failed external dacryocystorhinostomy. Otolaryngol Head Neck Surg 2014 May;150(5):901-5.
17
18. Shrestha S, Kafle PK, Pokhrel S, Maharjan M, Toran KC. Successes rate of endoscopic dacryocystorhinostomy at KMC. Kathmandu Univ Med J (KUMJ ) 2010 Apr;8(30):195-8.
18
19. Szubin L, Papageorge A, Sacks E. Endonasal laser-assisted dacryocystorhinostomy. Am J Rhinol 1999 Sep;13(5):371-4.
19
20. Lee BJ, Nelson CC, Lewis CD, Perry JD. External dacryocystorhinostomy outcomes in sarcoidosis patients.OphthalPlastReconstrSurg 2012 Jan;28(1):47-9.
20
21. Boboridis KG, Bunce C, Rose GE. Outcome of external dacryocystorhinostomy combined with membranectomy of a distal canalicular obstruction. Am J Ophthalmol 2005 Jun;139(6):1051-5.
21
22. Keerl R, Weber R. [Dacryocystorhinostomy - state of the art, indications, results]. Laryngorhinootologie 2004 Jan;83(1):40-50.
22
23. Eyigor H, Unsal AI, Unsal A. The role of accompanying sinonasal abnormalities in the outcome of endonasaldacryocystorhinostomy. Am J Rhinol 2006 Nov;20(6):620-4.
23
24. Golan S, Leibovitch I, Landsberg R. Unexpected pathologies in patients referred for endoscopic DCR. Eur Arch Otorhinolaryngol 2014 Nov;271(11):3053-8.
24
25. Fayet B, Racy E, Assouline M. Complications of standardized endonasaldacryocystorhinostomy with unciformectomy. Ophthalmology 2004 Apr;111(4):837-45.
25
ORIGINAL_ARTICLE
The diagnostic value of TTF1, P63, HMWK [34βE12], CK7, and CD56 immunostaining in classification of lung carcinoma
Background & objective: The histologic distinction of small cell from non-small cell lung carcinoma and correct identification of all subtypes of lung carcinoma are very important in treatment management. The main method for histologic classification of lung tumors is based on morphology. However, in small bronchoscopic biopsies in particular, distinction is very difficult upon morphology alone. The current study aimed at evaluating the utility of a panel of antibodies, consisting of thyroid transcription factor (TTF-1), P63, high molecular weight keratin [HMWK (34βE12)], cytokeratin (CK7), and cluster of differentiation (CD56) for accurate distinction of bronchogenic carcinomas. Methods: Bronchoscopic biopsies of 60 lung carcinoma cases including 20 small cell carcinomas, 20 adenocarcinomas, and 20 squamous cell carcinomas (SCCs) with typical morphologic features were selected. All these cases were immunohistochemically stained for TTF-1, P63, HMWK (34βE12), CK7, and CD56. All immunostained slides were scored as either positive or negative. Results: The mean age of the patients was 60 years; ranged from 35 to 81. Sixteen patients were female and 44 were male. All adenocarcinomas were positive for CK7 and most of them (18/20; 90%) were positive for TTF-1. Most of small cell lung carcinomas were positive for TTF-1 (17/20; 85%), and CD56 (18/20; 90%). All squamous cell carcinomas (SCCs) were negative for TTF-1, but most of them were positive for HMWK (34βE12) and P63. Conclusion: The obtained data showed that TTF-1, P63, CK7, CD56 and/or 34βE12 represent a useful panel of antibodies to identify lung carcinoma subtypes in small bronchoscopic biopsies.
https://ijp.iranpath.org/article_25041_a0b78c4786c88b619d62c298c0d4ec81.pdf
2017-07-01
195
201
10.30699/ijp.2017.25041
Immunohistochemistry
TTF1
P63
HMWK [34βE12]
CK7
CD56
lung carcinoma
Amir Hossein
Jafarian
jafarianah@mums.ac.ir
1
Dept. of Pathology, Faculty of Medicine, Mashhad University of Medical Sciences, Iran
AUTHOR
Masoumeh
Gharib
gharibm@mums.ac.ir
2
Dept. of Pathology, Faculty of Medicine, Mashhad University of Medical Sciences, Iran
LEAD_AUTHOR
Nema
Mohammadian Roshan
roshann@mums.ac.ir
3
Dept. of Pathology, Faculty of Medicine, Mashhad University of Medical Sciences, Iran
AUTHOR
Samaneh
Sherafatnia
samanehsherafatnia@yahoo.com
4
Dept. of Pathology, Faculty of Medicine, Mashhad University of Medical Sciences, Iran
AUTHOR
Abbas Ali
Omidi
omidiaa@mums.ac.ir
5
Dept. of Pathology, Faculty of Medicine, Mashhad University of Medical Sciences, Iran
AUTHOR
Sahar
Bagheri
bagheris892@mums.ac.ir
6
Dept. of Pathology, Faculty of Medicine, Mashhad University of Medical Sciences, Iran
AUTHOR
Forman D, Ferlay J, Stewart B, Wild C. The global and regional burden of cancer. World cancer report. 2014:16-53.
1
2. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2016. CA: a cancer journal for clinicians. 2016; 66 (1):7-30.
2
3. Siegel R, Naishadham D, Jemal A. Cancer statistics, 2013. CA: a cancer journal for clinicians. 2013;63 (1):11-30.
3
4. Travis WD, Brambilla E, Burke AP, Marx A, Nicholson AG. Introduction to the 2015 World Health Organization Classification of Tumors of the Lung, Pleura, Thymus, and Heart. Journal of Thoracic Oncology. 2015; 10 (9):1240-2.
4
5. Kargi A, Gurel D, Tuna B. The diagnostic value of TTF-1, CK 5/6, and p63 immunostaining in classification of lung carcinomas. Applied Immunohistochemistry & Molecular Morphology. 2007;15(4):415-20.
5
6. Au N, Gown A, Cheang M, Huntsman D, Yorida E, Elliott W, et al. P63 expression in lung carcinoma: a tissue microarray study of 408 cases. Applied Immunohistochemistry & Molecular Morphology. 2004;12(3):240-7.
6
7. Wang BY, Gil J, Kaufman D, Gan L, Kohtz DS, Burstein DE. P63 in pulmonary epithelium, pulmonary squamous neoplasms, and other pulmonary tumors. Human pathology. 2002;33 (9):921-6.
7
8. Jerome Marson V, Mazieres J, Groussard O, Garcia O, Berjaud J, Dahan M, et al. Expression of TTF‐1 and cytokeratins in primary and secondary epithelial lung tumours: correlation with histological type and grade. Histopathology. 2004;45(2):125-34.
8
9. Johansson L. Histopathologic classification of lung cancer: relevance of cytokeratin and TTF-1 immunophenotyping. Annals of diagnostic pathology. 2004;8(5):259-67.
9
10. Lyda MH, Weiss LM. Immunoreactivity for epithelial and neuroendocrine antibodies are useful in the differential diagnosis of lung carcinomas. Human pathology. 2000;31(8):980-7.
10
11. Rossi G, Marchioni A, Milani M, Scotti R, Foroni M, Cesinaro A, et al. TTF-1, cytokeratin 7, 34βE12, and CD56/NCAM immunostaining in the subclassification of large cell carcinomas of the lung. American journal of clinical pathology. 2004;122(6):884-93.
11
12. Sturm N, Lantuéjoul S, Laverrière M-H, Papotti M, Brichon P-Y, Brambilla C, et al. Thyroid transcription factor 1 and cytokeratins 1, 5, 10, 14 (34βE12) expression in basaloid and large-cell neuroendocrine carcinomas of the lung. Human pathology. 2001;32(9):918-25.
12
13. Viberti L, Bongiovanni M, Croce S, Bussolati G. 34βE 12 Cytokeratin Immunodetection in the Differential Diagnosis of Small Cell Tumors of Lung. International journal of surgical pathology. 2000;8(4):317-22.
13
14. Al-Zahrani IH. The value of immunohistochemical expression of TTF-1, CK7 and CK20 in the diagnosis of primary and secondary lung carcinomas. Saudi medical journal. 2008;29(7):957-61.
14
15. Ionescu DN, Treaba D, Gilks CB, Leung S, Renouf D, Laskin J, et al. Nonsmall cell lung carcinoma with neuroendocrine differentiation—an entity of no clinical or prognostic significance. The American journal of surgical pathology. 2007;31(1):26-32.
15
ORIGINAL_ARTICLE
The Core Needle and Surgical Biopsy Concordance to Detect Estrogen, Progesterone, and Her-2 Receptors in Breast Cancer: A Comparative Study
Background &Objectives: Evaluation of estrogen receptor (ER), progesterone receptor (PR), and (human epidermal growth factor receptor-2) Her-2 on core needle biopsies (CNBs) is increasingly in use to diagnosis early breast cancer, but its concordance with surgical excision (SE) is not well documented. Methods: The study included 100 formalin fixed, paraffin-embedded specimens of invasive breast carcinoma archived in Pathology Department of Cancer Institute, Tehran, Iran, from 2011 to 2014. Immunohistochemistry was applied to detect ER, PR, and Her-2. Results: The current study findings indicated a significant correlation of 90% between CNB and SE specimens for ER expression. The correlation between CNB and SE specimens was estimated as 81% and 97.3% for PR and Her-2, respectively. Discussion: CNB can be performed confidently to determine ER and Her-2. For PR, results obtained from CNB should be considered.
https://ijp.iranpath.org/article_25042_d9d52819e8185fe15f5f155b5f857544.pdf
2017-07-01
202
208
10.30699/ijp.2017.25042
Core Needle Biopsy
Breast cancer
Estrogen
progesterone
Her2
Fereshteh
Ensani
fensani@gmail.com
1
Dept. of Pathology, Cancer Institute Hospital, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Ramesh
Omranipour
omranipour@tums.ac.ir
2
Surgical Oncology Center Institute Hospital, Tehran University of Medical Science, Tehran, Iran
AUTHOR
Isa
Jahanzad
jahanzad@yahoo.com
3
Dept. of Immunohistochemistry, Cancer Institute, Tehran University of Medical Science, Tehran, Iran
AUTHOR
Azadeh
Jafari
jafari@yahoo.com
4
Dept. of Pathology, Cancer Institute Hospital, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Shima
Nafarzadeh
shima.nafar2004@yahoo.com
5
Dept. of Oral and Maxillofacial Pathology, Babol University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Pouyan
Aminishakib
aminishakib@tums.ac.ir
6
Dept. of Oral and Maxillofacial Pathology, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
1. Tamaki K, Sasano H, Ishida T, Miyashita M, Takeda M, Amari M,et al. Comparison of core needle biopsy (CNB) and surgical specimens for accurate preoperative evaluation of ER, PgR and HER2 status of breast cancer patients. Cancer sci. 2010 1;101(9):2074-9.
1
2. Arnedos M, Nerurkar A, Osin P, A'hern R, Smith IE, Dowsett M. Discordance between core needle biopsy (CNB) and excisional biopsy (EB) for estrogen receptor (ER), progesterone receptor (PgR) and HER2 status in early breast cancer (EBC). Ann Oncol. 2009 1;20(12):1948-52.
2
3. Sutela A, Vanninen R, Sudah M, Berg M, Kiviniemi V, Rummukainen J,et al. Surgical specimen can be replaced by core samples in assessment of ER, PR and HER-2 for invasive breast cancer. ActaOncologica. 2008 1;47(1):38-46.
3
4.Ma Soomi T,Shfaruddin, Kamali M, HasaniMehraban A, Omranipur R. Psychological responses to breast cancer:A qualitative study. J SABZEVAR Univ Med Sci. 2013 20; 1(67): 84-92.
4
5.Journal article on the Internet: Pusztai L, Viale G, Kelly CM, Hudis CA. Estrogen and HER-2 receptor discordance between primary breast cancer and metastasis. Oncologist. 2010, doi: 10.1634/theoncologist.2010-005915(11):1164-8.
5
6.Usami S, Moriya T, Amari M, Suzuki A, Ishida T, Sasano H. Reliability of prognostic factors in breast carcinoma determined by core needle biopsy. Japanese JClinOncol. 2007 1;37(4):250-5.
6
7. Omranipour R, Alipour S, Hadji M, Fereidooni F, Jahanzad I, Bagheri K. Accuracy of estrogen and progesterone receptor assessment in core needle biopsy specimens of breast cancer.Iran Red Crescent Med J. 2013;15(6):515.
7
8.D'Alfonso T, Liu YF, Monni S, Rosen PP, Shin SJ. Accurately assessing her-2/neu status in needle core biopsies of breast cancer patients in the era of neoadjuvant therapy: emerging questions and considerations addressed. Am J SurgPathol. 2010 1;34(4):575-81.
8
9. Al Sarakbi W, SalhabM, Thomas V, Mokbel K.Is preoperative core biopsy accurate in determining the hormone receptor status in women with invasive breast cancer? in International seminars in surgical oncology. 2005. BioMed Central Ltd.
9
10.Reisenbichler ES, Lester SC, Richardson AL, Dillon DA, Ly A, Brock JE. Interobserver Concordance in Implementing the 2010 ASCO/CAP Recommendations for Reporting ER in Breast Carcinomas. Am JClinPathol. 2013 1;140(4):487-94.
10
11.Cserni G, Francz M, Kálmán E, Kelemen G, Komjáthy DC, Kovács I, et al. Estrogen receptor negative and progesterone receptor positive breast carcinomas—How frequent are they?. PatholOncol. 2011 1;17(3):663-8.
11
12.Prati R, Apple SK, He J, Gornbein JA, Chang HR. Histopathologic Characteristics Predicting HER‐2/neu Amplification in Breast Cancer.Breast J. 2005 1;11(6):433-9.
12
13.Tsuda H, Kurosumi M, Umemura S, Yamamoto S, Kobayashi T, Osamura RY. HER2 testing on core needle biopsy specimens from primary breast cancers: interobserver reproducibility and concordance with surgically resected specimens. BMC cancer. 2010 7;10(1):1.
13
14. Li S, Yang X, Zhang Y, Fan L, Zhang F, Chen L. et al. Assessment accuracy of core needle biopsy for hormone receptors in breast cancer: a meta-analysis. Breast Cancers Treat. 2012 1;135(2):325-34.
14
15.Pettine S, Place R, Babu S, Williard W, Kim D, Carter P. Stereotactic breast biopsy is accurate, minimally invasive, and cost effective. AmJ J Surg. 1996 31;171(5):474-6.
15
16.Pijnappel RM, van Dalen A, Rinkes IH, van den Tweel JG, Willem PT. The diagnostic accuracy of core biopsy in palpable and non-palpable breast lesions. Europ J Radiol. 1997 28;24(2):120-3.
16
17.Chen X, Yuan Y, Gu Z, Shen K. Accuracy of estrogen receptor, progesterone receptor, and HER2 status between core needle and open excision biopsy in breast cancer: a meta-analysis. Breast Canc Res Treat. 2012 1;134(3):957-67.
17
18. Zidan A, Brown JC, Peston D, Shousha S. Oestrogen and progesterone receptor assessment in core biopsy specimens of breast carcinoma. J ClinPathol. 1997 1;50(1):27-9.
18
19. Bilous M. Breast core needle biopsy: issues and controversies. Mod Pathol. 2010 1;23:36-45.
19
20.Nadji M, Gomez-Fernandez C, Ganjei-Azar P, Morales AR. Immunohistochemistry of estrogen and progesterone receptors reconsidered. Am J ClinPathol. 2005 1;123(1):21-7.
20
21. Khoury T, Zakharia Y, Tan W, Kulkarni S, Liu W, Zhang S,et al. Breast hormonal receptors test should be repeated on excisional biopsy after negative core needle biopsy. Breast J. 2011 1;17(2):180-6.
21
22.Brenner RJ, Fajardo L, Fisher PR, Dershaw DD, Evans WP, Bassett L,et al. Percutaneous core biopsy of the breast: effect of operator experience and number of samples on diagnostic accuracy. Am J Roentgenol. 1996;166(2):341-6.
22
ORIGINAL_ARTICLE
Differentiating and Categorizing of Liposarcoma and Synovial Sarcoma Neoplasms by Fluorescence in Situ Hybridization
Background & Objective: Soft tissue sarcomas (STS) constitute an uncommon and heterogeneous group of tumors of mesenchymal origin and various cytogenetic abnormalities ranging from distinct genomic rearrangements, such as chromosomal translocations and amplifications, to more intricate rearrangements involving multiple chromosomes. Fluorescence in situ hybridization (FISH) can be used to identify these chromosomal translocations and amplifications, and sub classify STS precisely. The current study aimed at investigating the usefulness of FISH, as a diagnostic ancillary aid, to detect cytogenetic abnormalities such as MDM2 (murine double minute 2) amplification and CHOP(C/EBP homologous protein) rearrangement in liposarcoma, as well as SYT (synaptotagmin) rearrangement in synovial sarcoma. Methods: The FISH technique was used to analyze 17 specimens of liposarcoma for MDM2 amplification and CHOP rearrangement, and 10 specimens of synovial sarcoma for SYT rearrangement. The subtypes of liposarcoma and synovial sarcomas were reclassified according to the FISH results and compared with those of the respective histological findings. Results: According to the FISH results in 17 liposarcoma cases, well-differentiated liposarcoma(WDLPS), dedifferentiated liposarcoma (DDLPS), and myxoidliposarcoma (MLPS)subtypes were 41%, 53%, and 6%, respectively. In different subtypes of liposarcoma, a total of 30% mismatches were observed between pathologic and cytogenetic results. According to the histological findings from FISH analysis, SYT rearrangement was found only in three out of 10 (30%) synovial sarcomas. Conclusion: The detection of cytogenetic abnormalities in patients with liposarcoma and synovial sarcoma by FISH technique provides an important objective tool to confirm sarcoma diagnosis and sub classification of specific sarcoma subtypes in such patients.
https://ijp.iranpath.org/article_25043_ac79674409a98de9ac72f09068eb05fa.pdf
2017-07-01
209
217
10.30699/ijp.2017.25043
Liposarcoma
Synovial Sarcoma
Fish
CHOP
SYT
MDM2
Farhad
Shahi
fshahi@yahoo.com
1
Dept. of Hematology and Medical Oncology, Cancer Research Center, Cancer Institute, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Razieh
Alishahi
razieh.alishahi@gmail.com
2
Dept. of Biology, Faculty of Sciences, International Pardis, University of Guilan, Rasht, Iran
AUTHOR
Hossein
Pashaiefar
hossein.pashaiefar@gmail.com
3
Dept. of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Isa
Jahanzad
jahanzad@yahoo.com
4
Dept. of Pathology, Cancer Research Center, Cancer Institute, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Naser
Kamalian
kamaliann8@gmail.com
5
Dept. of Pathology, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Ardeshir
Ghavamzadeh
ghavamza@sina.tums.ac.ir
6
Hematology, Oncology and Stem Cell Transplantation Research center, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Marjan
Yaghmaie
m-yaghmaie@sina.tums.ac.ir
7
Hematology, Oncology and Stem Cell Transplantation Research center, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
1.Fletcher CD, Unni KK, Mertens F. Pathology and genetics of tumours of soft tissue and bone. World Health Organization classification of tumours. 2013.
1
2.Thway K, Fisher C. Histopathological diagnostic discrepancies in soft tissue tumours referred to a specialist centre. Sarcoma. 2009;2009.
2
3.Ray-Coquard I, Montesco M, Coindre J, Dei Tos A, Lurkin A, Ranchère-Vince D, et al. Sarcoma: concordance between initial diagnosis and centralized expert review in a population-based study within three European regions. Annals of oncology. 2012;23(9):2442-9.
3
4.Singer S, editor New diagnostic modalities in soft tissue sarcoma. Seminars in surgical oncology; 1999: Wiley Online Library.
4
5.Bovée JV, Hogendoorn PC. Molecular pathology of sarcomas: concepts and clinical implications. Virchows Archiv. 2010;456(2):193-9.
5
6.Toro JR, Travis LB, Wu HJ, Zhu K, Fletcher CD, Devesa SS. Incidence patterns of soft tissue sarcomas, regardless of primary site, in the surveillance, epidemiology and end results program, 1978–2001: an analysis of 26,758 cases. International Journal of Cancer. 2006;119(12):2922-30.
6
7.Fletcher CD, Organization WH, Cancer IAfRo. WHO classification of tumours of soft tissue and bone: IARC press; 2013.
7
8.Kindblom L-G. Lipomatous tumors—how we have reached our present views, what controversies remain and why we still face diagnostic problems: a tribute to Dr Franz Enzinger. Advances in anatomic pathology. 2006;13(6):279-85.
8
9.Suurmeijer A, de Bruijn D, Geurts van Kessel A, Miettinen M. Synovial sarcoma. WHO Classification of Tumours of Soft Tissue and Bone Lyon: IARC. 2013:213-5.
9
10.Rieker RJ, Weitz J, Lehner B, Egerer G, Mueller A, Kasper B, et al. Genomic profiling reveals subsets of dedifferentiated liposarcoma to follow separate molecular pathways. Virchows Archiv. 2010;456(3):277-85.
10
11.Lewis JJ, Antonescu CR, Leung DH, Blumberg D, Healey JH, Woodruff JM, et al. Synovial sarcoma: a multivariate analysis of prognostic factors in 112 patients with primary localized tumors of the extremity. Journal of Clinical Oncology. 2000;18(10):2087-94.
11
12.Coindre JM, Pelmus M, Hostein I, Lussan C, Bui BN, Guillou L. Should molecular testing be required for diagnosing synovial sarcoma? Cancer. 2003;98(12):2700-7.
12
13.Guillou L, Coindre J-M, Gallagher G, Terrier P, Gebhard S, Somerhausen NDSA, et al. Detection of the synovial sarcoma translocation t (X; 18)(SYT; SSX) in paraffin-embedded tissues using reverse transcriptase-polymerase chain reaction: a reliable and powerful diagnostic tool for pathologists: a molecular analysis of 221 mesenchymal tumors fixed in different fixatives. Human pathology. 2001;32(1):105-12.
13
14.De Vreeze RS, de Jong D, Nederlof PM, Ariaens A, Tielen IH, Frenken L, et al. Added value of molecular biological analysis in diagnosis and clinical management of liposarcoma: a 30-year single-institution experience. Annals of surgical oncology. 2010;17(3):686-93.
14
15.Weaver J, Downs-Kelly E, Goldblum JR, Turner S, Kulkarni S, Tubbs RR, et al. Fluorescence in situ hybridization for MDM2 gene amplification as a diagnostic tool in lipomatous neoplasms. Modern Pathology. 2008;21(8):943-9.
15
16.Neuville A, Ranchère-Vince D, Dei Tos AP, Montesco MC, Hostein I, Toffolatti L, et al. Impact of molecular analysis on the final sarcoma diagnosis: a study on 763 cases collected during a European epidemiological study. The American journal of surgical pathology. 2013;37(8):1259-68.
16
17.Dei Tos AP, Doglioni C, Piccinin S, Sciot R, Furlanetto A, Boiocchi M, et al. Coordinated expression and amplification of the MDM2, CDK4, and HMGI‐C genes in atypical lipomatous tumours. The Journal of pathology. 2000;190(5):531-6.
17
18.Cho J, Lee SE, Choi Y-L. Diagnostic Value of MDM2 and DDIT3 Fluorescence In Situ Hybridization in Liposarcoma Classification: A Single-Institution Experience. Korean journal of pathology. 2012;46(2):115-22.
18
19.Sirvent N, Coindre J-M, Maire G, Hostein I, Keslair F, Guillou L, et al. Detection of MDM2-CDK4 amplification by fluorescence in situ hybridization in 200 paraffin-embedded tumor samples: utility in diagnosing adipocytic lesions and comparison with immunohistochemistry and real-time PCR. The American journal of surgical pathology. 2007;31(10):1476-89.
19
20.Saboorian MH, Ashfaq R, Vandersteenhoven JJ, Schneider NR. Cytogenetics as an adjunct in establishing a definitive diagnosis of synovial sarcoma by fine‐needle aspiration. Cancer Cytopathology. 1997;81(3):187-92.
20
21.Ladanyi M, Antonescu CR, Leung DH, Woodruff JM, Kawai A, Healey JH, et al. Impact of SYT-SSX Fusion Type on the Clinical Behavior of Synovial Sarcoma A Multi-Institutional Retrospective Study of 243 Patients. Cancer research. 2002;62(1):135-40.
21
22.Surace C, Panagopoulos I, Pålsson E, Rocchi M, Mandahl N, Mertens F. A novel FISH assay for SS18–SSX fusion type in synovial sarcoma. Laboratory investigation. 2004;84(9):1185-92.
22
23.Ducimetière F, Lurkin A, Ranchère-Vince D, Decouvelaere A-V, Péoc'h M, Istier L, et al. Incidence of sarcoma histotypes and molecular subtypes in a prospective epidemiological study with central pathology review and molecular testing. PloS one. 2011;6(8):e20294.
23
24.Conyers R, Young S, Thomas DM. Liposarcoma: molecular genetics and therapeutics. Sarcoma. 2010;2011.
24
25.Sreekantaiah C, Ladanyi M, Rodriguez E, Chaganti R. Chromosomal aberrations in soft tissue tumors. Relevance to diagnosis, classification, and molecular mechanisms. The American journal of pathology. 1994;144(6):1121.
25
26.Haldar M, Randall RL, Capecchi MR. Synovial sarcoma: from genetics to genetic-based animal modeling. Clinical orthopaedics and related research. 2008;466(9):2156-67.
26
27.Sugita S, Asanuma H, Hasegawa T. Diagnostic use of fluorescence in situ hybridization in expert review in a phase 2 study of trabectedin monotherapy in patients with advanced, translocation-related sarcoma. Diagnostic Pathology. 2016;11(1):1.
27
28.Thway K, Wang J, Swansbury J, Min T, Fisher C. Fluorescence in situ hybridization for MDM2 amplification as a routine ancillary diagnostic tool for suspected well-differentiated and dedifferentiated liposarcomas: experience at a tertiary center. Sarcoma. 2015;2015.
28
29.Italiano A, Di Mauro I, Rapp J, Pierron G, Auger N, Alberti L, et al. Clinical effect of molecular methods in sarcoma diagnosis (GENSARC): a prospective, multicentre, observational study. The Lancet Oncology. 2016;17(4):532-8.
29
How to Cite This Article:
30
30.Horn H, Allmanritter J, Doglioni C, Marx A, Müller J, Gattenlöhner S, et al. Fluorescence in situ analysis of soft tissue tumor associated genetic alterations in formalin-fixed paraffin-embedded tissue. Pathology-Research and Practice. 2014;210(12):804-11.
31
31.Guan Z, Yu X, Wang H, Zhang J, Cao J, Li G, et al. Advances in the targeted therapy of liposarcoma. Onco Targets Ther. 2015;8:125-36.
32
ORIGINAL_ARTICLE
High Expression of Sphingosine Kinase 1 in Estrogen and Progesterone Receptors-Negative Breast Cancer
Background & objective: Breast cancer is the leading cause of cancer related death in females. Sphingosine kinase 1 (SPHK1) and its product sphingosine-1-phosphate (S1P) are the essential key regulator molecules in breast cancer through their ability to promote cell proliferation, angiogenesis, cell proliferation, and lymphagiogenesis. SPHK1 is overexpressed in multiple types of cancer including breast cancer and is associated with resistance to treatment. The current study aimed at investigating the expression of SPHK1 in estrogen and progesterone receptors (ER, PR) negative in comparison to ER, and PR positive breast cancer and their normal controls, and also finding the relationship between SPHK1 expression and high body index (BMI) in the selected groups with breast cancer. Methods: A total of 120 human breast cancer tissue specimens were analyzed for SPHK1 expression using quantitative real–time polymerase chain reaction (q RT-PCR) assay. Detection of hormonal status of breast cancer tissue samples was conducted by immunohistochemical assay. Result: The current study findings showed that the level of SPHK1expression in the breast cancer tissue was significantly higher in patients with estrogen and progesterone negative receptors, compared to the ones without them (P-value< 0.05). The obtained data confirmed that the obesity in patients with ER negative was higher than the ones with positive receptors (BMI> 25). Conclusion: The current study showed that expression of SPHK1gene was higher in the patients with ER and PR negative breast cancer and high BMI, compared with other groups.
https://ijp.iranpath.org/article_25049_246222ab6de884234b89ebe7bfc8ddc0.pdf
2017-07-01
218
224
10.30699/ijp.2017.25049
Sphingosine Kinase 1 phosphate
Estrogen and Progesterone Receptors
Real –time PCR
Breast cancer
Azadeh Sadat
Nazouri
nazouriazadeh@gmail.com
1
Dept. of Biology, Science Faculty, Shahid Beheshti University, Tehran, Iran
AUTHOR
omolbanin
asadpour
asadpour1391@yahoo.com
2
Dept. of Medical Biotechnology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
AUTHOR
Shahriar
Dabiri
dabiri12@yahoo.com
3
Pathology and Stem Cell Research Center, Pathology Department, Afzalipour School of Medicine, Kerman University of Medical Sciences, Kerman, Iran
LEAD_AUTHOR
Bahram
Pourseyedi
pourseyedib@yahoo.com
4
Surgery Department, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Mohamad reza
Lashkarizadeh
lashkarizadeh@kmu.ac.ir
5
Surgery Department, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Hamid
Zeinalyneghad
h.zeinaly-in-@yahoo.com
6
Surgery Department, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
1. World Cancer Report. International Agency for research on Cancer. 2008Retrieved 2011-02-26.
1
2. Beckmann MW, Bani MR, Fasching PA, Strick R and Lux MP. Risk and risk assessment for breast cancer: molecular and clinical aspects. Maturitas 2007.20; 57(1): 56-60.
2
3.Mousavi SM, Montazeri A, Mohagheghi MA, Jarrahi AM, Harirchi I, Najafi M, Ebrahimi M. Breast cancer in Iran: an epidemiological review. Breast J 2007; 13(4):383-91.
3
4. Lal P, Tan LK, Chen B. Correlation of HER-2 status with estrogen and progesterone receptors and histologic features in 3,655 invasive breast carcinomas. Am J Clin Pathol 2005; 123(4): 541-6.
4
5. Blanco G, Holli K, Heikkinen M, Kallioniemi OP, Taskinen P. Prognostic factors in recurrent breast cancer: relationship to site of recurrence, disease- free interval, female sex steroid receptors, ploidy and histological malignancy grading. Br J Cancer 1990; 62(1): 142-6.
5
6. Marzec KA, Baxter R C, and. Martin JL. Targeting Insulin-Like Growth Factor Binding Protein-3 Signaling in Triple-Negative Breast Cancer. BoiMed Res Int 2015; 2015:638526.
6
7. Cuvillier O, Nava VE, Murthy SK, Edsall LC, Levade T, Milstien S, Spiegel S. Sphingosine generation, cytochrome c release, and activation of caspase-7 in doxorubicin-induced apoptosis of MCF7 breast adenocarcinoma cells. Cell Death Differ2001; 8(2):162-71.
7
8. Herr DR, Chun J. Effects of LPA and S1P on the nervous system and implications for their involvement in disease. Curr Drug Targets2007;8 (1):155-67.
8
9. Spiegel S, Milstien S. Sphingosine-1-phosphate: an enigmatic signaling lipid. Nat Rev Mol Cell Biol2003; 4(5):397-407.
9
10. Shida D, Takabe K, Kapitonov D, Milstien S, Spiegel S. Targeting SphK1 as a new strategy against cancer. Curr Drug Targets 2008 Aug; 9(8):662-73.
10
11. Maceyka M, Spiegel S.Sphingolipid metabolites in inflammatory disease.Nature2014; 5;510(7503):58-67.
11
12. Pyne NJ, PyneS.Sphingosine 1-phosphate and cancer.Nat Rev Cancer 2010; 10(7):489-503.
12
13. Alshaker H, Sauer L, Monteil D, Ottavini S, Strivats S, Bohler T, Pchejetshki D. Therapeutic potential of targeting SK1 in human cancers.Adv Cancer Res 2013; 117:143-200.
13
14. Zheng XD, Zhang Y, Qi XW, Wang MH, Sun P, Zhang Y, et al. Role of Sphk1 in the malignant transformation of breast epithelial cells and breast cancer progression. Indian J Cancer 2014 Oct-Dec; 51(4):524-9.
14
15. XiaP,GambleJR,WangL,PitsonSM,MorettiPA,WattenbergBW,D'AndreaRJ,Vadas MA et al. An oncogenic role of sphingosine kinase.CurrBiol2000; 10(23):1527-30.
15
16. Ko P, Kim D, You E, Jung J, Oh S, Kim J et al. Extracellular Matrix Rigidity-dependent Sphingosine-1-phosphate Secretion Regulates Metastatic Cancer Cell Invasion and Adhesion. Sci Rep 2016 Feb 15; 6:21564.
16
17. Tian H, Yu Z. Resveratrol induces apoptosis of leukemia cell line K562 by modulation of sphingosine kinase-1 pathway. Int J Clin Exp Phathol 2015 Mar 1; 8(3):2755-62.
17
18. Salama MF, Carroll B, Adada M, PuLkoski-Gross M, Hannun YA, Obeid LM. A novel role of sphingosine kinase-1 in the invasion and angiogenesis of VHL mutant clear cell renal cell carcinoma. FASEB J 2015 Jul; 29(7):2803-13.
18
19. Beach JA, Aspuria PJ, Cheon DJ, Lawenson K, Agadjanian H, Walsh CS. Sphingosine kinase 1 is required for TGF-β mediated fibroblastto- myofibroblast differentiation in ovarian cancer. Oncotarget 2016 Jan 26; 7(4):4167-82.
19
20. Le ScolanE ,Pchejetski D,BannoY, DenisN, MayeuxP, Vainchenker W et al. Overexpression of sphingosine kinase 1 is an oncogenic event in erythroleukemic progression. Blood 2005;106(5):1808-16.
20
21. Zhao R, Milstien S, Zhou H, Spiegel S, Takabe K: Sphingosine-1-phosphateproduced by sphingosine kinase 1 promotes breast cancer progressionby stimulating angiogenesis and lymphangiogenesis. Cancer Res 2012 Feb 1; 72(3):726–735.
21
22. Wang E, NgalameY Panelli MC, Nguyen-Jackson H, Deavers M, Mueller P, HuW, Savary CA et al. Peritoneal and subperitoneal stroma may facilitate regional spread of ovarian cancer. Clin Cancer Res 2005; 11(1):113-22.
22
23. Butcher DT, Alliston T, Weaver VM. A tense situation: forcing tumour progression.Net Rev Cancer 2009 Feb; 9(2):108-22.
23
24. Leventl KR, Yu H, Kass L, Lakins JN, Egeblad M, ErlerJT, Fong SF et al. Matrix crosslinking forces tumor progression by enhancing integrin signaling. cell 2009 Nov 25;139(5):891-906..
24
25. Shirai K, Kaneshiro T, Wada M, Furuya H, Bielawski J, Hannun YA, Obeid LM, et al. A role of sphingosine kinase 1 in head & neck carcinogenesis. Cancer Prev Res (Phila). 2011 Mar; 4(3):454-62.
25
26. Tsuchida J, Nagahashi M, Nakajima M, Moro K, Tatsuda K, Ramanathan R. Breast cancer sphingosine-1-phosphate is associated with phospho-sphingosine kinase 1 and lymphatic metastasis.JSurgRes2016; 205(1):85-94.
26
27. Ruckhäberle E, Rody A, Engels K, Gaetje R, vonMinckwitz G, Schiffmann S et al. Microarray analysis of altered sphingolipid metabolism reveals prognostic significance of sphingosine kinase 1 in breast cancer. Breast Cancer Res Treat 2008; 112(1):41-52.
27
28. Long JS, Edwards J, Watson C, Tovey S, Mair KM, Schiff R et al. Sphingosine kinase 1 induces tolerance to human epidermal growth factor receptor 2 and prevents formation of a migratory phenotype in response to sphingosine 1-phosphate in estrogen receptor-positive breast cancer cells. Mol Cell Biol 2010 Aug; 30(15):3827-41.
28
29. Pyne NJ, Tonelli F, Lim KG, Long J, Edwards J, Pyne S: Targeting sphingosine kinase 1 in cancer. AdvBiolRegul 2012 Jan; 52:31–38.
29
30. Ohotski J, Long JS, Orange C, Elsberger B, Mallon E, Doughty J.Expression of sphingosine 1-phosphate receptor4 and sphingosine kinase 1 is associated with outcome in oestrogen receptor-negative breast cancer. Br J Cancer 2012; Apr 10; 106(8):1453-9.
30
31. French KJ,SchrecengostRS,LeeBD,ZhuangY,SmithSN,EberlyJL,YunJK,SmithCD.Discovery and evaluation of inhibitors of human sphingosine kinase.CancerRes2003; 63(18):5962-9.
31
32. Alshker H, Krell J, Frampton AE, Waxman J, BlyussO,Zaikin A. et al. Leptin induces upregulation of sphingosine kinase 1 in oestrogen receptor-negative breast cancer via Src family kinase-mediated, janus kinase 2-independent pathway. Breast Cancer Res 2014 Oct 25; 16(5):426.
32
33. Błachnio-ZabielskaAU,PułkaM,BaranowskiM,NikołajukA,ZabielskiP,Górska M.et al.Ceramidemetabolismisaffectedbyobesityanddiabetesinhumanadipose tissue.J Cell Physiol2012; 227(2):550-7.
33
34. Ruckhaberle E, Rody A, Engels K, Gaetje R, von Minckwitz G, Schiffmann S, Grosch S et al. Microarray analysis of altered sphingolipid metabolism reveals prognostic significance ofsphingosine kinase 1 in breast cancer. Breast Cancer Res Treat 2008 Nov; 112(1):41–52.
34
35. Blachnio-Zabielska AU, Pulka M, Baranowski M, Nikolajuk A, ZabielskiP,Gorska M. Ceramide metabolism is affected by obesity and diabetes in human adipose tissue. J Cell Physiol 2012 Feb; 227(2):550-7.
35
36. Miyoshi Y,FunahashiT, TanakaS, TaguchiT, TamakiY, Shimomura I et al High expression of leptin receptor mRNA in breast cancer tissue predicts poor prognosis for patients with high, but not low, serum leptin levels. Int J Cancer 2006; 118(6):1414-9.
36
37. MacciòA, MadedduC, GramignanoG, MulasC, FlorisC, Massa D et al. Correlation of body mass index and leptin with tumor size and stage of disease inhormone-dependent postmenopausal breast cancer preliminary results and the rapeuticimplications. JMol Med (Berl) 2010; 88(7):677-86.
37
38. Ishikawa M,Kitayama J, Nagawa H. Enhanced expression of leptin and leptin receptor (OB-R) in human breast cancer. Clin Cancer Res 2004; 10(13):4325-31.
38
39. Visentin B, Vekich JA, Sibbald BJ, Cavalli AL, Moreno KM, Matteo RG et al. Validation of an anti-sphingosine-1-phosphate antibody as a potential therapeutic in reducing growth, invasion, and angiogenesis in multiple tumor lineages. Cancer Cell 2006 ;9(3):225-38.
39
40. Nagahashi M, Ramachandran S, Kim EY, Alle good JC, Rashid OM, Yamada A et al.Sphingosine-1-phosphate produced by sphingosine kinase 1 promotes breast cancer progression by stimulating angiogenesis and lymphangiogenesis.CancerRes2012; 72(3):726-35.
40
41. Mukhopadhyay P, Ramanathan R, Takabe K.S1P promotes breast cancer progression by angiogenesis and lymphangiogenesis. Breast Cancer Manag2015; 4(5):241-244.
41
42. Sobue S, Lwasiki T, Suqisaki C, Nagatu K, Kikuchi R, Murakami M. QuantitativeRT-PCRanalysis of sphingolipid metabolic enzymes in acuteleukemia and myelodysplastic syndromes. Leukemia 2006 Nov; 20(11):2042-6.
42
43. Johnson KR, Johnson KY, Crellin HG, Ogretmen B, Boylan AM, Harley RA, et al. Immunohistochemical distribution of sphingosine kinase 1 in normal and tumor lung tissue. J Histochem Cytochem 2005 Sep; 53(9):1159-66.
43
44. TahaTA,KitataniK,El-Alwani M, Bielawski J, Hannun YA, Obeid LM. Loss of sphingosine kinase-1 activates the intrinsic pathway of programmed cell death: modulation of sphingolipid levels and the induction of apoptosis.FASEBJ2006; 20(3):482-4.
44
ORIGINAL_ARTICLE
Correlation of vascularization and inflammation with severity of oral leukoplakia
Background & objective: Changes in submucosal vascularization and inflammation, determined by immunohistochemistry staining, were shown to be correlated with the development of dysplasia and invasiveness of epithelial cells in premalignant and malignant lesions. This study evaluated changes in sections routinely stained with Hematoxylin and Eosin (H&E) in order to investigate vascular density and intensity of inflammatory cells infiltration during the progression of oral leukoplakia with mild dysplasia to Squamous Cell Carcinoma (SCC).The aim of the research was to determine whether changes in sub-mucosal vascularity and inflammatory infiltration of leukoplakia in routine H&E-stained sections could contribute to the assessment of severity of the lesion. Methods: In this cross-sectional, comparative and descriptive study, vascular density and inflammation intensity of 125 available samples of H&E-stained sections, consisting of 35 cases of mild and moderate dysplasia, 38 severe dysplasia and carcinoma in situ, and 52 SCC, were investigated. To analyze the data, chi-square test, Mann-Whitney test, Kruskal-Wallis test, Tukey’s post hoc test, and cumulative ordinal logistic regression were conducted. Results: There was a significantly higher vascular density in cases with severe dysplasia, in situ carcinoma, and SCC compared to those with mild to moderate dysplasia (P<0.0001). However, the difference in vascularity was not statically significant between severe dysplasia, carcinoma in situ, and SCC (P=0.78). Intensity of inflammatory cells infiltration in the underlying connective tissue was significantly different among the three groups (P<0.0001), and the highest intensity of inflammatory cells infiltration was seen in the SCC group. Conclusions: Increased submucosal vascularization and inflammatory cells infiltration can contribute further to predicting more aggressive epithelial dysplasia.
https://ijp.iranpath.org/article_25044_c3be0c4e897bc2c403995f1a72306189.pdf
2017-07-01
225
230
10.30699/ijp.2017.25044
Squamous cell carcinoma
Oral Leukoplakia
Inflammation
Blood Vessels
Fatemeh
Mashhadiabbas
fmashhadiabbas@yahoo.com
1
Dept. of Oral and Maxillofacial Pathology, Dental school, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Masoume
Fayazi-Boroujeni
fayazi_masoume@yahoo.com
2
Shahrekord University of Medical Sciences, Shahrekord, Iran
LEAD_AUTHOR
1. Warnakulasuriya S, Johnson NW, Van der Waal I. Nomenclature and classification of potentially malignant disorders of the oral mucosa. J Oral Pathol Med 2007; 36:575-580.
1
2. Regezi JA, Sciubba JJ, and Jordan RCK. Oral Pathology. 6th ed. Philadelphia USA: Elsevier Sunders. 2012: Chap. 3. 80-113.
2
3. Abbas NF, El-Sharkawy SL, Abbas EA, El-Shaer MAM. Immunohistochemical study of p53 and angiogenesis benign and preneoplastic oral lesions and oral squamous cell carcinoma. Oral Surg Oral Med Oral Pathol Oral RadiolEndod 2007; 103:385-90.
3
4. Gandolfo M, Keszler A, Lanfranchi H, Itoiz ME. Increased subepithelial vascularization and VEGF expression reveal potentially malignant changes in human oral mucosa lesions. Oral Surg Oral Med Oral Pathol Oral RadiolEndod 2011; 111(4): 486-493.
4
5. Michailidou EZ, Markopoulos AK, Antoniades DZ. Mast cells and angiogenesis in oral malignant and premalignant lesions, Open Dent J 2008; 2:126-132.
5
6. Aromando RF, Raimondi AR, Perez MA, Trivillin VA, Schwint AE, Itoiz M, Angiogenesis in potentially malignant lesions and carcinomas during experimental oral carcinogenesis:a preliminary study in the hamster cheek pouch. Anticancer Res 2014; 34(11):6381-6388.
6
7. Jin Y, Tipoe GL, White FH, Yang L. A quantitative investigation of immunocytochemically stained blood vessels in normal, benign, premalignant and malignant human oral cheek epithelium. Virchows Arch 1995; 427: 145-151.
7
8. Ribatti D, Crivellato E. Mast cells, angiogenesis and tumour growth. BiochimBiophysActa 2012; 1822: 2–8.
8
9. Macluskey M, Chandrachud LM, Pazouki S, Green M, Chisholm DM, Ogden GR, Schor SL, Schor AM. Apoptosis, proliferation and angiogenesis in oral tissues possible relevance to tumour progression. J Pathol 2000; 191(4): 368-375.
9
10. Pazouki S, Chisholm DM, Adi MM, Carmichael G, Farquharson G, Ogden GR, Schor SL, Schor AM. The association between tumour progression and vascularity in the oral mucosa. J Pathol 1997; 183(1): 39-43.
10
11. Harris MK, Oral Cancer: Causes, Diagnosis and Treatment. New York. Nova Science Publishers Inc. 2011: 253-270.
11
12. Loening T, Broemel H, Becker WM, Otto HF. Identification of inflammatory cell phenotypes in human oral carcinomas by means of monoclonal antibodies. Arch Oral Biol 1983; 28(12): 1093–1100.
12
13. Gannot G, Gannot I, Vered H, Buchner A, Keisari Y. Increase in immune cell infiltration with progression of oral epithelium from hyperkeratosis to dysplasia and carcinoma. Brit J Cancer 2002; 86: 1444-1448.
13
14. Hamidi S, Salo T, Kainulainen T, Epstein J, Lerner K, Larjava H.Expression of avb6 integrin in oral leukoplakia. Brit J Cancer 2000; 82(8): 1433–1440.
14
15. Syafriadi M, Cheng J, Jen KY, Ida-Yonemochi H, Suzuki M, Saku T. Two-phase appearance of oral epithelial dysplasia resulting from focal proliferation of parabasal cells and apoptosis of prickle cells. J Oral Pathol Med 2005; 34: 140–9.
15
16. Manchanda A, Shetty DC. Reproducibility of grading systems in oral epithelial dysplasia. Med Oral Patol Oral Cir Bucal 2012; 17(6): 935-942.
16
17. JalayerNaderi N, Semyari H, Elahinia Z. The impact of smoking on gingiva: a histopathological study. Iran J Pathol. 2015; 10(3): 214-220.
17
18. Gomes-filho J, Duarte P, Oliveria C, Watanabe S, Simonetti C. Tissue reaction to a triantibiotic paste used for endodontic self-generation of nonvital immature permanent teeth. J Endod 2012; 38(1):91-95.
18
19. Coussens LM, Werb Z. Inflammation and cancer. Nature 2002;420: 860–867.
19
20. Yu JL, Rak JW. Inflammatory and immune cells in tumor angiogenesis and arteriogenasis. Breast Cancer Res 2003; 5: 83-8.
20
21. Mor F, Quintana F J., Cohan I R. Angiogenesis-Inflammation cross talk: VEGF is secreted by activated T cells and induces Th1 polarization. Journal of immunology, 2004; 172:4618-4623.
21
ORIGINAL_ARTICLE
Expression of Apoptosis Related and Proliferative Proteins in Malignant Lympho-Proliferative Disorders
Background & objective: The current study aimed to perform an immunohistochemical analysis of patterns of apoptotic and cell proliferative related protein expression in different histological grades and immune phenotypes of malignant lymphomas and other lymphoproliferative disorders Methods:This observational study was carried on 60lymph node biopsies of lymphoproliferative disorders. The biopsies were analyzed histologically and immunohistochemically. Results:A total of 60 lymph node biopsies were included in the study, of which 81.6% were of malignant lympho-proliferative lesions. The majority of the biopsies were B-cell (66%) and were grouped in the intermediate grade. Bax and BCL-2 protein expression was presented by percentage of immune positive neoplastic cells per 10fields and graded on a scale of 1 to4. A Bcl-2, Bax Protein Ratio (BBPR) was determined for each case by dividing the estimated Bcl-2 protein (percentage of Bcl-2 positive cells x Bcl-2 staining intensity) by the estimated Bax protein (percentage of Bax positive cells x Bax immunostaining intensity). The mean BBPR was found to be significantly higher in indolent lymphomas (2.64 ± 1.3) as compared to aggressive lymphomas (0.47 ± 0.9) (P<0.01). The expression of P53 and PCNA in 35 biopsies of Non Hodgkin Lymphomas (NHL) was found to increase from low to high grade tumors. Conclusions: A significant correlation was found between BBPR and predicted biological behavior of indolent and aggressive lymphomas. This indicates the important role of Bcl-2 and Bax in biological behavior of lymphomas. Furthermore, P53 and PCNA expression were found to increase from low to high-grade tumors suggesting their prognostic value in NHL.
https://ijp.iranpath.org/article_25051_9ab586e95005b1017c5d4d3d532387a7.pdf
2017-07-01
231
240
10.30699/ijp.2017.25051
Apoptosis
Malignant lymphoproliferative
Bcl2
Bax
Zeeba
Jairajpuri
jairajpurizs@gmail.com
1
Dept. of Pathology, Hamdard Institute of Medical Sciences and Research, Jamia Hamdard, New Delhi, India
LEAD_AUTHOR
Rekha
Ghai
rekhaghai@gmail.com
2
National Institute of Pathology, Indian Council Of Medical Research, Safdarjung Hospital Complex, New Delhi India
AUTHOR
Sumita
Saluja
drssaluja@gmail.com
3
Dept. of Haematology Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India
AUTHOR
Sujala
Kapur
sujalakapur@gmail.com
4
National Institute of Pathology, Indian Council Of Medical Research, Safdarjung Hospital Complex, New Delhi India
AUTHOR
K.T
Bhowmick
bhowmik@yahoo.com
5
Dept. of Radiotherapy, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India
AUTHOR
1. Canioni D, Jabado N, MacIntyre E, Patey N, Emile JF, Brousse N. Lymphoproliferative disorders in children with primary immunodeficiency; immunological status may be more predictive of the outcome than other criteria. Histopathol2001;38:146-159.
1
2. Rizzo K, NassiriM.Diagnostic Workup of Small B Cell Lymphomas: A Laboratory Perspective Lymphoma
Volume 2012:Article ID 346084,doi:10.1155/2012/346084
2
3. Dorfman RF, Gelb AB, Hendrickson MR. Composite lymphoma Am J Pathol 1992; 40: 959-76
3
4. Kerr JFR, Winterford CM, Harmon BV. Apoptosis. –Its significance in cancer and cancer therapy. Cancer 1994; 73:2013-26.
4
5. Anderson MA, Huang D,RobertsA. Targeting BCL2 for the Treatment of Lymphoid Malignancies. SeminHematol 2014; 51:219–227.
5
6. Gaulard P, Agay MF, M. Peuchmaur, N Brousse, C. Gisselbrecht, P. Solal-Celignyet al. Bcl-2 expression in diffuse aggressive lymphoma. Am J Pathol 1992; 140:1089-95.
6
7. Wheaton S, Netser J, Guinee D, Rahn M, Perkins S.BCL-2 and Bax protein expression and indolent versus aggressive B-cell non- Hodgkin’s lymphomas. Human Pathology 1998;29: 820-25.
7
8. Korsemeyer SJ, Shutter JR, Veis DJ, Merry DE, Oltvai ZN. BCL-2 / Bax: a rheostat that regulates an antioxidant pathway and cell death. Semin Cancer Biol. 1993; 4: 327-32.
8
9. Sahu SK, Choudhuri T. Lack of Association between Bax Promoter (-248G>A) Single Nucleotide Polymorphism and Susceptibility towards Cancer: Evidence from a Meta-Analysis. PLoS ONE 2013; 8(10): e77534. doi:10.1371/journal.pone.0077534
9
10. Soiniy Y, Paakko P. Apoptosis and ex-pression of caspases 3, 6 and 8 in malignant non- Hodkins lymphomas. APMIS. 1999;107: 1043- 50.
10
11. Oltavi ZN, Millman CL & Korsmeyer SJ.Bcl-2 heterodimers in vivo with a conserved homologue, Bax, that accelerates programmed cell death. 1993.Cell;74 :609–619.
11
12. M R. Hussein, TM Al-SabaeMarcelle, N. Georgis. Analysis of the Bcl-2 and p53 Protein Expression
in the LymphoproliferativeLesions in the Upper Egypt. Cancer Biology & Therapy 2005;4: 324-28.
12
13. Gascoyne RD, Krajewska M, Krajewski S, Connors JM, Reed JC . Prognostic significance of Bax protein expression in diffuse agressive non-Hodkin’ s lymphoma. Blood. 1997; 90: 3173-8
13
14. Winter JNN, Andersen J, Reed JC,KrajewskiS,Variakojis D, Bauer KDet.al. Bcl-2 expression correlates with lower proliferative activity in the intermediate-and high grade non- Hodkins lymphomas: an Eastern Cooperative Oncology group and southwest Oncology group cooperative laboratory study. Blood. 1998; 91: 1391-8.
14
15. Flora Tzifi, Christina Economopoulou, DimitriosGourgiotis, AlexandrosArdavanis,SotiriosPapageorgiou,AndreasScorilas. The Role of BCL2 Family of Apoptosis Regulator Proteins in Acute and Chronic Leukemias. Advances in Hematology
Volume 2012, Article ID 524308, 15 pages
15
16. El-Esawy, B. H. The Immunohistochemistry Based Evaluation of Bcl-2 in B Non Hodgkin lymphoma & Its Prognostic Significance. Life Sci J 2013;10: 3290-3295
16
17. NY Samuel, Matthew S. Davids. Selective Bcl-2 Inhibition to Treat Chronic Lymphocytic Leukemia and Non-Hodgkin Lymphoma. Clinical Advances in Hematology & Oncology 2014;12: 224-29.
17
18. CD Goia, AR Lupu, C Bleotu, C Antipa, Lvelt, E Popa, G Constantinescu, Correlation Between Pro- And Anti-Apoptotic Gene Expression And Telomerase Activity In B- Cell Lymphomas. Proc. Rom. Acad2008;3:169–174
18
19. Charalambous GK, Gomatos IP, Konstadoulakis MM, MessarisEG, Manouras AJ,
Apostolou AE et.al. Protein expression of bax, bcl-2, and p53 in patients with nonHodgkin’s gastric lymphoma: Prognostic significance. World J Surg 2000; 24:608-14.
19
20. Burra U, Shanthi P, Krishnan KB, Madhavan M. P 53 and PCNA in Non Hodgkin’s lymphoma—an immunohistochemical evaluation. Indian J PatholMicrobiol 2000; 43:61-4.
20
21. Miyashita T, Harigai M, Hanada M, Reed JC. Identification of a p53-dependent negative response element in the bcl-2 gene. Cancer Res 1994; 54:3131-5.
21
22. Korkolopoulou P, Oates J, Kittas C, Crocker J. P-53, c-myc, P-62 and proliferating cell nuclear antigen (PCNA) expression in no Hodgkin’s lymphomas. J Clin Pathol.1994; 47: 9-14.
22
23. Rabenhorst SH, Burini RC, Schmitt FC. Proliferating cell nuclear antigen (PCNA) in non-Hodgkin's lymphomas: correlation with working formulation and Kiel classification in formalin-fixed paraffin-embedded material. Pathology. 1996; 28:12-6.
23
24. Marafioti T, Hummel M, Foss HD, Laumen H, Korbjuhn P, Ioannis A.et al: Hodgkin and Reed-Sternberg cells represent an expansion of a single clone originating from a germinal center B-cell with functional immuno- globulin gene rearrangements but defective immunoglobulin transcription. Blood 2000;95:1443-50.
24
25. Garcia JF, Camacho FI, MorenteM,Fraga M, Montalban C, Alvaro T.et.al. Hodgkin and Reed-Sternberg cells harbor alterations in the major tumor suppressor pathways and cell-cycle checkpoints: Analyses using tissue microarrays. Blood 2003;101:681-689
25
26. SJ. Sup, C A. Aleman ̃y, B Pohlman, P Elson, S Malhi, SThakkar. Expression of bcl-2 in Classical Hodgkin’s Lymphoma: An Independent Predictor of Poor Outcome. J ClinOncol 2005;23:3773-79.
26
27. EDerenzin,AYounes. Predicting treatment outcome in classical Hodgkin lymphoma: genomic advances. Genome Medicine 2011, 3:26
27
28. Brousset P, Benharroch D, Krajewski S, Laurent G, Meggetto F, Rigal-Huguet F.et.al. Frequent expression of cell death inducing gene Bax in Reed Sternberg cells of Hodgkin’s disease. Blood 1996; 87: 2470-5.
28
29. KanavarosP, Stefanaki K, Viachonikolis J. Expression of P-53, P-21 / Waf1, BCL-2, Bax, Rb and Ki67 proteins in Hodgkin’s lymphomas. Histopathol 2000;15: 445-53.
29
30. Smolewski P, Niewiadomska H, Blonski JZ, Robak T, Krykowski E.et.al. Expression of proliferating cell nuclear antigen (PCNA) and P-53, BCL-2 or C-erb B -2 proteins on Reed Sternberg cells: prognostic significance in Hodgkin’s disease. Neoplasma.1998; 45: 140-7.
30
ORIGINAL_ARTICLE
Basic Characteristics of Oligodendrogliomas: The Shohada-e Tajrish Hospital Experience (2008-2014)
Background and Objectives: Gliomas are the most prevalent subgroup of primary brain tumors with a relatively high mortality. However, oligodendrogliomas have a better prognosis compared to other subtypes due to their sensitivity to chemotherapy. Considering the low incidence and the resulting lack of information about oligodendrogliomas, particularly in Iran, this study aimed at assessing their basic characteristics. Methods:In this descriptive retrospective study, patients with definite diagnosis of oligodendroglioma were identified by reviewing the archives of pathology reports at the department of pathology of Shohada-e Tajrish Hospital during years 2008 to 2014. Age, gender, location, and the grade of the tumor were extracted and entered to the SPSS statistical software for analysis. Results: A total of 182 patients, including 115 males (63.2%) and 67 females (36.8%), were included with a mean age of 38.5±13.36 years. Frontal lobe was involved in 53 patients (29.1%), parietal lobe in 31 (17.0%), temporal lobe in 22 (12.1%), frontoparietal area in 15 (8.2%), parieto-occipital area in 11 (6.0%), temporoparietal and frontotemporal areas each in 9 subjects (4.9%), occipital lobe in 5 (2.7%), and the brainstem in 4 (2.2%). Furthermore, 108 cases (59.3%) had grade-2 and the remaining74 patients (40.7%) had grade-3 anaplastic oligodendrogliomas. The mean age of subjects with brainstem oligodendrogliomas was significantly lower than the other patients (p=0.025). Conclusion: Oligodendrogliomas commonly effects the frontal lobe, followed by the parietal and temporal lobes. The mean age of subjects with brainstem lesions was significantly lower than other patients. Age, gender or location of the tumor did not independently predict a higher grade lesion.
https://ijp.iranpath.org/article_25050_2537827a5dd7e7d2e3e8979e38d2ec37.pdf
2017-07-01
241
247
10.30699/ijp.2017.25050
Oligodendrogliomas
Central nervous system
Location
Grade
age
Mahsa
Ahadi
mahsaamehr@yahoo.com
1
Cancer Research Center, Shohada-e Tajrish Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Afshin
Moradi
afshinmo2002@gmail.com
2
Cancer Research Center, Shohada-e Tajrish Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Azadeh
Rakhshan
azadehrakhshan@yahoo.com
3
Cancer Research Center, Shohada-e Tajrish Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Alireza
Arefian
alireza.arefian@hotmail.com
4
Cancer Research Center, Shohada-e Tajrish Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Mitra
Rafizadeh
m.rafiezadeh@yahoo.com
5
Cancer Research Center, Shohada-e Tajrish Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Hanieh
Zham
zhamhanieh@gmail.com
6
Cancer Research Center, Shohada-e Tajrish Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
1. Allison RR, Schulsinger A, Vongtama V, Barry T, Shin KH. Radiation and chemotherapy improve outcome in oligodendroglioma. IJROBP. 1997;37(2):399-403.
1
2. Karim AB, Afra D, Cornu P, Bleehan N, Schraub S, De Witte O, et al. Randomized trial on the efficacy of radiotherapy for cerebral low-grade glioma in the adult: European Organization for Research and Treatment of Cancer Study 22845 with the Medical Research Council study BRO4: an interim analysis. IJROBP. 2002;52(2):316-24.
2
3. Ellis TL, Stieber VW, Austin RC. Oligodendroglioma. Curr Treat Options Oncol. 2003;4(6):479-90.
3
4. Engelhard HH, Stelea A, Mundt A. Oligodendroglioma and anaplastic oligodendroglioma:: Clinical features, treatment, and prognosis. Surg Neurol. 2003;60(5):443-56.
4
5. Van den Bent M, Taphoorn M, Brandes Aa, Menten J, Stupp R, Frenay M, et al. Phase II study of first-line chemotherapy with temozolomide in recurrent oligodendroglial tumors: the European Organization for Research and Treatment of Cancer Brain Tumor Group Study 26971. J Clin Oncol. 2003;21(13):2525-8.
5
6. Fleury A, Menegoz F, Grosclaude P, Daures JP, Henry‐Amar M, Raverdy N, et al. Descriptive epidemiology of cerebral gliomas in France. Cancer. 1997;79(6):1195-202.
6
7. Van den Bent M. Advances in the biology and treatment of oligodendrogliomas. Curr Opin Neurol. 2004;17(6):675-80.
7
8. Hashimoto N, Murakami M, Takahashi Y, Fujimoto M, Inazawa J, Mineura K. Correlation between genetic alteration and long‐term clinical outcome of patients with oligodendroglial tumors, with identification of a consistent region of deletion on chromosome arm 1p. Cancer. 2003;97(9):2254-61.
8
9. Jacob R, Jyothirmayi R, Dalal Y, Nambiar U, Rajan B, Nair M. Oligodendroglioma: clinical profile and treatment results. Neurol India. 2002;50(4):462.
9
10. HELSETH A, MØRK SJ, JOHANSEN A, TRETLI S. Neoplasms of the central nervous system in Norway. APMIS. 1989;97(7‐12):646-54.
10
11. Nutt CL, Mani D, Betensky RA, Tamayo P, Cairncross JG, Ladd C, et al. Gene expression-based classification of malignant gliomas correlates better with survival than histological classification. Cancer Res. 2003;63(7):1602-7.
11
12. Peterson K, Cairncross JG. Oligoden-droglioma. Cancer Invest. 1996;14(3):243-51.
12
13.Kleihues P, Cavenee WK. Pathology and genetics of tumours of the nervous system: International Agency for Research on Cancer; 2000.
13
14.Celli P, Nofrone I, Palma L, Cantore G, Fortuna A. Cerebral oligodendroglioma: prognostic factors and life history. Neurosurgery. 1994;35(6):1018-35.
14
15. Daumas-Duport C, Varlet P, Tucker M-L, Beuvon F, Cervera P, Chodkiewicz J-P. Oligodendrogliomas. Part I: Patterns of growth, histological diagnosis, clinical and imaging correlations: a study of 153 cases. J Neurooncol. 1997;34(1):37-59.
15
16.Engelhard HH, Stelea A, Cochran EJ. Oligodendroglioma: pathology and molecular biology. Surg Neurol. 2002;58(2):111-7.
16
17. Paleologos NA, Cairncross JG. Treatment of oligodendroglioma: an update. Neuro Oncol. 1999;1(1):61-8.
17
18.Louis DN, Ohgaki H, Wiestler OD, Cavenee WK, Burger PC, Jouvet A, et al. The 2007 WHO classification of tumours of the central nervous system. Acta Neuropathol. 2007;114(2):97-109.
18
19.Feigenberg SJ, Amdur RJ, Morris CG, Mendenhall WM, Marcus Jr RB, Friedman WA. Oligodendroglioma: does deferring treatment compromise outcome? Am J Clin Oncol. 2003;26(3):e60-e6.
19
20.Fortin D, Cairncross GJ, Hammond RR. Oligodendroglioma: an appraisal of recent data pertaining to diagnosis and treatment. Neurosurgery. 1999;45(6):1279.
20
21.Sunyach M, Pommier P, Lafay IM, Guyotat J, Ginestet G, Jouanneau E, et al. Conformal irradiation for pure and mixed oligodendroglioma: the experience of Centre Leon Berard Lyon. IJROBP. 2003;56(1):296-303.
21
22. Shaw EG, Scheithauer BW, O'Fallon JR, Tazelaar HD, Davis DH. Oligodendrogliomas: the Mayo clinic experience. J Neurosurg. 1992;76(3):428-34.
22
23. SPSS I. IBM SPSS statistics 22. Algorithms Chicago: IBM SPSS Inc. 2013.
23
24. Nielsen MS, Christensen HC, Kosteljanetz M, Johansen C. Incidence of and survival from oligodendroglioma in Denmark, 1943–2002. Neuro Oncol. 2009;11(3):311-7.
24
25. Mørk SJ, Lindegaard K-F, Halvorsen TB, Lehmann EH, Solgaard T, Hatlevoll R, et al. Oligodendroglioma: incidence and biological behavior in a defined population. J Neurosurg. 1985;63(6):881-9.
25
26. Chin HW, Hazel JJ, Kim TH, Webster JH. Oligodendrogliomas I. A clinical study of cerebral oligodendrogliomas. Cancer. 1980;45(6):1458-66.
26
27.Reyes-Botero G, Mokhtari K, Martin-Duverneuil N, Delattre J-Y, Laigle-Donadey F. Adult brainstem gliomas. The oncologist. 2012;17(3):388-97.
27
ORIGINAL_ARTICLE
Comparison of Interferon-Gamma (IFNG) +874 T/A Single Nucleotide Polymorphism in Hepatitis C Virus Infected Patients and Non-Infected Controls in Mashhad, Iran
Background and Objectives: Interferon-gamma is an important cytokine, which facilitates immunity against intracellular pathogens. Several factors, including genetic variations of cytokine-producing genes have been shown to influence the progression and severity of Hepatitis C virus (HCV) infection. Methods: Between January and December 2012, 87 HCV-infected individuals and 89 individuals without HCV infection were recruited for the study of Single Nucleotide Polymorphism (SNP) at Interferon Gamma (IFNG) +874 T/A. After extraction of genomic DNA from Peripheral Blood Mononuclear Cells (PBMCs) in blood sample of the individuals, Amplification Refractory Mutation System (ARMS) polymerase chain reaction was performed to evaluate the SNP at this position. Results: The frequency of genotype TA was 62.1% in the HCV-infected group, while it was 47.2% for the control group (p=0.033). However, after adjusting for confounders (including alcohol consumption, drug addiction, transfusion, and tattoos), the genotypes at this position did not show any statistically significant association with HCV infection (adjusted P values were above 0.05). The frequency of allele A was slightly higher in patients than the controls (55.2% versus 48.3%).Carriers of A allele were more frequent in patients with HCV infection compared to the control group (55.17% in patients versus 48.31% in the control group; P=0.02). However, after adjustment for confounders, the results were no longer statistically significant (P=0.2). Conclusion: A carrier status for certain alleles and genotypes at Interferon Gamma (IFNG) +874 T/A may lead to higher susceptibility to HCV infection in a certain population.
https://ijp.iranpath.org/article_25046_d601b9dcfa93371eb8aabba7f426fbee.pdf
2017-07-01
248
256
10.30699/ijp.2017.25046
Interferon-gamma
single nucleotide polymorphism
Hepatitis C Virus
Sina
Rostami
sin.fum@gmail.com
1
Dept. of Laboratory Medicine, Children's and Women's Health, NTNU - Norwegian University of Science and Technology, NO-7491 Trondheim, Norway
AUTHOR
Alireza
Pasdar
pasdara@mums.ac.ir
2
Dept. of Modern Sciences and Technologies, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Sina
Gerayli
sina.gerayli@gmail.com
3
Dept. of Biology, University of Western Ontario, London, Ontario N6A5BF, Canada
AUTHOR
Hamed
Hatami
hatamih911@mums.ac.ir
4
Dept. of Immunology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Samaneh
Sepahi
sepahis931@mums.ac.ir
5
Targeted Drug Delivery Research Centre, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Fatemeh
Nategh
f_nategh@yahoo.com
6
Applied Biotechnology Research Center, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran
AUTHOR
Mojtaba
Meshkat
mesh6280@gmail.com
7
Islamic Azad University, Mashhad Branch, Mashhad, Iran
AUTHOR
Seyed Mousalreza
Hoseini
hoseinimr@mums.ac.ir
8
Dept. of Internal Medicine, Qaem Hospital, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mitra
Ahadi
ahadim@mums.ac.ir
9
Dept. of Internal Medicine, Qaem Hospital, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Hamid Reza
Sima
simahr@mums.ac.ir
10
Dept. of Internal Medicine, Imam Reza Hospital, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Hasan
Vosughinia
vosoghiniah@mums.ac.ir
11
Dept. of Internal Medicine, Imam Reza Hospital, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mohammad Reza
Sarvghad
sarvghadmr@mums.ac.ir
12
Dept. of Infectious Diseases, Imam Reza Hospital, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Abbas
Esmaeelzade
esmaeelzadeha@mums.ac.ir
13
Dept. of Internal Medicine, Qaem Hospital, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Hosein
Nomani
nomanih1@mums.ac.ir
14
Antimicrobial Resistance Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Homan
Mosanan Mozafari
mozaffarih@mums.ac.ir
15
Dept. of Internal Medicine, Qaem Hospital, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Fariba
Rezai Talab
rezaitalabf@mums.ac.ir
16
Dept. of Internal Medicine, Imam Reza Hospital, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mohammad Taghi
Shakeri
shakerimt@mums.ac.ir
17
Dept. of Biostatistics, Public Health School, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Zahra
Meshkat
meshkatz@mums.ac.ir
18
Antimicrobial Resistance Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1. Lavanchy D. Evolving epidemiology of hepatitis C virus. Clinical Microbiology and Infection. 2011;17(2):107-15.
1
2. Hajarizadeh B, Grebely J, Dore GJ. Epidemiology and natural history of HCV infection. Nat Rev Gastroenterol Hepatol. 2013 09//print;10(9):553-62.
2
3.Kolls JK, Szabo G. The genetics of hepatitis C virus underlie its ability to escape humoral immunity. Journal of Clinical Investigation. 2015;125(1):97.
3
4. Brenndörfer ED, Sällberg M. Hepatitis C virus-mediated modulation of cellular immunity. Archivum immunologiae et therapiae experimentalis. 2012;60(5):315-29.
4
5. Koziel MJ, editor Cytokines in viral hepatitis2008: © 1999 by Thieme Medical Publishers, Inc.
5
6. Hold GL, Untiveros P, Saunders KA, El-Omar EM. Fibrogenesis & Tissue Repair. 2009;2(6).
6
7. Awad MR, El-Gamel A, Hasleton P, Turner DM, Sinnott PJ, Hutchinson IV. Genotypic variation in the transforming growth factor-[beta] 1 gene: association with transforming growth factor-[beta] 1 production, fibrotic lung disease, and graft fibrosis after lung transplantation. Transplantation. 1998;66(8):1014-20.
7
8. Fishman D, Faulds G, Jeffery R, Mohamed-Ali V, Yudkin JS, Humphries S, et al. The effect of novel polymorphisms in the interleukin-6 (IL-6) gene on IL-6 transcription and plasma IL-6 levels, and an association with systemic-onset juvenile chronic arthritis. Journal of Clinical Investigation. 1998;102(7):1369-76.
8
9. Sun Y, Lu Y, Li T, Xie L, Deng Y, Li S, et al. Interferon Gamma+ 874T/A Polymorphism Increases the Risk of Hepatitis Virus-Related Diseases: Evidence from a Meta-Analysis. PloS one. 2015;10(5):e0121168.
9
10. Castelli JC, Hassel BA, Wood KA, Li X-L, Amemiya K, Dalakas MC, et al. A study of the interferon antiviral mechanism: apoptosis activation by the 2–5A system. The Journal of experimental medicine. 1997;186(6):967-72.
10
11. Goodbourn S, Didcock L, Randall R. Interferons: cell signalling, immune modulation, antiviral response and virus countermeasures. Journal of General Virology. 2000;81(10):2341-64.
11
12. Huang Y, Chen XC, Konduri M, Fomina N, Lu J, Jin L, et al. Mechanistic link between the anti‐HCV effect of interferon gamma and control of viral replication by a ras‐MAPK signaling cascade. Hepatology. 2006;43(1):81-90.
12
13. Carlo-Stella N, Badulli C, De Silvestri A, Bazzichi L, Martinetti M, Lorusso L, et al. A first study of cytokine genomic polymorphisms in CFS: Positive association of TNF-857 and IFNgamma 874 rare alleles. Clinical and experimental rheumatology. 2006;24(2):179-82.
13
14. Lalor PF, Shields P, Grant AJ, Adams DH. Recruitment of lymphocytes to the human liver. Immunology and cell biology. 2002;80(1):52-64.
14
15. Pravica V, Perrey C, Stevens A, Lee JH, Hutchinson IV. A single nucleotide polymorphism in the first intron of the human IFN-γ gene:: Absolute correlation with a polymorphic CA microsatellite marker of high IFN-γ production. Human immunology. 2000;61(9):863-6.
15
16. Makhatadze NJ. Tumor necrosis factor locus: genetic organisation and biological implications. Human immunology. 1998;59(9):571-9.
16
17. Smith A, Humphries SE. Cytokine and cytokine receptor gene polymorphisms and their functionality. Cytokine & growth factor reviews. 2009;20(1):43-59.
17
18. Frese M, Schwärzle V, Barth K, Krieger N, Lohmann V, Mihm S, et al. Interferon‐γ inhibits replication of subgenomic and genomic hepatitis C virus RNAs. Hepatology. 2002;35(3):694-703.
18
19.Lanford RE, Guerra B, Lee H, Averett DR, Pfeiffer B, Chavez D, et al. Antiviral effect and virus-host interactions in response to alpha interferon, gamma interferon, poly (i)-poly (c), tumor necrosis factor alpha, and ribavirin in hepatitis C virus subgenomic replicons. Journal of virology. 2003;77(2):1092-104.
19
20.Napoli J, Bishop G, McCaughan G. Increased intrahepatic messenger RNA expression of interleukins 2, 6, and 8 in human cirrhosis. Gastroenterology. 1994;107(3):789-98.
20
21.Bonilla N, Barget N, Andrieu M, Roulot D, Letoumelin P, Grando V, et al. Interferon gamma‐secreting HCV‐specific CD8+ T cells in the liver of patients with chronic C hepatitis: relation to liver fibrosis–ANRS HC EP07 study*. Journal of viral hepatitis. 2006;13(7):474-81.
21
22. Afshari R, Nomani H, Zaniani FR, Nabavinia MS, Mirbagheri Z, Meshkat M, et al. Genotype distribution of hepatitis C virus in Khorasan Razavi Province, Iran. Turkish Journal of Medical Sciences. 2014;44(4):656-60.
22
23.Ohno O, Mizokami M, Wu R, Saleh M, Ohba K, E O, et al. New hepatitis C virus (HCV) genotyping system that allows for identification of HCV genotypes 1a, 1b, 2a, 2b, 3a, 3b, 4, 5a, and 6a. J Clin Microbiol. 1997;35:201-7.
23
24. Shakeri MT, Nomani H, Mobarhan MG, Sima HR, Gerayli S, Shahbazi S, et al. The prevalence of hepatitis C virus in mashhad, iran: a population-based study. Hepatitis Monthly. 2013;13(3).
24
25. Afshari R, Nomani H, Zaniani FR, Nabavinia MS, Mirbagheri Z, Meshkat M, et al. Genotype distribution of hepatitis C virus in Khorasan Razavi Province, Iran. Turkish Journal of Medical Sciences. 2014;44.
25
26.Wang X-H, Netski DM, Astemborski J, Mehta SH, Torbenson MS, Thomas DL, et al. Progression of fibrosis during chronic hepatitis C is associated with rapid virus evolution. Journal of virology. 2007;81(12):6513-22.
26
27. Hu SX, Kyulo NL, Xia VW, Hillebrand DJ, Hu K-Q. Factors associated with hepatic fibrosis in patients with chronic hepatitis C: a retrospective study of a large cohort of US patients. Journal of clinical gastroenterology. 2009;43(8):758-64.
27
28.Hoffmann SC, Stanley EM, Cox ED, DiMercurio BS, Koziol DE, Harlan DM, et al. Ethnicity greatly influences cytokine gene polymorphism distribution. American Journal of Transplantation. 2002;2(6):560-7.
28
29. Lloyd AR, Jagger E, Post JJ, Crooks L-A, Rawlinson WD, Hahn YS, et al. Host and viral factors in the immunopathogenesis of primary hepatitis C virus infection. Immunology and cell biology. 2007;85(1):24-32.
29
30. Lechmann M, Woitas RP, Langhans B, Kaiser R, Ihlenfeldt HG, Jung G, et al. Decreased frequency of HCV core-specific peripheral blood mononuclear cells with type 1 cytokine secretion in chronic hepatitis C. Journal of hepatology. 1999;31(6):971-8.
30
31. Perrey C, Pravica V, Sinnott PJ, Hutchinson IV. Genotyping for polymorphisms in interferon-γ, interleukin-10, transforming growth factor-β1 and tumour necrosis factor-α genes: a technical report. Transplant Immunology. 1998;6(3):193-7.
31
32. Albuquerque MCd, Aleixo ALQdC, Benchimol EI, Leandro ACCS, Neves LBd, Vicente RT, et al. The IFN-³+ 874T/A gene polymorphism is associated with retinochoroiditis toxoplasmosis susceptibility. Memórias do Instituto Oswaldo Cruz. 2009;104(3):451-5.
32
33.Karaoglan I, Pehlivan S, Namiduru M, Pehlivan M, Kilinçarslan C, Balkan Y, et al. TNF-alpha, TGF-beta, IL-10, IL-6 and IFN-gamma gene polymorphisms as risk factors for brucellosis. New Microbiol. 2009;32(2):173-8.
33
34.Tso H, Ip W, Chong W, Tam C, Chiang A, Lau Y. Association of interferon gamma and interleukin 10 genes with tuberculosis in Hong Kong Chinese. Genes and Immunity. 2005;6(4):358-63.
34
35.Kerr J, McCoy M, Burke B, Mattey D, Pravica V, Hutchinson I. Cytokine gene polymorphisms associated with symptomatic parvovirus B19 infection. Journal of clinical pathology. 2003;56(10):725-7.
35
36.Cheong JY, Cho SW, Chung SG, Lee JA, Yeo M, Wang HJ, et al. Genetic polymorphism of interferon-γ, interferon-γ receptor, and interferon regulatory factor-1 genes in patients with hepatitis B virus infection. Biochemical genetics. 2006;44(5-6):246-55.
36
37. Karatayli S, Ulger Z, Ergul A, Keskin O, Karatayli E, Albayrak R, et al. Tumour necrosis factor‐alpha, interleukin‐10, interferon‐gamma and vitamin D receptor gene polymorphisms in patients with chronic hepatitis delta. Journal of viral hepatitis. 2014;21(4):297-304.
37
38.Gao Q-J, Liu D-W, Zhang S-Y, Jia M, Wang L-M, Wu L-H, et al. Polymorphisms of some cytokines and chronic hepatitis B and C virus infection. World journal of gastroenterology: WJG. 2009;15(44):5610-9.
38
39.Dai C-Y, Chuang W-L, Chang W-Y, Chen S-C, Lee L-P, Hsieh M-Y, et al. Polymorphisms in the interferon-γ gene at position+ 874 in patients with chronic hepatitis C treated with high-dose interferon-α and ribavirin. Antiviral research. 2005;67(2):93-7.
39
40.Sarvari J, Norozian H, Fattahi MR, Pirbonyeh N, Moattari A. The Role of Interferon Gamma Gene Polymorphism (+ 874A/T,+ 2109A/G, and-183G/T) in Response to Treatment Among Hepatitis C Infected Patients in Fars Province, Southern Iran. Hepatitis Monthly. 2014;14(1).
40
41.Dai C-Y, Chuang W-L, Hsieh M-Y, Lee L-P, Hou N-J, Chen S-C, et al. Polymorphism of interferon–gamma gene at position+ 874 and clinical characteristics of chronic hepatitis C. Translational Research. 2006;148(3):128-33.
41
42.Ben-Ari Z, Pappo O, Druzd T, Sulkes J, Klein T, Samra Z, et al. Role of cytokine gene polymorphism and hepatic transforming growth factor β1 expression in recurrent hepatitis C after liver transplantation. Cytokine. 2004;27(1):7-14.
42
43. Bouzgarrou N, Hassen E, Farhat K, Bahri O, Gabbouj S, Maamouri N, et al. Combined analysis of interferon-γ and interleukin-10 gene polymorphisms and chronic hepatitis C severity. Human immunology. 2009;70(4):230-6.
43
44. Huang Y, Yang H, Borg BB, Su X, Rhodes SL, Yang K, et al. A functional SNP of interferon-γ gene is important for interferon-α-induced and spontaneous recovery from hepatitis C virus infection. Proceedings of the National Academy of Sciences. 2007;104(3):985-90.
44
45. Frodsham AJ, Zhang L, Dumpis U, Taib NAM, Best S, Durham A, et al. Class II cytokine receptor gene cluster is a major locus for hepatitis B persistence. Proceedings of the National Academy of Sciences. 2006;103(24):9148-53.
45
ORIGINAL_ARTICLE
Evaluation of Association Between the Serum Levels of MMP-9 and MMP-9/TIMPs With Soluble Forms of Selectins and Itching Induced by Sulfur Mustard
Background & objective: Pruritus is the most frequent chronic dermal complication of sulfur mustard (SM), which negatively influences the quality of life. Exact pathophysiology of SM-induced itching is unknown. The current study aimed at evaluating the possible association between SM-induced itching and the serum levels of matrix metalloproteinase (MMP)-9 and their endogenous inhibitors, and serum levels of soluble forms of selectins (sL-, sP-, and sE-selectins) as adhesion molecules involved in the development of different inflammatory reactions. Methods: Serum levels of MMP-9, MMP-9/ tissue inhibitors of metalloproteinases (TIMPs), and selectins were measured by the enzyme-linked immunosorbent assay (ELISA), and compared between the groups (n=368) with and without itching, and matched control groups (n=126). Results: Serum levels of MMP-9 were significantly higher in the SM exposed group with itching, compared with that of the group without itching (medians: 894 and 624 pg/mL respectively; P-value =0.034). There was no relationship between the serum levels of MMP-9/TIMP-1, MMP-9/TIMP-2, MMP-9/TIMP-4, and itching in the patients exposed to SM. Median serum levels of sE- and sL-selectins in the exposed group with itching were higher than those of the exposed group without itching. These differences were statistically insignificant (P-values =0.084 and 0.095, respectively). Conclusion: According to the results of the current study, the increased serum levels of MMP-9 and selectins 20 years after exposure may play role in the pathogenesis and persistence of SM-induced itching in the exposed individuals.
https://ijp.iranpath.org/article_25646_79aae9948481ca0ccf4be0736da1ae93.pdf
2017-07-01
257
264
10.30699/ijp.2017.25646
Mustard Gas
Pruritus
MMP-9
MMP-9/TIMPs
Selectins
Nayere
Askari
askari.nr@gmail.com
1
Dept. of Biology, Faculty of Basic Sciences, Shahid Bahonar University of Kerman, Kerman, Iran
AUTHOR
Tooba
Ghazanfari
tghazanfari@yahoo.com
2
Immunoregulation Research Center, Shahed University, Tehran, Iran
LEAD_AUTHOR
Mohammad Mehdi
Naghizadeh
mmnaghi2@yahoo.com
3
Immunoregulation Research Center, Shahed University, Tehran, Iran
AUTHOR
Athar
Moin
si812003@yahoo.com
4
Immunoregulation Research Center, Shahed University, Tehran, Iran
AUTHOR
Ali
Khamesipour
khamesipour@tums.ac.ir
5
Center for Research and Training in Skin Diseases and Leprosy, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Shahryar
Pourfarzam
shahr773@hotmail.com
6
Immunoregulation Research Center, Shahed University, Tehran, Iran
AUTHOR
Zuhair Mohammad
Hassan
hasan_zm@modares.ac.ir
7
Dept. of Immunology, Tarbiat Moddares University, Tehran, Iran
AUTHOR
1. Moin A, Ghazanfari T, Davoudi SM, Emadi N, Panahi Y, Hassan ZM, et al. Long-term skin findings of sulfur mustard exposure on the civilians of Sardasht, Iran. Toxin Reviews. 2009;28(1):24-9.
1
2. Fekri A. Late cutaneous complications in chemical warfare victims in Kerman province. Journal of Kerman University of Medical Sciences. 1995;2(3):108-19.
2
3. Toosi P, Amir jA, Heydarian M, Keshvarz S, Fayaz M. Delayed Cutaneous complications in soldiers attacked by chemical agents. Pejouhandeh. 2002;7:209–12.
3
4. Hefazi M, Maleki M, Mahmoudi M, Tabatabaee A, Balali‐Mood M. Delayed complications of sulfur mustard poisoning in the skin and the immune system of Iranian veterans 16–20 years after exposure. International journal of dermatology. 2006;45(9):1025-31.
4
5. Heidari M, Karaminejad Ranjbar M, Ansari H. Prevalence of late toxic complication in chemical warfare victims. Daneshvar Medicine, Scientific Research Journal of Shahed University. 1999;7:67-72.
5
6. Greaves M. Pruritus. In: Bolognia JL, Jorizzo J, Rapini R, eds. Dermatology Edinburgh: Mosby. 2003:pp. 85-90.
6
7. William J, Berger T, Elston D. Andrews' diseases of the skin. 10 ed.: Philadelphia: WB Saunders; 2006.
7
8. Norton S. The skin in bioterrorism and biologic warfare. In: Wolff K, Goldsmith LA, Katz SI, Glchrest BA, Paller AS, Leffell DJ, eds. 7th ed.: New York: McGraw Hill; 2008.
8
9. Lateef F. Of pruritus and terrorism. Singapore Med J. 2007;48(5):380-2.
9
10. Potenzieri C, Undem BJ. Basic mechanisms of itch. Clin Exp Allergy. 2012;42(1):8-19.
10
11. Heyl T. Brachioradial pruritus. Archives of dermatology. 1983;119(2):115-6.
11
12. Moin A, Khamesipour A, Hassan ZM, Ebtekar M, Davoudi SM, Vaez-Mahdavi MR, et al. Pro-inflammatory cytokines among individuals with skin findings long-term after sulfur mustard exposure: Sardasht-Iran Cohort Study. Int Immunopharmacol. 2013;17(3):986-90.
12
13. Roosterman D, Goerge T, Schneider SW, Bunnett NW, Steinhoff M. Neuronal control of skin function: the skin as a neuroimmunoendocrine organ. Physiological reviews. 2006;86(4):1309-79.
13
14. Dziankowska-Bartkowiak B, Waszczykowska E, Żebrowska A. The role of metaloproteinases and their inhibitors in the patomechanism of skin diseases. Alerg Astma Immun. 2004;9:71-9.
14
15. Groneberg D, Bester C, Grützkau A, Serowka F, Fischer A, Henz B, et al. Mast cells and vasculature in atopic dermatitis–potential stimulus of neoangiogenesis. Allergy. 2005;60(1):90-7.
15
16. Fakhoury H, Hillarby M, Weiss J. Increased gelatinase activity in systemic sclerosis dermal fibroblast cultures with unaltered gelatinase A mRNA expression. Journal of dermatological science. 2002;29(1):62-9.
16
17. Suomela S, Kariniemi AL, Snellman E, Saarialho‐Kere U. Metalloelastase (MMP‐12) and 92‐kDa gelatinase (MMP‐9) as well as their inhibitors, TIMP‐1 and‐3, are expressed in psoriatic lesions. Experimental dermatology. 2001;10(3):175-83.
17
18. Suomela S, Kariniemi A-L, Impola U, Karvonen S-L, Snellman E, Uurasmaa T, et al. Matrix metalloproteinase-19 is expressed by keratinocytes in psoriasis. Acta dermato-venereologica. 2003;83(2):108-14.
18
19. Sekhon BS. Matrix metalloproteinases-an overview. Res Rep Biol. 2010;1:1-20.
19
20. Bell J, McQueen D, Rees J. Involvement of histamine H4 and H1 receptors in scratching induced by histamine receptor agonists in BalbC mice. British journal of pharmacology. 2004;142(2):374-80.
20
21. Gutgesell C, Heise S, Seubert A, Stichtenoth D, Frölich J, Neumann C. Comparison of different activity parameters in atopic dermatitis: correlation with clinical scores. British Journal of Dermatology. 2002;147(5):914-9.
21
22. Schon MP. Inhibitors of selectin functions in the treatment of inflammatory skin disorders. Ther Clin Risk Manag. 2005;1(3):201-8.
22
23. Ghazanfari T, Faghihzadeh S, Aragizadeh H, Soroush MR, Yaraee R, Mohammad Hassan Z, et al. Sardasht-Iran cohort study of chemical warfare victims: design and methods. Arch Iran Med. 2009;12(1):5-14.
23
24. Brew K, Nagase H. The tissue inhibitors of metalloproteinases (TIMPs): an ancient family with structural and functional diversity. Biochimica et Biophysica Acta (BBA)-Molecular Cell Research. 2010;1803(1):55-71.
24
25. Cawston T. Metalloproteinase inhibitors and the prevention of connective tissue breakdown. Pharmacology & therapeutics. 1996;70(3):163-82.
25
26. Johnson LL, Dyer R, Hupe DJ. Matrix metalloproteinases. Current opinion in chemical biology. 1998;2(4):466-71.
26
27. Shohrati M, Haji Hosseini R, Esfandiari MA, Najafian N, Najafian B, Golbedagh A. Serum matrix metalloproteinase levels in patients exposed to sulfur mustard. Iran Red Crescent Med J. 2014;16(3):e15129.
27
28. Shohrati M, Ahmadi M, Esfandiari MA, Soleimani N, Davari SM, Najafian B. Level of matrix metalloproteinases and their inhibitors in skin tissue samples of sulfur mustard exposed chemical patients. Trauma Monthly. 2011;2011(3, Autumn):163-7.
28
29. Shakarjian MP, Bhatt P, Gordon MK, Chang YC, Casbohm SL, Rudge TL, et al. Preferential expression of matrix metalloproteinase-9 in mouse skin after sulfur mustard exposure. J Appl Toxicol. 2006;26(3):239-46.
29
30. Zebrowska A, Wagrowska-Danilewicz M, Danilewicz M, Stasikowska-Kanicka O, Kulczycka-Siennicka L, Wozniacka A, et al. Mediators of mast cells in bullous pemphigoid and dermatitis herpetiformis. Mediators Inflamm. 2014;2014:936545.
30
31. Tengara S, Tominaga M, Kamo A, Taneda K, Negi O, Ogawa H, et al. Keratinocyte-derived anosmin-1, an extracellular glycoprotein encoded by the X-linked Kallmann syndrome gene, is involved in modulation of epidermal nerve density in atopic dermatitis. Journal of dermatological science. 2010;58(1):64-71.
31
32. Tominaga M, Takamori K. Recent advances in pathophysiological mechanisms of itch. 2010.
32
33. Tominaga M, Kamo A, Tengara S, Ogawa H, Takamori K. In vitro model for penetration of sensory nerve fibres on a Matrigel basement membrane: implications for possible application to intractable pruritus. British Journal of Dermatology. 2009;161(5):1028-37.
33
34. Asaduzzaman M, Rahman M, Jeppsson B, Thorlacius H. P‐selectin glycoprotein‐ligand‐1 regulates pulmonary recruitment of neutrophils in a platelet‐independent manner in abdominal sepsis. British journal of pharmacology. 2009;156(2):307-15.
34
35. Hayashi S, Abe Ky, Matsuoka H, Goya S, Morishita H, Mori M, et al. Increased level of soluble E-selectin in the serum from patients with idiopathic pulmonary fibrosis. Inflammation. 2004;28(1):1-5.
35
36. Hall RP, 3rd, Takeuchi F, Benbenisty KM, Streilein RD. Cutaneous endothelial cell activation in normal skin of patients with dermatitis herpetiformis associated with increased serum levels of IL-8, sE-Selectin, and TNF-alpha. J Invest Dermatol. 2006;126(6):1331-7.
36
37. Thestrup-Pedersen K, Ring J. Atopic Dermatitis. Summary of the 1st Georg Rajka Symposium 1998 and a Literature Review. Acta Dermatovenereologica-Stockholm-. 1999;79:257-64.
37
38. Barker J, editor. Adhesion molecules in cutaneous inflammation. Ciba Found Symp; 1995.
38
39. Cordero MM, Casas BB, Reyes RN, Avila CL, del Río NB, Sienra MJ. [Cyclosporin A in atopic dermatitis]. Revista alergia Mexico (Tecamachalco, Puebla, Mexico: 1993). 2001;49(4):129-34.
39
40. Shimada Y, Sato S, Hasegawa M, Tedder TF, Takehara K. Elevated serum L-selectin levels and abnormal regulation of L-selectin expression on leukocytes in atopic dermatitis: soluble L-selectin levels indicate disease severity. Journal of allergy and clinical immunology. 1999;104(1):163-8.
40
41. Nakamura M, Toyoda M, Morohashi M. Pruritogenic mediators in psoriasis vulgaris: comparative evaluation of itch‐associated cutaneous factors. British Journal of Dermatology. 2003;149(4):718-30.
41
42. Kneuer C, Ehrhardt C, Radomski MW, Bakowsky U. Selectins–potential pharmacological targets? Drug discovery today. 2006;11(21):1034-40.
42
ORIGINAL_ARTICLE
Acute Myeloid Leukemia as the Main Cause of Pancytopenia in Iranian Population
Background & objective: Pancytopenia is the reduction in the number of all 3 major cellular elements of blood and leads to anemia, leukopenia, and thrombocytopenia. A wide variety of etiologies result in pancytopenia including leukemia, aplastic anemia, and megaloblastic anemia. The current study identified the different etiologies of pancytopenia based on bone marrow examination in Iranian patients with pancytopenia. Methods: A total of 683 cases of pancytopenia with various etiologies were selected for this retrospective study. Bone marrow biopsy was performed with the standard technique using Jamshidi needle. The inclusion criteria for patients with pancytopenia were hemoglobin (Hb) 9/L, and platelet count 9/L. Results: In the present study acute leukemia was the first most common etiology detected in 235 (35.4%) patients in which acute myeloid leukemia (AML) comprised the majority of cases 142 (21.4%), followed by myelodysplastic syndrome (MDS) 100 (15%). In patients less than 20 years old, acute leukemia was also the commonest cause identified in 56 (57.7%) cases in which acute lymphoblastic leukemia (ALL) with 38.7% was the most common etiology; however in adults (>45 year old), AML accounted for the majority of cases 76 (53.5%). Conclusion: Since acute leukemia was the commonest etiology in both young and adults in which AML accounted for the majority of cases with pancytopenia in Iranian population, there was an urgent need to identify the underlying molecular or genetic mechanism of this malignancy for better further medical management and patients` survival.
https://ijp.iranpath.org/article_25647_5a9118ef5878bb93fdc314106eb2df44.pdf
2017-07-01
265
271
10.30699/ijp.2017.25647
Pancytopenia
Acute Leukemia
Myelodysplastic Syndrome
AML
Hasan
Jalaeikhoo
researchnew010@gmail.com
1
AJA Cancer Research Center (ACRC), AJA University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Seyed Mohammad Hossein
Kashfi
kashfihossein@yahoo.com
2
Gastroenterology and Liver Diseases Research center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Pedram
Azimzadeh
azimzadeh.pedram@gmail.com
3
Gastroenterology and Liver Diseases Research center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Ahmad
Narimani
doctornarimani@gmail.com
4
AJA Cancer Research Center (ACRC), AJA University of Medical Sciences, Tehran, Iran
AUTHOR
Katayon
Gouhari Moghadam
kgohari@gmail.com
5
AJA Cancer Research Center (ACRC), AJA University of Medical Sciences, Tehran, Iran
AUTHOR
Mohsen
Rajaeinejad
mrajaei@gmail.com
6
AJA Trauma and Surgery Research Center, AJA University of Medical Sciences, Tehran, Iran
AUTHOR
Mehdi
Ariana
mehdi.ariana2010@gmail.com
7
AJA Trauma and Surgery Research Center, AJA University of Medical Sciences, Tehran, Iran
AUTHOR
Manouchehr
Keyhani
mkeyhani@hotmail.com
8
Hematology and Oncology Research Center, Vali Asr Hospital, Tehran University of Medical Science, Tehran, Iran
AUTHOR
1. DM. W, Pancytopenia, Aplastic anemia and Pure red cell aplasia., ed. W.s.C. Hematology. Vol. 10th Ed. 1993, Baltimore: William and Willkins. 1449- 84.
1
2. Ishtiaq O, Baqai H Z, Anwer F, and Hussain N. Patterns of pancytopenia patients in a general medical ward and a proposed diagnostic approach. J Ayub Med Coll Abbottabad 2004; 16(1): 8-13.
2
3. Alter B P. Fanconi's anemia and malignancies. Am J Hematol 1996; 53(2): 99-110.
3
4. Jha A, Sayami G, Adhikari R C, Panta A D, and Jha R. Bone marrow examination in cases of pancytopenia. JNMA J Nepal Med Assoc 2008; 47(169): 12-7.
4
5. Gupta V, Tripathi S, Tilak V, and Bhatia B D. A study of clinico-haematological profiles of pancytopenia in children. Trop Doct 2008; 38(4): 241-3.
5
6. Pizzo PA D A A, The pancytopenias. Nelson textbook of pediatrics. Vol. 17th ed. 2003, Behrman RE: Kleigman RM, Jenson HB. . Philadelphia: Saunders.
6
7. Bhatnagar S K, Chandra J, Narayan S, Sharma S, Singh V, and Dutta A K. Pancytopenia in children: etiological profile. J Trop Pediatr 2005; 51(4): 236-9.
7
8. Tilak V and Jain R. Pancytopenia--a clinico-hematologic analysis of 77 cases. Indian J Pathol Microbiol 1999; 42(4): 399-404.
8
9. Varma N and Dash S. A reappraisal of underlying pathology in adult patients presenting with pancytopenia. Trop Geogr Med 1992; 44(4): 322-7.
9
10. Safaei A, Shokripour M, and Omidifar N. Bone marrow and karyotype findings of patients with pancytopenia in southern iran. Iran J Med Sci 2014; 39(4): 333-40.
10
11. Gayathri B N and Rao K S. Pancytopenia: a clinico hematological study. J Lab Physicians 2011; 3(1): 15-20.
11
12. Hayat AS K A, Baloch GH, Shaikh N. Pancytopenia;. study for clinical features and etiological pattern of at tertiary care settings in Abbottabad. Professional Med J 2014; 21(1): 060-65.
12
13. Santra G and Das B K. A cross-sectional study of the clinical profile and aetiological spectrum of pancytopenia in a tertiary care centre. Singapore Med J 2010; 51(10): 806-12.
13
14. Ito S, Takada N, Ozasa A, Hanada M, Sugiyama M, Suzuki K, et al. Secondary hemophagocytic syndrome in a patient with methicillin-sensitive Staphylococcus Aureus bacteremia due to severe decubitus ulcer. Intern Med 2006; 45(5): 303-7.
14
15. Keisu M and Ost A. Diagnoses in patients with severe pancytopenia suspected of having aplastic anemia. Eur J Haematol 1990; 45(1): 11-4.
15
16. Nafil H, Tazi I, Sifsalam M, Bouchtia M, and Mahmal L. [Etiological profile of pancytopenia in adults in Marrakesh, Morocco]. East Mediterr Health J 2012; 18(5): 532-6.
16
17. Thakkar B B, Bhavsar U N, Trivedi N, and Agnihotri A. A Study of Pancytopenia in Adult Patients More than 12 Years of Age in North West Region of Saurashtra. National Journal of Medical Research 2013: 48.
17
18. Redaelli A, Laskin B L, Stephens J M, Botteman M F, and Pashos C L. A systematic literature review of the clinical and epidemiological burden of acute lymphoblastic leukaemia (ALL). Eur J Cancer Care (Engl) 2005; 14(1): 53-62.
18
19. Yamamoto J F and Goodman M T. Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002. Cancer Causes Control 2008; 19(4): 379-90.
19
20. Mirzai A Z, Hosseini N, and Sadeghipour A. Indications and diagnostic utility of bone marrow examination in different bone marrow disorders in Iran. Lab Hematol 2009; 15(4): 38-44.
20
21. Ley T J, Ding L, Walter M J, McLellan M D, Lamprecht T, Larson D E, et al. DNMT3A mutations in acute myeloid leukemia. N Engl J Med 2010; 363(25): 2424-33.
21
22. SEER Cancer Statistics Factsheets: Acute Myeloid Leukemia. National Cancer Institute. Bethesda, MD,.
22
23. Altekruse S, Kosary C, Krapcho M, Neyman N, Aminou R, Waldron W, et al. SEER cancer statistics review, 1975-2007. Bethesda, MD: National Cancer Institute 2010; 7.
23
24. Ries L A G, Smith M A, Gurney J, Linet M, Tamra T, Young J, et al. Cancer incidence and survival among children and adolescents: United States SEER Program 1975-1995. Cancer incidence and survival among children and adolescents: United States SEER Program 1975-1995 1999.
24
25. Dash A and Gilliland D G. Molecular genetics of acute myeloid leukaemia. Best Pract Res Clin Haematol 2001; 14(1): 49-64.
25
26. Gilliland D G and Tallman M S. Focus on acute leukemias. Cancer Cell 2002; 1(5): 417-20.
26
27. Dohner H, Estey E H, Amadori S, Appelbaum F R, Buchner T, Burnett A K, et al. Diagnosis and management of acute myeloid leukemia in adults: recommendations from an international expert panel, on behalf of the European LeukemiaNet. Blood 2010; 115(3): 453-74.
27
28. Chiste M, Vrotsos E, Zamora C, and Martinez A. Chronic lymphocytic leukemia/small lymphocytic lymphoma involving the aortic valve. Ann Diagn Pathol 2013; 17(3): 295-7.
28
29. Rangaswamy M, Prabhu, Nandini N M, and Manjunath G V. Bone marrow examination in pancytopenia. J Indian Med Assoc 2012; 110(8): 560-2, 66.
29
30. Ma X, Does M, Raza A, and Mayne S T. Myelodysplastic syndromes: incidence and survival in the United States. Cancer 2007; 109(8): 1536-42.
30
31. Sekeres M A, Schoonen W M, Kantarjian H, List A, Fryzek J, Paquette R, et al. Characteristics of US patients with myelodysplastic syndromes: results of six cross-sectional physician surveys. J Natl Cancer Inst 2008; 100(21): 1542-51.
31
32. Weinzierl E P and Arber D A. Bone marrow evaluation in new-onset pancytopenia. Hum Pathol 2013; 44(6): 1154-64.
32
33. Doshi D, Shah A N, Somani S, Jain A, Jivarajani H, and Kothari P. Study of clinical and aetiological profile of 100 patients of pancytopenia at a tertiary care centre in India. Hematology 2012; 17(2): 100-5.
33
34. Incidence of aplastic anemia: the relevance of diagnostic criteria. By the International Agranulocytosis and Aplastic Anemia Study. Blood 1987; 70(6): 1718-21.
34
35. Khan F S and Hasan R F. Bone marrow examination of pancytopenic children. J Pak Med Assoc 2012; 62(7): 660-3.
35
36. Pine M and Walter A W. Pancytopenia in hospitalized children: a five-year review. J Pediatr Hematol Oncol 2010; 32(5): e192-4.
36
37. Arcaini L, Zibellini S, Boveri E, Riboni R, Rattotti S, Varettoni M, et al. The BRAF V600E mutation in hairy cell leukemia and other mature B-cell neoplasms. Blood 2012; 119(1): 188-91.
37
38. Brochamer W L, Jr. and Keeling M M. The bone marrow biopsy, osteoscan, and peripheral blood in non-hematopoietic cancer. Cancer 1977; 40(2): 836-40.
38
ORIGINAL_ARTICLE
Duodenal Metastases From Renal Cell Carcinoma Presented With Melena: Review and Case Report
Renal cell carcinoma (RCC) metastasis to duodenum is very rare and only a few case reports are available in the literature. We here reported a patient with solitary duodenal metastasis presented with melena six years after right nephrectomy. The patient underwent upper gastrointestinal endoscopy showing ulcerative mass at the second portion of duodenum and biopsy of this mass was consistent with metastatic RCC. Metastasis work up did not find any other site of malignancy, thus Whipple’s operation (Pancreaticoduodenectomy) was performed. In conclusion metastasis from RCC should be considered in mind in patients with history of nephrectomy presenting with gastrointestinal symptoms and a complete evaluation, especially endoscopic examination followed by biopsy, is suggested.
https://ijp.iranpath.org/article_25687_bed934950c921b90b8a226ed6a9e7019.pdf
2017-07-01
272
276
10.30699/ijp.2017.25687
Duodenum
Renal cell carcinoma
Pancreaticoduodenectomy
melena
Ramesh
Omranipour
0mranipour@sina.tums.ac.ir
1
Cancer Institute of Tehran University of medical science, Tehran, Iran
AUTHOR
Habibollah
Mahmoudzadeh
drhabib94@yahoo.com
2
Farabi Hospital, Tehran University of Medical Science, Tehran, Iran
AUTHOR
Freshteh
Ensani
fensani@gmail.com
3
Research Center of Cancer, Tehran University of Medical Science, Tehran, Iran
AUTHOR
Samira
Yadegari
yadegarisamira@yahoo.com
4
Cancer Institute of Tehran University of Medical Science, Tehran, Iran
AUTHOR
Seyed Rohollah
Miri
drsrmiri@yahoo.com
5
Cancer Institute of Tehran University of Medical Science, Tehran, Iran
LEAD_AUTHOR
1. Gajendra S, Sachdev R, Mohapatra I, Goel R, Goel S. Metastatic Renal Cell Carcinoma: An Unusual Cause of Bleeding Pancreatic Mass. J Clin Diagn Res 2015;9(9):7-15.
1
2. Willis RA. Secondary tumors of the intestines. in: The Spread of Tumor's in the Human Body. ed 3. London. Butterworth & Co Ltd; 1973.
2
3. Vootla VR, Kashif M, Niazi M, Nayudu SK. Recurrent Renal Cell Carcinoma with Synchronous Tumor Growth in Azygoesophageal Recess and Duodenum: A Rare Cause of Anemia and Upper Gastrointestinal Bleeding. Case Rep Oncol Med 2015;2015:143934.
3
4. Rustagi T, Rangasamy p, Versland m.Duodenal Bleeding from Metastatic Renal Cell Carcinoma. Case Rep Gastroenterol 2011;5:249–257.
4
5. Sellner F, Tykalsky N, DeSantes M, Pont J, Klimpfinger M. Solitary and multiple isolated metastasis of clear cell renal cell carcinoma to the pancreas: An indication for pancreatic surgery. Ann Surg Oncol 2006; 13:75-85.
5
6. Crippa S, Angelini C, Mussi C, Bonardi C, Romano F, Sartori P. Surgical treatment of metastatic tumour to the pancreas: A single center experience and review of the literature. World J Surg 2006; 30:1536-42.
6
7. Eidt S, Jergas M, Schmidt R, Siedek M. Metastasis to the pancreas- an indication for pancreatic resection. Langenbecks Arch Surg 2007; 392:539-42.
7
8. Rustagi T, Rangasamy P, Versland M. Duodenal bleeding from metastatic renalcellcarcinoma. Case Rep Gastroenterol 2011; 5(1):249–57.
8
9. Bhatia A, Das A, Kumar Y, Kochhar R. Renal cell carcinoma metastasizing to duodenum: a rare occurrence. Diagn Pathol2006; 1: 29-31.
9
10. Waalkes S, Schrader AJ, Kuczyk MA. Current treatment options for disseminated Renal Cell Carcinoma. Eur Urol Suppl 2012; 11:73–8.
10
11. Espinoza E, Hassani A, Vaishampayan U, Shi D, Pontes JE, Weaver DW. Surgical excision of duodenal/pancreatic metastatic renal cell carcinoma. Front Oncol 2014; 14 (4):214-218
11
12. Lynch-Nyhan A, Fishman EK, Kadir S. Diagnosis and management of massive gastrointestinal bleeding owing to duodenal metastasis from renal cell carcinoma. J Urol 1987; 138:611-613.
12
13. Nabi G, Gandhi G, Dogra PN. Diagnosis and management of duodenal obstruction due to renal cell carcinoma. Trop Gastroenterol2001; 22: 47-49.
13
14. Cherian SV, Subhraleena D Garcha AS. Recurrent renal cell cancer presenting as gastrointestinal Bleeding .World J Gastrointest Oncol2011 ;15 3(6): 99-102.
14
15. Geramizadeh B Mostaghni AH ,Ranjbar Z. An Unusual Case of Metastatatic Renal Cell Carcinoma Presenting as Melena and Duodenal Ulcer, 16 Years After Nephrectomy; a Case Report and Review of the Literature .Iran J Med Sci March 2015; 40 (2);175-180.
15
16. Hsu CC, Chen JJ, Changchien CS. Endoscopic features of metastatic tumors in the upper gastrointestinal tract. Endoscopy1996; 28: 249-253.
16
17. Teo MY, Ryan B, Swan N, McDermott RS. A Case of Metastatic Renal Cell Cancer Presenting as Jaundice. World J OncoL 2010;1:218-20.
17
18. Toh SK, Hale JE. Late presentation of a solitary metastasis of renal cell carcinoma as an obstructive duodenal mass. Postgrad Med J 1996;72:178-9.
18
19. Zhao H, Han K, Li J, Liang P, Zuo G, Zhang Y. A case of wedge resection of duodenum for massive gastrointestinal bleeding due to duodenal metastasis by renal cell carcinoma. World J Surg Oncol 2012;10:199.
19
20. Antonelli A, Arrighi N, Corti S, Legramanti S, Zanotelli T, Cozzoli A, et al. Surgical. treatment of atypical metastasis from renal cell carcinoma (RCC). BJU Int 2012;110: 559-563.
20
21. Sadler GJ, Anderson MR, Moss MS, Wilson PG. Metastases from renal cell carcinoma presenting as gastrointestinal bleeding: two case reports and a review of the literature. BMC Gastroenterol 2007; 7: 4-6.
21
22. Hsu CC, Chen JJ, Changchein CS. Endoscopic features of metastatic tumor's in upper gastrointestinal tract. Endoscopy 1996;28:249–253.
22
23. Toh SK, Hale JE. Late presentation of a solitary metastasis of renal cell carcinoma as an obstructive duodenal mass. Postgrad Med J 1996;72:178–179.
23
24. Le Borgne J, Partensky C, Glemain P.Pancreaticoduodenectomy for metastatic ampullary and pancreatic tumors. Hepatogastroenterology2000;47:540–544.
24
25. Freedman AI, Tomaszewski JE, Van Arsdalen KN. Solitary late recurrence of renal cell carcinoma presenting as duodenal ulcer. Urology 1992;39:461–463.
25
26. Mascarenhas B, Konety B, Rubin JT .Recurrent metastatic renal cell carcinoma presenting as a bleeding gastric ulcer after a complete response to high-dose interleukin-2 treatment. Urology 2001;57:168–169.
26
ORIGINAL_ARTICLE
A Carcinoid Tumor in the Urinary Bladder With Uncommon Clinicopathological Presentation
Background: Carcinoid tumors usually originate from the enterochromaffin cells located in gastrointestinal tract and bronchopulmonary system. They may rarely arise in the urinary bladder, where this can be eventually miscued as any other commoner bladder neoplasms. The current study was conducted to connote an uncommon clinicopathological presentation by a carcinoid tumor in the urinary bladder. Case: A 52-year-old male, who initially experienced obstructive urinary symptoms, underwent cystourethroscopy to remove a tumor in the urinary bladder. The tumor exhibited insular, trabecular, and organoid architecture on histology without any necrosis or mitosis, stained positively with chromogranin A, and thereby, confirmed the diagnosis of a pure carcinoid tumor. Conclusion: Carcinoid tumors rarely arise in the urinary bladder and other genitourinary organs. But, several other and relatively more common bladder neoplasms may often deceptively simulate it. This dilemma could be resolved easily with the application of proper immunohistochemistry (IHC) in neuroendocrine tumors.
https://ijp.iranpath.org/article_25688_91cf900c3a6f7a1c6967baff025382af.pdf
2017-07-01
277
280
10.30699/ijp.2017.25688
Carcinoid Tumor
Chromogranin A
Cystourethroscopy
Immunohistochemistry Urinary Bladder
Krishnendu
Mondal
kaminakriss@gmail.com
1
Dept. of Pathology, Sonoscan Healthcare, Malda, India
LEAD_AUTHOR
Rupali
Mandal
krishnendu.kriss@gmail.com
2
Dept. of Pathology, Sonoscan Healthcare, Malda, India
AUTHOR
1. Martignoni G, Eble JN. Carcinoid tumors of the urinary bladder: immunohistochemical study of two cases and review of the literature. Arch Pathol Lab Med 2003; 127: e22–e24.
1
2. Chen Y, Epstein JI. Primary carcinoid tumors of the urinary bladder and prostatic urethra: a clinicopathologic study of 6 cases. Am J Surg Pathol 2011; 35(3): 442-6.
2
3. Eble JN, Grignon DJ, Young RH. Tumors of the urinary bladder and urethra. In: Fletcher CDM, editor. Diagnostic histopathology of tumors. 4th ed. Philadelphia: Elsevier Saunders; 2013. p. 610-37.
3
4. Manunta A, Vincendeau S, Kiriakou G, Lobel B, Guillé F. Non-transitional cell bladder carcinomas. BJU Int 2005; 95: 497-502.
4
5. Peterson RO, Sesterhenn IA, Davis CJ, editors. Urologic pathology. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2009. p. 245-9.
5
6. Sugihara A, Kajio K, Yoshimoto T et al. Primary carcinoid tumor of the urinary bladder. Int Urol Nephrol 2002; 33: 53-7.
6
7. Mascolo M, Altieri M, Mignogna C, Napodano G, De Rosa G, Insabato L. Calcitonin-producing well-differentiated neuroendocrine carcinoma (carcinoid tumor) of the urinary bladder: case report. BMC Cancer 2005; 5: 88.
7
ORIGINAL_ARTICLE
Immunohistochemical Expression of Nuclear β-Catenin and STAT-6 in a Solitary Fibrous Tumor of the Soft Palate: A Case Report and Review of the Literature
The solitary fibrous tumors (SFT) are rare tumors in the head and neck region and there have been only 5 cases reported in the literature in the soft palate. The current paper presents a unique case of a 62-year-old male with TFS arising in the soft palate. The tumor was highly cellular, composed of bland looking haphazardly arranged spindle cells. The signal transducer and activator of transcription (STAT)-6 and nuclear β-catenin were reactive by immunohistochemistry (IHC). The current case highlights the importance of the STAT-6 and the β-catenin as IHC markers to make a differential diagnosis with other entities. In summary, the paper presents the first reported case of a SFT of the soft palate in a male patient with nuclear expression of STAT-6 and β-catenin.
https://ijp.iranpath.org/article_25689_9edebe408d43b71a34f9b0b6dcc01c16.pdf
2017-07-01
281
285
10.30699/ijp.2017.25689
Solitary Fibrous Tumor (SFT)
Immunohistochemistry (IHQ)
Mesenchymal Tumors
Soft Palate
STAT-6
β-Catenin
Ivonne A.
Montes-Mojarro
mmai_0207@hotmail.com
1
Surgical Pathology Department, The American British Cowdray Medical Center, Mexico city 01120, Mexico
AUTHOR
Javier
Baquera-Heredia
cbaquera@abchospital.com
2
Surgical Pathology Department, The American British Cowdray Medical Center, Mexico city 01120, Mexico
AUTHOR
Juan
Felipe Sanchez-Marle
fsanchezm@abchospital.com
3
Head and Neck Surgery Department, The American British Cowdray Medical Center, Mexico city 01120, Mexico
AUTHOR
Carlos
Ortiz-Hidalgo
cortiz@abchospital.com
4
Surgical Pathology Department, The American British Cowdray Medical Center, Mexico city 01120, Mexico
LEAD_AUTHOR
1. Chan J. K. C. Solitary fibrous tumor- everywhere and a diagnosis in vogue. Histopathology. 1997; 31:568-576.
1
2. Alawi F, Stratton D, Freedman P. Solitary fibrous tumor of the oral soft tissues. A clinicopathologic and immunohistochemical study of 16 cases. Am J Surg Pathol. 2001;25:900-910
2
3. Li X-M, Yu J-Q, Xu GH. Solitary fibrous tumor of the soft palate: a report of two cases. Oncology letters. 2014; 7: 1975-1977.
3
4. Shimoyama T, Horte N, Ide F. Solitary Fibrous tumor of the palate: a case report and review of the literature. J Oral Maxillofac Surg. 2004; 62: 895-897.
4
5. Sánchez-Legaza E, Guerrero-Cauqui R, Miranda Caravallo JI, Murga Tejada C. Solitary fibrous tumor of the smooth palate. Acta Otorrinolaringol Esp. 2011;62:239-241.
5
6. Suster S, Nasciemiento AG, Miettinen M, Sickel J, Moran C A. Solitary fibrous tumors of soft tissue: a clinicopatologic and inmunohistochemical study of 12 cases. Am J Surg Pathol. 1995; 19: 1257-1266.
6
7. Torsten Hansen . Kathrin Katenkamp .Detlef Katenkamp. D2-40 staining in sinonasal-type hemangiopericytoma—further evidence of distinction from conventional hemangiopericytoma and solitary fibrous tumor. Virchows Arch . 2006; 448: 459–462.
7
8. Doyle L. A, Vivero M, Flecher C, Mertens F, Hornick J.L. Nuclear expression of STAT6 distinguishes solitary fibrous tumor from histologic mimics. Modern Pathology. 2014; 27:390-395.
8
9. Koelsche C, Schweizer L, Renner M, Warth A. et al. Nuclear relocation of STAT-6 reliably predicts NAB2/STAT-6 fusion for the diagnosis of solitary fibrous tumor. Histopathology .2014; 65(5):613-22.
9
10. Mohajeri A., Tayebwa J, Collin A et al. Comprehensive genetic analysis identifies a pathognomonic NAB2-STAT6 fusion in solitary fibrous tumors. Nat Genet.2013; 45:180-185.
10
11. Rakheja D, Molberg KH, Roberts CA, Jaiswal VR. Immunohistochemical expression of β-Catenin in Solitary Fibrous Tumor. Arch Pathol Lab Med 2005;129;776-779.
11
12. Ng T. L, Gown A M, Barry T.S, Cheang M C, Chan K A, Turbin S A, Hsu F D, West R. B, Nielsen T. O. Nuclear beta-catenin in mesenchymal tumors. Modern Pathology. 2005; 18: 68-74
12
13. Hansen T, Katenkamp K and Katenkamp D. D2-40 staining in sinonasal-type hemangiopericytoma—further evidence of distinction from conventional hemangiopericytoma and solitary fibrous tumor. Virchows Arch .2006; 448: 459–462.
13
ORIGINAL_ARTICLE
CD99: A potential Diagnostic Marker for Differentiating Sub-ependymal Giant Cell Astrocytoma From Other Mimickers: A Report of Five Cases
Background: Tuberous sclerosis (TSC) is inherited as an autosomal dominant disease, characterized by skin lesion and tubers in vital organs, especially brain in three categories including subependymal nodules, cortical tubers and subependymal giant cell astrocytoma. Subependymal giant cell astrocytoma (SEGA) is an indolent neoplasm which usually arises at the cauda thalamic groove near foramen monro, although it occurs usually in the clinical settings of TSC, a few number of SEGA has been reported without such history. Its morphology with special cytoarchitecture could be mistaken with other glial brain tumors with similar morphology. Therefore, investigating new markers for differentiating SEGA from other mimickers seems logical rather than other glioneural immunohistochemical markers introduced before. Case: We investigated CD99 expression in SEGA as an adjunctive marker for diagnostic purposes. Five reported cases of SEGA were studied and all of them showed CD99 expression besides usual glioneural markers. Conclusion: CD99 may be a useful adjunctive marker in differentiating SEGA from other mimickers
https://ijp.iranpath.org/article_25706_0732c5ab7e3ecee4393c191ef27a6b8f.pdf
2017-07-01
286
290
10.30699/ijp.2017.25706
Sub Ependymal Giant Cell Astrocytoma
CD99
Immunohistochemical Staining
Tumor
Alireza
Sadeghipour
sadeghipour.alireza@gmail.com
1
Dept of Pathology, Iran university of medical sciences, Tehran, Iran
AUTHOR
Navid
Abdi
navid_abdi@yahoo.com
2
Dept of Pathology, Iran university of medical sciences, Tehran, Iran
AUTHOR
Pegah
Babaheidarian
pegibh@gmail.com
3
Dept of Pathology, Iran university of medical sciences, Tehran, Iran
LEAD_AUTHOR
1-O'Callaghan FJ, Lux A, Osborne J.Early diagnosis of subependymal giant cell astrocytoma in children with tuberous sclerosis. J Neurol Neurosurg Psychiatry. 2000 Jan; 68(1):118
1
.2-Roth J1, Roach ES, Bartels U, Jóźwiak S, Koenig MK, Weiner HLet al.Subependymal giant cell astrocytoma: diagnosis, screening, and treatment. Recommendations from the InternationaTuberous Sclerosis Complex Consensus Conference 2012.Pediatr Neurol. 2013 Dec; 49(6):439-44.
2
3Erol İ1, Savaş T1, Şekerci S2, Yazıcı N3, Erbay A3, Demir Ş4,et al.TuberousHYPERLINK "/pubmed/26078697" sclerosis complex; single center experience.TurkPediatriArs. 2015 Mar 1; 50(1):51-60
3
4-Jung TY1, Kim YH1, Jung S1, Baek HJ2, Lee KH3.The clinical characteristics of subependymal giant cell astrocytoma: five cases.Brain Tumor Res Treat. 2015 Apr; 3(1):44-7
4
5-Lopes MB1, Altermatt HJ, Scheithauer BW, Shepherd CW, VandenBergSR.Immunohistochemical characterization of subependymal giant cell astrocytomas.ActaNeuropathol. 1996; 91(4):368-75
5
6-JozwiaHYPERLINK "JozwiakJozwiakJ"k J1, JozwiakHYPERLINK JozwiakJozwiaSkopinski .Immunohistochemical and microscopic studies on giant cells in tuberous sclerosis.Histol Histopathol2005 Oct; 20(4):1321-6.
6
7-Ishizawa K1, Komori T, Shimada S, Hirose T.Olig2 and CD99 are useful negative markers for the diagnosis of brain tumors.ClinNeuropathol. 2008 May-Jun; 27(3):118-28.
7
8-Cenacchi G, GiangasperoF.Emerging tumor entities and variants of CNS neoplasms.JNeuropatholExp Neurol. 2004 Mar; 63(3):185-92.
8
9-Sterman H1, Furlan AB, Matushita H, Teixeira MJ.Subependymal giant cell astrocytoma associated with tuberous sclerosis presenting with intratumoral bleeding. Case report and review of literature.ChildsNerv Syst. 2013 Feb; 29(2):335-9.
9
10-Beaumont TL1, Godzik J1, Dahiya S2, Smyth MD.Subependymal giant cell astrocyto ma in the absence of tuberous sclerosis complex: case JNeurosurgPediatr. 2015 Aug; 16(2):134-7.
10
11-Grajkowska W, Kotulska K, Jurkiewicz E, Roszkowski M, Daszkiewicz P, Jóźwiak S, Matyja E. Subependymal giant cell astrocytomas with atypical histological features mimicking malignant gliomas. Folia Neuropathol. 2011;49(1):39-46
11
12-Mahfouz S1, Aziz AA, Gabal SM, el-Sheikh S.Immunohistochemical study of CD99 and EMA expression in ependymomas.Medscape J Med. 2008 Feb 19;10(2):41
12
13-Ouyang T, Zhang N, Benjamin T, Wang L, Jiao J, Zhao Y, et al.Subependymal giant cell astrocytoma: current concepts, management, and future directions.ChildsNerv Syst. 2014 Apr; 30(4):561-70
13
14-Siedlecka M, Szlufik S, Grajkowska W, Roszkowski M, Jóźwiak J1.Erk activation as a possible mechanism of transformation of subependymal nodule into subependymal giant cell astrocytoma.FoliaNeuropathol. 2015; 53(1):8-14.
14
15-Svajdler M Jr1, Deák L, Rychlý B, Talarčík P, FröhlichováL.Subependymal giant cell astrocytoma with atypical clinical and pathological features: a diagnostic pitfall.CeskPatol. 2013 Apr; 49(2):76-9.
15
ORIGINAL_ARTICLE
Benign Phyllodes Tumor With Cystic Squamous Metaplasia: A Cytohistological Correlation of a Rare Case
Background: Phyllodes tumors (PTs) are uncommon biphasic fibroepithelial neoplasms of the breast occurring in elderly females with a peak incidence between 45 and 49 years. Depending on various histological criteria, they are subdivided into benign, borderline, and malignant forms. Metaplastic changes occur, but are quite infrequent and cystic squamous metaplasia is very rare among the observed metaplastic changes in PT. Case: The current paper presents the case of a 41-year-old female with a progressively enlarging swelling in the left breast. Subsequent histopathological examination revealed benign PT with cystic squamous metaplasia. The previously done fine needle aspiration smears were also reviewed, which showed important diagnostic clues to this rare entity, but were ignored due to the rarity of the lesion. Conclusion: The case was presented because of its unique cytological and histopathological morphology and also to determine the role of aspiration cytology to diagnose such a rare occurrence.
https://ijp.iranpath.org/article_25837_80126bc415fec05357234430e3893557.pdf
2017-07-01
291
294
10.30699/ijp.2017.25837
Benign Phyllodes Tumor
Cystic Squamous Metaplasia
Cytology
Indranil
Chakrabarti
drinch@rediffmail.com
1
Dept. of Pathology, North Bengal Medical College, The West Bengal University of Health Sciences, Siliguri, Darjeeling, West Bengal, India
LEAD_AUTHOR
Priyanka
Agarwala
drinch@mail.com
2
Dept. of Pathology, North Bengal Medical College, The West Bengal University of Health Sciences, Siliguri, Darjeeling, West Bengal, India
AUTHOR
Pranati
Bera
drindranil79@gmail.com
3
Dept. of Pathology, North Bengal Medical College, The West Bengal University of Health Sciences, Siliguri, Darjeeling, West Bengal, India
AUTHOR
Sankarshan
Bhaduri
timingil2008@gmail.com
4
Anadaloke Sonoscan Centre, Siliguri, Darjeeling, West Bengal, India
AUTHOR
1. Bellocq JP, Magro G. Fibroepithelial tumours. In: Tavassoli FA, Devilee P, editors. World Health Organization Classification of Tumours. Pathology and Genetics of Tumours of the Breast and Female Genital Tract. Lyon: IARC Press; 2003. pp. 99–103.
1
2. Bernstein L, Deapen D, Ross RK. The descriptive epidemiology of malignant cystosarcoma phyllodes tumors of the breast. Cancer 1993 May;71(10):3020–4.
2
3. Chua CL, Thomas A, Ng BK. Cystosarcoma phyllodes—Asian variations. Aust N Z J Surg 1988 Apr;58(4):301–5.
3
4. Rosen PP. Rosen’s Breast Pathology. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2001.
4
5. Sugie T, Takeuchi E, Kunishima F, Yotsumoto F, Kono Y. A case of ductal carcinoma with squamous differentiation in malignant phyllodes tumor. Breast Cancer 2007;14(3):327–32.
5
6. Grimes MM. Cystosarcoma phyllodes of the breast: histologic features, flow cytometric analysis, and clinical correlations. Mod Pathol 1992 May;5(3):232–9.
6
7. Norris HJ, Taylor HB. Relationship of histologic features to behavior of cystosarcoma phyllodes. Analysis of ninety-four cases. Cancer 1967 Dec;20(12):2090–9.
7
8. Quinlan-Davidson S, Hodgson N, Elavathil L, Shangguo T. Borderline phyllodes tumor with an incidental invasive tubular carcinoma and lobular carcinoma in situ component: a case report. J Breast Cancer 2011 Sep;14(3):237–40.
8
9. Salvadori B, Cusumano F, Del Bo R, Delledonne V, Grassi M, Rovini D et al. Surgical treatment of phyllodes tumors of the breast. Cancer 1989 Jun;63(12):2532–6.
9
10. Bernstein L, Deapen D, Ross RK. The descriptive epidemiology of malignant cystosarcoma phyllodes tumors of the breast. Cancer 1993 May;71(10):3020–4.
10
11. Rajan PB, Cranor ML, Rosen PP. Cystosarcoma phyllodes in adolescent girls and young women: a study of 45 patients. Am J Surg Pathol 1998 Jan;22(1):64–9.
11
12. Mishra SP, Tiwary SK, Mishra M, Khanna AK. Phyllodes Tumor of Breast: A Review Article. ISRN Surgery 2013;2013:1-8. https://doi.org/10.1155/2013/361469.
12
13. Kumar H, Iqbal MB, Buch A, Panicker N. Extensive squamous metaplasia in a benign phyllodes tumor: A rare case report. Med J DY Patil Univ 2015;8(3):404–6.
13
14. Gottfried MR. Extensive squamous metaplasia in gynecomastia. Arch Pathol Lab Med 1986 Oct;110(10):971–3.
14
15. Söderstrom KO, Toikkanen S. Extensive squamous metaplasia simulating squamous cell carcinoma in benign breast papillomatosis. Hum Pathol 1983 Dec;14(12):1081–2.
15
16. Rosen PP. Fibroepithelial Neoplasms. In: Pine JW, editor. Rosen’s Breast Pathology, 3rd.
16
17. Philadelphia. Lippincott Williams & Wilkins; 2009. pp. 202–26.
17
ORIGINAL_ARTICLE
Nosocomial Jejunal Mucormycosis - an Unusual Cause of Perforation Peritonitis
Mucormycosis is a rare but highly invasive opportunistic fungal infection. Gastrointestinal disease although uncommon is highly fatal. We report a case of jejunal mucormycosis in a 24 year old undernourished female with preceding surgical intervention for acute intestinal obstruction of tubercular etiology. On 8th post-operative day, she developed oozing from suture line, prompting exploratory laparotomy, bowel resection, jejunostomy and ileal mucus fistula. Resected bowel showed one perforation and several areas of impending perforations. Characteristic broad, pauci-septate hyaline, empty looking hyphae with infrequent branching were found transmurally and showing angio-invasion. Local intestinal tissue trauma coupled with her sub-normal immune status permitted this unusual nosocomial infection. Histopathologic demonstration of the fungus in surgical specimens remains cornerstone of diagnosis of mucormycosis in view of its non-specific symptoms, low isolation rates of mycologic culture and lack of other rapid tests.
https://ijp.iranpath.org/article_25840_947fc9a2e4886e2a64642cb879aeba3c.pdf
2017-07-01
295
300
10.30699/ijp.2017.25840
Mucormycosis
nosocomial infection
Jejunum
Small Bowel
Chandan
Kumar
drchandan.ucms@gmail.com
1
Dept. of Pathology, University College of Medical Sciences, University of Delhi, Delhi, India
AUTHOR
Pragya
Jain
drpragyajain9@gmail.com
2
Dept. of Pathology, University College of Medical Sciences, University of Delhi, Delhi, India
AUTHOR
Neelam
Wadhwa
drneelam428@yahoo.co.in
3
Dept. of Pathology, University College of Medical Sciences, University of Delhi, Delhi, India
LEAD_AUTHOR
Preeti
Diwaker
diwaker_preeti@yahoo.in
4
Dept. of Pathology, University College of Medical Sciences, University of Delhi, Delhi, India
AUTHOR
Nirupma
Khan
nirupmapanikar@rediffmail.com
5
Dept. of Pathology, Guru Teg Bahadur Hospital, Shahdra, Delhi, India
AUTHOR
1. Petrikkos G, Skiada A, Lortholary O, Roilides E, Walsh TJ, Kontoyiannias DP. Epidemiology and clinical manifestations of mucormycosis. Clin Infect Dis. 2012; 54: Suppl 1: S23–34.
1
2. Roden MM, Zaoutis TE, Buchanan WL, Knudsen TA, Sarkisova TA, Schaufele RL, et al. Epidemiology and outcome of zygomycosis: a review of 929 reported cases. Clin Infect Dis. 2005; 41(5):634–53.
2
3. Bitar D, Van Cauteren D, Lanternier F, Dannaoui E, Che D, Dromer F, et al. Increasing incidence of zygomycosis (mucormycosis), France, 1997-2006. Emerg Infect Dis. 2009; 15(9): 1395-401.
3
4. Chakrabarti A, Chatterjee SS, Das A, Panda N, Shivaprakash MR, Kaur A, et al. Invasive zygomycosis in India: experience in a tertiary care hospital. Postgrad Med J. 2009; 85(1009): 573-81.
4
5. Agha FP, Lee HH, Boland CR, Bradley SF. Mucormycoma of the colon: early diagnosis and successful management. Am J Roentgenol. 1985; 145(4): 739–41.
5
6. Kwon-Chung K. Taxonomy of fungi causing mucormycosis and entomophthoramycosis (zygomycosis) and nomenclature of the disease: molecular and mycologic perspectives. Clin Infect Dis. 2012; 54 Suppl 1: S8–S15.
6
7. Rammaert B, Lanternier F, Zahar JR, Dannaoui E, Bougnoux ME, Lecuit M, et al. Healthcare-associated mucormycosis. Clin Infect Dis. 2012; 54 Suppl 1:S44-54.
7
8. Ribes JA, Vanover-Sams CL, Baker DJ. Zygomycetes in human disease. Clin Microbiol Rev. 2000; 13(2): 236-301.
8
9. Zaoutis TE, Roilides E, Chiou CC, Buchanan WL, Knudsen TA, Sarkisova TA, et al. Zygomycosis in children: a systematic review and analysis of reported cases. Pediatr Infect Dis J. 2007;26(8): 723-7.
9
10. Patra S, Vij M, Chirla DK, Kumar N, Samal SC. Unsuspected invasive neonatal gastrointestinal mucormycosis: A clinicopathological study of six cases from a tertiary care hospital. J Indian Assoc Pediatr Surg. 2012; 17(4): 153-6.
10
11. Maraví-Poma E, Rodríguez-Tudela JL, de Jalón JG, Manrique-Larralde A, Torroba L, Urtasun J, et al. Outbreak of gastric mucormycosis associated with the use of wooden tongue depressors in critically ill patients. Intensive Care Med. 2004; 30(4): 724-8.
11
12. Karanth M, Taniere P, Barraclough J, Murray JA. A rare presentation of zygomycosis (mucormycosis) and review of the literature. J Clin Pathol. 2005: 58(8): 879-81.
12
13. Martinello M, Nelson A, Bignold L, Shaw D. "We are what we eat!" Invasive intestinal mucormycosis: A case report and review of the literature. Med Mycol Case Rep. 2012;1(1):52-5.
13
ORIGINAL_ARTICLE
Gorham’s Disease of the Maxilla and Mandible With Distinctive Cone Beam Computerized Tomographic Features
Gorham’s disease is a rare and atypical disorder epitomized by progressive osteolysis of bone with eventual total disappearance of bone. The etiology is poorly understood with variable clinical presentation. Most times it is initially misdiagnosed as temporomandibular joint dysfunction, periodontal disease or odontogenic tumors clinically and radiographically in routine dental practice. Radiographic examination, such as Cone Beam Computerized Tomography (CBCT) play a vital role in diagnosing such disorder resulting in disappearance of the involved bone entirely, which is a definitive distinguishing feature of this condition. Regarding the rarity of the condition, the current study presents a case of Gorham’s disease with distinctive clinical, radiological, and histological, features involving maxilla and mandible.
https://ijp.iranpath.org/article_25855_268bb5f9f26f4c782a00c00e8f61803c.pdf
2017-07-01
301
306
10.30699/ijp.2017.25855
Gorham’s disease
Maxilla
Mandible
Massive Osteolysis
Resorption
Rupam
Sinha
rupamsinha@yahoo.com
1
Dept. of Oral Medicine & Radiology, Haldia Institute of Dental Sciences and Research, Haldia, West Bengal, India
LEAD_AUTHOR
Soumyabrata
Sarkar
dr.rupsarkar@gmail.com
2
Dept. of Oral Medicine & Radiology, Haldia Institute of Dental Sciences and Research, Haldia, West Bengal, India
AUTHOR
Tanya
Khaitan
tanyakhaitan@gmail.com
3
Dept. of Dentistry, Murshidabad Medical College and Hospital, Berhampore, West Bengal, India
AUTHOR
Deepsikha
Ramani
dr.deepsikha.ramani@gmail.com
4
Dept. of Oral Medicine & Radiology, Haldia Institute of Dental Sciences and Research, Haldia, West Bengal, India
AUTHOR
1. R. Dominguez, T. L. Washowich. Gorham's disease or vanishing bone disease: Plain film, CT, and MRI findings of two cases. Pediatr Radiol.1994;24(5):316-8.
1
2. Patel DV. Gorham’s Disease or Massive Osteolysis. Clin Med Res. 2005;3(2):65-74.
2
3. Raghuveer HP, Jayalekshmy R. Gorham’s massive osteolysis of the mandible – a progressive radiographic presentation. Dentomaxillofac Radiol. 2009;38(5):292–5.
3
4. Saify FY, Gosavi SR. Gorham's disease: A diagnostic challenge. J Oral Maxillofac Pathol.2014;18(3):411-4.
4
5. Nikolaou VS, Chytas D, Korres D, Efstathopoulos N. Vanishing bone disease (Gorham-Stout syndrome): A review of a rare entity. World J Orthop 2014;5(5):694-8.
5
6. Kothari P. Gorham Disease an Enigma. Webmed Central Dentistry 2012;3(1):WMC002898.
6
7. Kiran DN, Anupama A. Vanishing Bone Disease: A Review. J Oral Maxillofac Surg 2011;69(1):199-203.
7
8. Nagaveni NB, Radhika NB, Umashankara KV, Satisha TS. Vanishing (Disappearing) Bone Disease in children – A review. J Clin Exp Dent. 2011;3(4):e328-35.
8
9. Patrick JH. Massive osteolysis complicated by chylothorax successfully treated by pleurodesis. J Bone Joint Surg Br. 1976;58(3):347-9.
9
10. Gul SK, Oruc AF, Gedik D, Gul HL, Aksu A, Mayadagli A. Gorham’s Disease that Gave Response to Radiotherapy. Journal of Cancer Treatment and Research 2014;2(5):45-7.
10
11. Mignogna MD, Fedele S, Lo Russo L, Lanza A, Marenzi G, Sammartino G. Gorham’s disease of the mandible mimicking periodontal disease on radiograph. J Clin Periodontol 2005;32(9):1022–6.
11
ORIGINAL_ARTICLE
Placental Mesenchymal Dysplasia With Normal Fetus: A Rare Case Report
Placental mesenchymal dysplasia (PMD) is a rare benign placental abnormality. It is characterized by hydropic degeneration of stem villi, placentomegaly, and increased maternal serum alpha-fetoprotein(AFP). It can be associated with different congenital abnormalities, karyotype abnormalities, and feto-maternal morbidities. It is difficult to differentiate PMDfrom partial mole, complete mole with twin pregnancy in ultrasound, and in macroscopic examination. The current paper presentsa rare case of placental mesenchymal dysplasia in a young primigravida mother who delivered a normal fetus withnormal karyotype.
https://ijp.iranpath.org/article_25856_86b53d38bcb0d2a51d9dec94bd87faa4.pdf
2017-07-01
307
310
10.30699/ijp.2017.25856
Placental mesenchymal dysplasia (PMD)
normal fetus
partial mole
Subrata
Pal
subratapal1985@gmail.com
1
Dept. of Pathology, College of Medicine and Sagore Dutta Hospital. Kolkata, India
LEAD_AUTHOR
Kingshuk
Bose
kingshukbosepath@gmail.com
2
Dept. of Pathology, Bankura Sammilani Medical College, Bankura, India.
AUTHOR
Palash
Ch Mondal
drpalashmondal@gmail.com
3
Dept. of Gynaecology and Obstretics, Bankura Sammilani Medical College, Bankura, India
AUTHOR
Srabani
Chakrabarti
banerjee.srabani@yahoo.co.in
4
Dept. of Pathology, Culcutta National Medical College, Kolkata, India
AUTHOR
Mrinal
Sikder
mrinalsikder@gmail.com
5
Dept. of Pathology, R G Kar Medical College, Kolkata, India
AUTHOR
1. Woo, G.W., Rocha, F.G., Gaspar-Oishi, M. et al, Placental mesenchymal dysplasia. Am J ObstetGynecol 2011;205(6):e3–e5.
1
2. Li H, Li L, Tang X, Yang F, Yang K-X. Placental mesenchymal dysplasia: a case of a normal-appearing fetus with intrauterine growth restriction.Int Jour of Clin and ExpPathol 2014;7(8):5302-7.
2
3. Ohira S, Ookubo N, Kobara H, Tanaka K, Kikuchi N, Takatsu A et al. Placental Mesenchymal Dysplasia: Chronological Observation of Placental Images during Gestation and Review of the Literature. GynecolObstet Invest 2013;75(4):217–23.
3
4. Pawoo N and Heller DS. Placental Mesenchymal Dysplasia. Arch Pathol Lab Med 2014,138(9):1247-9.
4
5. Sheeja S, Usha P, Shiny MP and Renu T. Placental mesenchymal dysplasia: a report of two cases with review of literature. Indian J PatholMicrobiol 2013; 56(1):57–9.
5
6. Taga S, Haraga J, Sawada M, Nagai A, Yamamoto D, Hayase R. A case of placental mesenchymal dysplasia. Case Rep ObstetGynecol2013 doi:10.1155/2013/265159. Epub.
6
7. Nayeri UA, West AB, Nardini HKG, Copel JA, Sfakianaki AK. Systematic review of sonographic findings of placental mesenchymal dysplasia and subsequent pregnancy outcome. Ultrasound Obstetrics and Gynecology 2012;41(4):366–74.
7
8. Kaiser-Rogers KA, McFadden DE, Livasy CA, Dansereau J, Jiang R and Knops JF et al. Androgenetic/biparentalmosaicism causes placental mesenchymal dysplasia. J Med Genet2006;43(2):187–92.
8
9. Parveen Z, Tongson-Ignacio JE, Fraser CR, Killeen JL, Thompson KS. Placental Mesenchymal Dysplasia. Arch Pathol Lab Med 2007;131(1):131–7.
9
10. Cohen MC, Roper EC, Sebire NJ, Stanek J, Anumba DO. Placental mesenchymal dysplasia associated with fetal aneuploidy. PrenatDiagn 2005;25(3):187-92.
10
ORIGINAL_ARTICLE
Dark Chocolate Intake Acutely Enhances Neutrophil Count in Peripheral Venous Blood
Beside the well-established impact on decreasing the risk of cardiovascular diseases (1), recent attention has been paid to the relationship between cocoa-containing foods and the immune system (2), showing that dark chocolate consumption enhances the systemic defense against bacterial (3) and viral (4) infections. Hence, the current study aimed at investigating the acute effect of dark chocolate intake on peripheral blood leukocytes.
https://ijp.iranpath.org/article_25047_6e9ee7f191711739b11e312076e1c84d.pdf
2017-07-01
311
312
10.30699/ijp.2017.25047
chocolate
cocoa
Leukocytes
neutrophils
Infection
Martina
Montagnana
martina.montagnana@univr.it
1
Section of Clinical Biochemistry, University of Verona, Verona, Italy
AUTHOR
Elisa
Danese
elisa.danese@univr.it
2
Section of Clinical Biochemistry, University of Verona, Verona, Italy
AUTHOR
Gabriel
Lima-Oliveira
dr.g.lima.oliveira@gmail.com
3
Section of Clinical Biochemistry, University of Verona, Verona, Italy
AUTHOR
Gian Luca
Salvagno
gianluca.salvagno@univr.it
4
Section of Clinical Biochemistry, University of Verona, Verona, Italy
AUTHOR
Giuseppe
Lippi
ulippi@tin.it
5
Section of Clinical Biochemistry, University of Verona, Verona, Italy
LEAD_AUTHOR
Lippi G, Franchini M, Montagnana M, Favaloro EJ, Guidi GC, Targher G. Dark chocolate: consumption for pleasure or therapy? J Thromb Thrombolysis 2009; 28:482-8.
1
Pérez-Cano FJ, Massot-Cladera M, Franch A, Castellote C, Castell M. The effects of cocoa on the immune system. Front Pharmacol 2013;4:71.
2
Niehues M, Stark T, Keller D, Hofmann T, Hensel A. Antiadhesion as a functional concept for prevention of pathogens: N-Phenylpropenoyl-L-amino acid amides as inhibitors of the Helicobacter pylori BabA outer membrane protein. Mol Nutr Food Res 2011;55:1104-17.
3
Kamei M, Nishimura H, Takahashi T, Takahashi N, Inokuchi K, Mato T, Takahashi K. Anti-influenza virus effects of cocoa. J Sci Food Agric 2016;96:1150-8.
4
Simundic AM, Cornes M, Grankvist K, Lippi G, Nybo M. Standardization of collection requirements for fasting samples: for the Working Group on Preanalytical Phase (WG-PA) of the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM). Clin Chim Acta 2014;432:33-7.
5
Ellinger S, Stehle P. Impact of Cocoa Consumption on Inflammation Processes-A Critical Review of Randomized Controlled Trials. Nutrients 2016;8(6). pii: E321.
6
ORIGINAL_ARTICLE
Current Diagnostic Status of Pheochromocytomaand Future Perspective: A Mini Review
Pheochromocytomas (PCCs) are rare neuroendocrine tumors. The current diagnostic tools are based on biochemistry and histopathology results, but heterogeneity of diagnostic markers, signs and symptoms of PCCs bring a lot of difficulties for these two current methods. Unfortunately microscopic understanding of PCCs is not adequate for its confident prognosis and management. There are data linking specific genotypes of PCCs tumors to specific locations, typical biochemical phenotypes or future clinical behaviors. The detection of a germ-line mutation possibly can guide us to an early diagnosis, appropriate treatment, and regular surveillance with better prognosis not only for the patient but also for their family members. Moreover, the latest discoveries in gene sequencing, circulating DNA (ctDNA) and circulating tumor cells (CTCs) will support the exact molecular pathogenesis of PCCs in order to provide an important basis for future PCCs managements.
https://ijp.iranpath.org/article_26267_5da06a3b200b12e7a8dca36dfd5f967f.pdf
2017-07-01
313
322
10.30699/ijp.2017.26267
Pheochromocytomas (PCCs)
Histopathology
genes
catecholamines
metanephrines
Fatemeh
Khatami
f-khatami@farabi.tums.ac.ir
1
Chronic Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Seyed Mohammad
Tavangar
tavangar@ams.ac.ir
2
Dept. of Pathology, Dr. Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
1. Boulpaep EL, Boron WF, Caplan MJ, Cantley L, Igarashi P, Aronson PS et al. Medical Physiology a Cellular and Molecular Approach. Signal Transduct 2009;48:27.
1
2. Beard CM, Sheps SG, Kurland LT, Carney JA, Lie JT. Occurrence of pheochromocytoma in Rochester, Minnesota, 1950 through 1979. Mayo Clin Proc 1983;58(12):802–4.
2
3. Haghpanah V, Soliemanpour B, Heshmat R, Mosavi-Jarrahi AR, Tavangar SM, Malekzadeh R et al. Endocrine cancer in Iran: based on cancer registry system. Indian J Cancer 2006;43(2):80–5.
3
4. Larijani B, Shirzad M, Mohagheghi MA, Haghpanah V, Mosavi-Jarrahi AR, Tavangar SM et al. Epidemiologic analysis of the Tehran cancer institute data system registry (TCIDSR). Asian Pac J Cancer Prev 2004;5(1):36–9.
4
5. Guerrero MA, Schreinemakers JM, Vriens MR, Suh I, Hwang J, Shen WT et al. Clinical spectrum of pheochromocytoma. J Am Coll Surg 2009;209(6):727–32.
5
6. Tsirlin A, Oo Y, Sharma R, Kansara A, Gliwa A, Banerji MA. Pheochromocytoma: a review. Maturitas 2014;77(3):229–38.
6
7. Lenders JW, Eisenhofer G, Mannelli M, Pacak K. Phaeochromocytoma. Lancet 2005; 366(9486):665–75.
7
8. Tavangar SM, Larijani B, Mahta A, Hosseini SM, Mehrazine M, Bandarian F. Craniopharyngioma: a clinicopathological study of 141 cases. Endocr Pathol 2004;15(4):339–44.
8
9. Tavangar SM, Shojaee A, Moradi Tabriz H, Haghpanah V, Larijani B, Heshmat R et al. Immunohistochemical expression of Ki67, c-erbB-2, and c-kit antigens in benign and malignant pheochromocytoma. Pathol Res Pract 2010 ;206(5):305–9.
9
10. Larijani B, Mohagheghi MA, Bastanhagh MH, Mosavi-Jarrahi AR, Haghpanah V, Tavangar SM et al. Primary thyroid malignancies in Tehran, Iran. Med Princ Pract 2005;14(6):396–400.
10
11. Larijani B, Bastanhagh MH, Pajouhi M, Kargar Shadab F, Vasigh A, Aghakhani S. Presentation and outcome of 93 cases of craniopharyngioma. Eur J Cancer Care (Engl) 2004 ;13(1):11–5.
11
12. Kong A, Leboucher P, Leek R, Calleja V, Winter S, Harris A et al. Prognostic value of an activation state marker for epidermal growth factor receptor in tissue microarrays of head and neck cancer. Cancer Res 2006;66(5):2834–43.
12
13. Bravo EL, Tagle R. Pheochromocytoma: state-of-the-art and future prospects. Endocr Rev 2003;24(4):539–53.
13
14. Smythe GA, Edwards G, Graham P, Lazarus L. Biochemical diagnosis of pheochromocytoma by simultaneous measurement of urinary excretion of epinephrine and norepinephrine. Clin Chem 1992;38(4):486–92.
14
15. Eisenhofer G, Timmers HJ, Lenders JW, Bornstein SR, Tiebel O, Mannelli M et al. Age at diagnosis of pheochromocytoma differs according to catecholamine phenotype and tumor location. J Clin Endocrinol Metab 2011;96(2):375–84.
15
16. Cooper ME, Goodman D, Frauman A, Jerums G, Louis WJ. Phaeochromocytoma in the elderly: a poorly recognised entity? Br Med J (Clin Res Ed) 1986;293(6560):1474–5.
16
17. Munakata M, Aihara A, Imai Y, Noshiro T, Ito S, Yoshinaga K. Altered sympathetic and vagal modulations of the cardiovascular system in patients with pheochromocytoma: their relations to orthostatic hypotension. Am J Hypertens 1999 ;12(6):572–80.
17
18. Haghpanah V, Shooshtarizadeh P, Heshmat R, Larijani B, Tavangar SM. Immunohistochemical analysis of survivin expression in thyroid follicular adenoma and carcinoma. Appl Immunohistochem Mol Morphol 2006;14(4):422–5.
18
19. Omidfar K, Moinfar Z, Sohi AN, Tavangar SM, Haghpanah V, Heshmat R et al. Expression of EGFRvIII in thyroid carcinoma: immunohistochemical study by camel antibodies. Immunol Invest 2009;38(2):165–80.
19
20. Attaran SY, Omrani GH, Tavangar SM. Lymphoepithelial-like intrathyroidal thymic carcinoma with foci of squamous differentiation. Case report. APMIS 1996;104(6):419–23.
20
21. Tischler AS, Kimura N, Mcnicol AM. Pathology of pheochromocytoma and extra-adrenal paraganglioma. Ann N Y Acad Sci 2006 ;1073(1):557–70.
21
22. Bravo EL, Tarazi RC, Gifford RW, Stewart BH. Circulating and urinary catecholamines in pheochromocytoma. Diagnostic and pathophysiologic implications. N Engl J Med 1979;301(13):682–6.
22
23. Rosano TG, Swift TA, Hayes LW. Advances in catecholamine and metabolite measurements for diagnosis of pheochromocytoma. Clin Chem 1991;37(10 Pt 2):1854–67.
23
24. Young WF Jr. Pheochromocytoma: issues in diagnosis & treatment. Compr Ther 1997;23(5):319–26.
24
25. Eisenhofer G, Goldstein DS, Kopin IJ, Crout JR. Pheochromocytoma: rediscovery as a catecholamine-metabolizing tumor. Endocr Pathol 2003;14(3):193–212.
25
26. Gardet V, Gatta B, Simonnet G, Tabarin A, Chêne G, Ducassou D et al. Lessons from an unpleasant surprise: a biochemical strategy for the diagnosis of pheochromocytoma. J Hypertens 2001;19(6):1029–35.
26
27. Gerlo EA, Sevens C. Urinary and plasma catecholamines and urinary catecholamine metabolites in pheochromocytoma: diagnostic value in 19 cases. Clin Chem 1994;40(2):250–6.
27
28. Guller U, Turek J, Eubanks S, Delong ER, Oertli D, Feldman JM. Detecting pheochromocytoma: defining the most sensitive test. Ann Surg 2006;243(1):102–7.
28
29. Lenders JW, Pacak K, Walther MM, Linehan WM, Mannelli M, Friberg P et al. Biochemical diagnosis of pheochromocytoma: which test is best? JAMA 2002;287(11):1427–34.
29
30. van der Harst E, de Herder WW, de Krijger RR, Bruining HA, Bonjer HJ, Lamberts SW et al. The value of plasma markers for the clinical behaviour of phaeochromocytomas. Eur J Endocrinol 2002;147(1):85–94.
30
31. O’Connor DT, Bernstein KN. Radioimmunoassay of chromogranin A in plasma as a measure of exocytotic sympathoadrenal activity in normal subjects and patients with pheochromocytoma. N Engl J Med 1984 Sep;311(12):764–70.
31
32. John H, Ziegler WH, Hauri D, Jaeger P. Pheochromocytomas: can malignant potential be predicted? Urology 1999 Apr;53(4):679–83.
32
33. Proye CA, Vix M, Jansson S, Tisell LE, Dralle H, Hiller W. “The” pheochromocytoma: a benign, intra-adrenal, hypertensive, sporadic unilateral tumor. Does it exist? World J Surg 1994 Jul-Aug;18(4):467–72.
33
34. Eisenhofer G, Walther M, Keiser HR, Lenders JW, Friberg P, Pacak K. Plasma metanephrines: a novel and cost-effective test for pheochromocytoma. Braz J Med Biol Res 2000;33(10):1157–69.
34
35. Dove AE, Marathe PH, Gao HX, Close KL. American Association of Clinical Endocrinologists 2017. J Diabetes 2017. https://doi.org/10.1111/1753-0407.12573.
35
36. Sinclair D, Shenkin A, Lorimer AR. Normal catecholamine production in a patient with a paroxysmally secreting phaeochromocytoma. Ann Clin Biochem 1991;28(Pt 4):417–9.
36
37. Stewart MF, Reed P, Weinkove C, Moriarty KJ, Ralston AJ. Biochemical diagnosis of phaeochromocytoma: two instructive case reports. J Clin Pathol 1993;46(3):280–2.
37
38. Shawar L, Svec F. Pheochromocytoma with elevated metanephrines as the only biochemical finding. The Journal of the Louisiana State Medical Society: official organ of the Louisiana State Medical Society. 1996;148(12):535-8.
38
39. Lenders JW, Keiser HR, Goldstein DS, Willemsen JJ, Friberg P, Jacobs MC et al. Plasma metanephrines in the diagnosis of pheochromocytoma. Ann Intern Med 1995 Jul;123(2):101–9.
39
40. Elijovich F, Lenders J, Keiser H. Plasma metanephrines in the diagnosis of pheochromocytoma. Ann Intern Med 1996;124(7):694–5.
40
41. Salmenkivi K. Tumor Markers in Pheochromocytomas: Kaisa Salmenkivi; 2003.
41
42. Leibowitz-Amit R, Mete O, Asa SL, Ezzat S, Joshua AM. Malignant pheochromocytoma secreting vasoactive intestinal peptide and response to sunitinib: a case report and literature review. Endocr Pract 2014;20(8):e145–50.
42
43. Lauring BP, Hoda SA. Tumors of the Adrenal Gland and Extra-Adrenal Paraganglia. Arch Pathol Lab Med 1998;122(5):480.
43
44. Linnoila RI, Keiser HR, Steinberg SM, Lack EE. Histopathology of benign versus malignant sympathoadrenal paragangliomas: clinicopathologic study of 120 cases including unusual histologic features. Hum Pathol 1990;21(11):1168–80.
44
45. Unger PD, Cohen JM, Thung SN, Gordon R, Pertsemlidis D, Dikman SH. Lipid degeneration in a pheochromocytoma histologically mimicking an adrenal cortical tumor. Arch Pathol Lab Med 1990;114(8):892–4.
45
46. Vassallo G, Capella C, Solcia E. Grimelius’ silver stain for endocrine cell granules, as shown by electron microscopy. Stain Technol 1971;46(1):7–13.
46
47. Chetty R, Clark SP, Taylor DA. Pigmented pheochromocytomas of the adrenal medulla. Hum Pathol 1993;24(4):420–3.
47
48. van der Harst E, Bruining HA, Jaap Bonjer H, van der Ham F, Dinjens WN, Lamberts SW et al. Proliferative index in phaeochromocytomas: does it predict the occurrence of metastases? J Pathol 2000;191(2):175–80.
48
49. Mete O, Tischler AS, de Krijger R, McNicol AM, Eisenhofer G, Pacak K et al. Protocol for the examination of specimens from patients with pheochromocytomas and extra-adrenal paragangliomas. Arch Pathol Lab Med 2014;138(2):182–8.
49
50. Mete O, Asa SL. Endocrine Pathology with Online Resource. Cambridge University Press; 2016.
50
51. Thompson LD. Pheochromocytoma of the Adrenal gland Scaled Score (PASS) to separate benign from malignant neoplasms: a clinicopathologic and immunophenotypic study of 100 cases. Am J Surg Pathol 2002;26(5):551–66.
51
52. Srivastava A, Tischler AS, Delellis RA. Endogenous biotin staining as an artifact of antigen retrieval with automated immunostaining. Endocr Pathol 2004;15(2):175–8.
52
53. Tischler AS, Tsokas P, Shahsavari M, Powers JF. Immunoreactivity of normal rabbit serum with epinephrine (E) cells of the rat adrenal medulla after microwave antigen retrieval. Cell Tissue Res 1998 ;293(3):563–6.
53
54. Amousha MR, Kish NS, Heshmat R, Rajabiani A, Saffar H, Haghpanah V et al. Corrigendum: Expression of the Pituitary Tumor Transforming Gene (PTTG1) in Pheochromocytoma as a Potential Marker for Distinguishing Benign Versus Malignant Tumors. Acta Med Iran 2015;53(6):392.
54
55. Tavangar SM, Monajemzadeh M, Larijani B, Haghpanah V. Immunohistochemical study of oestrogen receptors in 351 human thyroid glands. Singapore Med J 2007;48(8):744–7.
55
56. Saffar H, Sanii S, Emami B, Heshmat R, Panah VH, Azimi S et al. Evaluation of MMP2 and Caspase-3 expression in 107 cases of papillary thyroid carcinoma and its association with prognostic factors. Pathol Res Pract 2013;209(3):195–9.
56
57. Sarmadi S, Izadi-Mood N, Sotoudeh K, Tavangar SM. Altered PTEN expression; a diagnostic marker for differentiating normal, hyperplastic and neoplastic endometrium. Diagn Pathol 2009;4(1):41.
57
58. Glinicki P, Jeske W, Bednarek-Papierska L, Kasperlik-Załuska A, Rosłonowska E, Gietka-Czernel M et al. Chromogranin A (CgA) in adrenal tumours. Endokrynol Pol 2013;64(5):358–62.
58
59. Jahn R, Schiebler W, Ouimet C, Greengard P. A 38,000-dalton membrane protein (p38) present in synaptic vesicles. Proc Natl Acad Sci USA 1985;82(12):4137–41.
59
60. Leong AS, Cooper K, Leong FJ. Manual of diagnostic antibodies for immunohistology. Cambridge University Press; 2003.
60
61. Wiedenmann B, Huttner WB. Synaptophysin and chromogranins/ secretogranins—widespread constituents of distinct types of neuroendocrine vesicles and new tools in tumor diagnosis. Virchows Arch B Cell Pathol Incl Mol Pathol 1989;58(2):95–121.
61
62. Wick MR, Scheithauer BW, Kovacs K. Neuron-specific enolase in neuroendocrine tumors of the thymus, bronchus, and skin. Am J Clin Pathol 1983;79(6):703–7.
62
63. Rutishauser U, Acheson A, Hall AK, Mann DM, Sunshine J. The neural cell adhesion molecule (NCAM) as a regulator of cell-cell interactions. Science 1988;240(4848):53–7.
63
64. Grignon DJ, Ro JY, Mackay B, Ordóñez NG, el-Naggar A, Molina TJ et al. Paraganglioma of the urinary bladder: immunohistochemical, ultrastructural, and DNA flow cytometric studies. Hum Pathol 1991;22(11):1162–9.
64
65. Komminoth P, De Krijger R, Tischler A. Paraganglia and the adrenal medulla. Endocrine pathology Churchill Livingstone, Philadelphia. 2002:149-69.
65
66. Dabbs DJ. Diagnostic immunohisto-chemistry: Elsevier Health Sciences; 2013.
66
67. Mahta A, Haghpanah V, Lashkari A, Heshmat R, Larijani B, Tavangar SM. Non-functioning pituitary adenoma: immunohistochemical analysis of 85 cases. Folia Neuropathol 2007;45(2):72–7.
67
68. Sharifi R, Allameh A, Biramijamal F, Mohammadzadeh SH, Rasmi Y, Tavangar SM et al. Relationship between genetic polymorphism of glutathione S-transferase-p1 and p53 protein accumulation in Iranian esophageal squamous cell carcinoma patients. Indian J Cancer 2008;45(1):8–12.
68
69. Kelishomi RB, Ejtemaeemehr S, Tavangar SM, Rahimian R, Mobarakeh JI, Dehpour AR. Morphine is protective against doxorubicin-induced cardiotoxicity in rat. Toxicology 2008; 243(1-2):96–104.
69
70. Momeny M, Sabourinejad Z, Zarrinrad G, Moghaddaskho F, Eyvani H, Yousefi H et al. Anti-tumour activity of tivozanib, a pan-inhibitor of VEGF receptors, in therapy-resistant ovarian carcinoma cells. Sci Rep 2017;7:45954.
70
71. Khatami F, Aghayan HR, Sanaei M, Heshmat R, Tavangar SM, Larijani B. The potential of circulating tumor cells in personalized management of breast cancer: A systematic review. Acta Med Iran 2017;55(3):175–93.
71
72. Bryant J, Farmer J, Kessler LJ, Townsend RR, Nathanson KL. Pheochromocytoma: the expanding genetic differential diagnosis. J Natl Cancer Inst 2003;95(16):1196–204.
72
73. Benn DE, Robinson BG. Genetic basis of phaeochromocytoma and paraganglioma. Best Pract Res Clin Endocrinol Metab 2006 ;20(3):435–50.
73
74. Burnichon N, Brière JJ, Libé R, Vescovo L, Rivière J, Tissier F et al. SDHA is a tumor suppressor gene causing paraganglioma. Hum Mol Genet 2010;19(15):3011–20.
74
75. Papathomas TG, Gaal J, Corssmit EP, Oudijk L, Korpershoek E, Heimdal K et al. Non-pheochromocytoma (PCC)/paraganglioma (PGL) tumors in patients with succinate dehydrogenase-related PCC-PGL syndromes: a clinicopathological and molecular analysis. Eur J Endocrinol 2013; 170(1):1–12.
75
76. Assadipour Y, Sadowski SM, Alimchandani M, Quezado M, Steinberg SM, Nilubol N et al. SDHB mutation status and tumor size but not tumor grade are important predictors of clinical outcome in pheochromocytoma and abdominal paraganglioma. Surgery 2017;161(1):230–9.
76
77. Hao HX, Khalimonchuk O, Schraders M, Dephoure N, Bayley JP, Kunst H et al. SDH5, a gene required for flavination of succinate dehydrogenase, is mutated in paraganglioma. Science 2009;325(5944):1139–42.
77
78. Bayley JP, Kunst HP, Cascon A, Sampietro ML, Gaal J, Korpershoek E et al. SDHAF2 mutations in familial and sporadic paraganglioma and phaeochromocytoma. Lancet Oncol 2010;11(4):366–72.
78
79. Qin Y, Yao L, King EE, Buddavarapu K, Lenci RE, Chocron ES et al. Germline mutations in TMEM127 confer susceptibility to pheochromocytoma. Nat Genet 2010;42(3):229–33.
79
80. Comino-Méndez I, Gracia-Aznárez FJ, Schiavi F, Landa I, Leandro-García LJ, Letón R et al. Exome sequencing identifies MAX mutations as a cause of hereditary pheochromocytoma. Nat Genet 2011;43(7):663–7.
80
81. Hernandez KG, Ezzat S, Morel CF, Swallow C, Otremba M, Dickson BC et al. Familial pheochromocytoma and renal cell carcinoma syndrome: TMEM127 as a novel candidate gene for the association. Virchows Arch 2015;466(6):727–32.
81
82. Timmers HJ, Kozupa A, Eisenhofer G, Raygada M, Adams KT, Solis D et al. Clinical presentations, biochemical phenotypes, and genotype-phenotype correlations in patients with succinate dehydrogenase subunit B-associated pheochromocytomas and paragangliomas. J Clin Endocrinol Metab 2007;92(3):779–86.
82
83. Amar L, Baudin E, Burnichon N, Peyrard S, Silvera S, Bertherat J et al. Succinate dehydrogenase B gene mutations predict survival in patients with malignant pheochromocytomas or paragangliomas. J Clin Endocrinol Metab 2007;92(10):3822–8.
83
84. Eisenhofer G, Lenders JW, Timmers H, Mannelli M, Grebe SK, Hofbauer LC et al. Measurements of plasma methoxytyramine, normetanephrine, and metanephrine as discriminators of different hereditary forms of pheochromocytoma. Clin Chem 2011;57(3):411–20.
84
85. Karasek D, Frysak Z, Pacak K. Genetic testing for pheochromocytoma. Curr Hypertens Rep 2010;12(6):456–64.
85
86. Schlisio S, Kenchappa RS, Vredeveld LC, George RE, Stewart R, Greulich H et al. The kinesin KIF1Bbeta acts downstream from EglN3 to induce apoptosis and is a potential 1p36 tumor suppressor. Genes Dev 2008;22(7):884–93.
86
87. Opocher G, Schiavi F. Genetics of pheochromocytomas and paragangliomas. Best Pract Res Clin Endocrinol Metab 2010;24(6):943–56.
87
88. Welander J, Söderkvist P, Gimm O. Genetics and clinical characteristics of hereditary pheochromocytomas and paragangliomas. Endocr Relat Cancer 2011;18(6):R253–76.
88
89. Dahia PL, Ross KN, Wright ME, Hayashida CY, Santagata S, Barontini M et al. A HIF1α regulatory loop links hypoxia and mitochondrial signals in pheochromocytomas. PLoS Genet 2005;1(1):72–80.
89
90. Karasek D, Shah U, Frysak Z, Stratakis C, Pacak K. An update on the genetics of pheochromocytoma. J Hum Hypertens 2013;27(3):141–7.
90
91. Timmers HJ, Gimenez-Roqueplo AP, Mannelli M, Pacak K. Clinical aspects of SDHx-related pheochromocytoma and paraganglioma. Endocr Relat Cancer 2009;16(2):391–400.
91
92. Petri BJ, van Eijck CH, de Herder WW, Wagner A, de Krijger RR. Phaeochromocytomas and sympathetic paragangliomas. Br J Surg 2009;96(12):1381–92.
92
93. Müller U, Troidl C, Niemann S. SDHC mutations in hereditary paraganglioma/ pheochromocytoma. Fam Cancer 2005;4(1):9–12.
93
94. Korpershoek E, Favier J, Gaal J, Burnichon N, van Gessel B, Oudijk L et al. SDHA immunohistochemistry detects germline SDHA gene mutations in apparently sporadic paragangliomas and pheochromocytomas. J Clin Endocrinol Metab 2011 Sep;96(9):E1472–6.
94
95. Neumann HP, Pawlu C, Pęczkowska M, Bausch B, McWhinney SR, Muresan M et al.; European-American Paraganglioma Study Group. Distinct clinical features of paraganglioma syndromes associated with SDHB and SDHD gene mutations. JAMA 2004 Aug;292(8):943–51.
95
96. Jiang S, Dahia PL. Minireview: the busy road to pheochromocytomas and paragangliomas has a new member, TMEM127. Endocrinology 2011 Jun;152(6):2133–40.
96
97. Amar L, Bertherat J, Baudin E, Ajzenberg C, Bressac-de Paillerets B, Chabre O et al. Genetic testing in pheochromocytoma or functional paraganglioma. J Clin Oncol 2005;23(34):8812–8.
97
98.Gill AJ, Benn DE, Chou A, Clarkson A, Muljono A, Meyer-Rochow GY, et al. Immunohistochemistry for SDHB triages genetic testing of SDHB, SDHC, and SDHD in paraganglioma-pheochromocytoma syndromes. Human pathology. 2010;41(6):805-14.
98
99. van Nederveen FH, Gaal J, Favier J, Korpershoek E, Oldenburg RA, de Bruyn EM, et al. An immunohistochemical procedure to detect patients with paraganglioma and phaeochromocytoma with germline SDHB, SDHC, or SDHD gene mutations: a retrospective and prospective analysis. The lancet oncology. 2009;10(8):764-71.
99
100.Baysal BE, Ferrell RE, Willett-Brozick JE, Lawrence EC, Myssiorek D, Bosch A, et al. Mutations in SDHD, a mitochondrial complex II gene, in hereditary paraganglioma. Science. 2000;287(5454):848-51.
100
101.Hensen EF, Bayley J-P. Recent advances in the genetics of SDH-related paraganglioma and pheochromocytoma. Familial cancer. 2011;10(2):355-63.
101
102.Mannelli M, Castellano M, Schiavi F, Filetti S, Giacche M, Mori L, et al. Clinically guided genetic screening in a large cohort of Italian patients with pheochromocytomas and/or functional or nonfunctional paragangliomas. J Clin Endocrinol Metab 2009;94(5):1541-7.
102
103.Venter JC, Adams MD, Myers EW, Li PW, Mural RJ, Sutton GG, et al. The sequence of the human genome. Science. 2001;291(5507):1304-51.
103
104.Khatami F, Noorinayer B, Mohebi SR, Ghiasi S, Mohebi R, Hashemi M, et al. Effects of amino acid substitution polymorphisms of two DNA methyltransferases on susceptibility to sporadic colorectal cancer. Asian Pac J Cancer Prev. 2009;10(6):1183-8.
104
105. Khatami F, Mohebi SR, Ghiasi S, Haghighi MM, Safaee A, Hashemi M, et al. Amino acid substitution polymorphisms of two DNA methyltransferases and susceptibility to sporadic colorectal cancer. Gastroenterology and Hepatology from bed to bench. 2009;1(3).
105
106.Mohammadi-asl J, Larijani B, Khorgami Z, Tavangar SM, Haghpanah V, Kheirollahi M, et al. Qualitative and quantitative promoter hypermethylation patterns of the P16, TSHR, RASSF1A and RARβ2 genes in papillary thyroid carcinoma. Medical Oncology. 2011;28(4):1123-8.
106
107.Alix-Panabières C, Pantel K. Circulating tumor cells: liquid biopsy of cancer. Clinical chemistry. 2013;59(1):110-8.
107
108. Khatami F, Larijani B, Tavangar S. Circulating Tumor BRAF Mutation and Personalized Thyroid Cancer Treatment. Asian Pacific journal of cancer prevention: APJCP. 2017;18(2):293.
108
109. Mardis ER. The impact of next-generation sequencing technology on genetics. Trends in genetics. 2008;24(3):133-41.
109