ORIGINAL_ARTICLE
The changes of Coagulation State in Patients Contracted with SARS-COV-19
Coronaviruses are considered to be one of the most significant human and animal pathogens. In late 2019, a new species of coronavirus was recognized as the cause of some pneumonia cases in Wuhan, China. The disease spread rapidly and made an epidemic in China and subsequently in almost all countries in the world. In February 2020, the World Health Organization (WHO) named it as COVID-19 standing for Coronavirus 2019 (1). Due to being a pandemic issue, it is needed to discuss various aspects of this viral disease. Recently, Yan Zhang et al. reported a case of coagulopathy and antiphospholipid antibodies in the patient with severe COVID-19 infection (2). Thus, one of the serious complications of COVID-19 that should be taken into consideration is coagulopathy with possible anti-phospholipid antibodies syndrome in these patients. In this regard, some studies also claimed that COVID-19 could cause venous and arterial thromboembolism because of excessive inflammation, hypoxia, immobility, and diffuse intravascular coagulation (3). Antiphospholipid syndrome is a systemic autoimmune disease with vascular and hematologic complications as venous and arterial thrombosis or pregnancy morbidity (4). It is well known that infectious agents are one of the major stimulators of the antiphospholipid antibodies in vivo (5), thus, COVID-19 can be a possible cause of this phenomenon within its infection period and consequently, positive results of antiphospholipid antibodies detection are not unexpected.
https://ijp.iranpath.org/article_43487_ffd726278030d174e2b46df4a18e0966.pdf
2020-10-01
259
260
10.30699/ijp.2020.129354.2427
Coagulation changes
COVID-19
DIC
Anahita
Nosrati
anahita785@gmail.com
1
Department of Pathology, Imam Hospital, Mazandaran University of Medical Sciences, Sari, Iran
LEAD_AUTHOR
Organization WH. Director-General's remarks at the media briefing on 2019-nCoV on 11 Febr uary 2020 -2019-ncov-on-11-february-2020 (Accessed on February 12, 2020).
1
Zhang Y, Xiao M, Zhang S, Xia P, Cao W, Jiang W, Chen H, Ding X, Zhao H, Zhang H, Wang C. Coagulopathy and antiphospholipid antibodies in patients with Covid-19. New Engl J Med. 2020 Apr 23;382(17):e38. [DOI:10.1056/NEJMc2007575] [PMID] [PMCID]
2
Klok F, Kruip M, van der Meer N, Arbous M, Gommers D, Kant K, et al. Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thromb Res. 2020. [DOI:10.1016/j.thromres.2020.04.041] [PMID] [PMCID]
3
Lim W. Antiphospholipid syndrome. Hematol. 2013 Dec 6;2013(1):675-80. [DOI:10.1182/asheducation-2013.1.675] [PMID]
4
Nasiri N, Golafshan H, Kohan Mozaffari S. New clinical and laboratory finding in anti-phospholipid syndromes. Laboratory & Diagnosis. 2019;11(44):10-8. .
5
Long QX, Liu BZ, Deng HJ, Wu GC, Deng K, Chen YK, et al. Antibody responses to SARS-CoV-2 in patients with COVID-19. Nat Med. 2020 Apr 29.
6
Bowles L, Platton S, Yartey N, Dave M, Lee K, Hart DP, MacDonald V, Green L, Sivapalaratnam S, Pasi KJ, MacCallum P. Lupus anticoagulant and abnormal coagulation tests in patients with Covid-19. New Engl J Med. 2020 May 5. [DOI:10.1056/NEJMc2013656] [PMID] [PMCID]
7
Tang N, Li D, Wang X, Sun Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J Thromb Haemost. 2020 Apr;18(4):844-7. [DOI:10.1111/jth.14768] [PMID] [PMCID]
8
Tang N, Bai H, Chen X, Gong J, Li D, Sun Z. Anticoagulant treatment is associated with decreased mortality in severe coronavirus disease 2019 patients with coagulopathy. J Thromb Haemost. 2020 May;18(5):1094-9. [DOI:10.1111/jth.14817] [PMID]
9
Giannis D, Ziogas IA, Gianni P. Coagulation disorders in coronavirus infected patients: COVID-19, SARS-CoV-1, MERS-CoV and lessons from the past. J Clin Virol. 2020 Apr 9:104362. [DOI:10.1016/j.jcv.2020.104362] [PMID] [PMCID]
10
ORIGINAL_ARTICLE
Clinical Validation of Eleven Formulas for Calculating LDL-C in Iran
Background & Objective: Concentration of low-density lipoprotein (LDL) is a known risk factor for cardiovascular disease which is routinely measured or calculated as LDL-C in clinical laboratories. In order to decrease the cost, instead of its measuring, it is recommended to calculate it using multiple formulas that have been introduced up to now. The aim of this study was to assess the results of various formulas and comparison of these results with those of measuring method and to clarify the best formula for the Iranian population. Methods: Concentrations of total cholesterol (TC), triglyceride (TG), cholesterol of high-density lipoprotein (HDL-C) and LDL-C in serums of 471 overnight fasting individuals were measured and also LDL-Cs of these samples were calculated by eleven different formulas according to their TC, TG, and HDL-C concentrations. Subsequently, results of measured and calculated LDL-C were analyzed statistically by paired t-test, correlation coefficient, and Passing-Bablok regression. In addition, for clinical evaluation, the differences between calculated and measured mean results were calculated and compared with an allowable total error. Result: Paired t-test unraveled a significant difference between the results of measured and calculated LDL-C by various formulas. But for some formulas, these differences were not clinically significant. The best clinical and statistical agreement (correlation coefficient) was obtained by the Friedewald equation. Conclusion: By using validated methods which have correct calibration and control system for measuring TC, TG, and HDL-C, we can use the Friedewald formula for calculating LDL-C in serum samples with TG up to 400 mg/dL.
https://ijp.iranpath.org/article_43483_ad6be4eae7271d961529cd7304f66110.pdf
2020-10-01
261
267
10.30699/ijp.2020.110379.2174
cardiovascular disease
LDL
Friedewald formula
HDL
TG
Fereshteh
Atabi
f.atabi@iautmu.ac.ir
1
Department of Biochemistry and Biophysics, Faculty of Advanced Sciences and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
AUTHOR
Reza
Mohammadi
rmohamadi@iautmu.ac.ir
2
Department of Biochemistry, Faculty of Medicine, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
LEAD_AUTHOR
Rim JH, Lee YH, Lee MH, Kim HY, Choi J, Lee BW, Kang ES, Lee HC, Kim JH, Lee SG, Cha BS. Comparison and validation of 10 equations including a novel method for estimation of LDL-cholesterol in a 168,212 Asian population. Med. 2016 Apr;95(14). [DOI:10.1097/MD.0000000000003230] [PMID] [PMCID]
1
de Cordova CMM, de Cordova MM. A new accurate, simple formula for LDL-cholesterol estimation based on directly measured blood lipids from a large cohort. Ann Clin Biochem. 2013;50(1):13-9. [DOI:10.1258/acb.2012.011259] [PMID]
2
Onyenekwu CP, Hoffmann M, Smit F, Matsha TE, Erasmus RT. Comparison of LDL-cholesterol estimate using the Friedewald formula and the newly proposed de Cordova formula with a directly measured LDL-cholesterol in a healthy South African population. Ann Clin Biochem. 2014;51(6):672-9. [DOI:10.1177/0004563214520750] [PMID]
3
Theodoraki TG, Tsoukatos DC, Karabina S-A, Rallidis LS, Papageorgakis NH, Tselepsis AD. LDL subfractions in patients with myocardial infarction: effect of smoking and β-blocker treatment. Ann Clin Biochem. 2000;37(3):313-8. [DOI:10.1258/0004563001899456] [PMID]
4
Teerakanchana T, Puavilai W, Suriyaprom K, Tungtrongchitr R. Comparative study of LDL-cholesterol levels in Thai patients by the direct method and using the Friedewald formula. Southeast Asian J Trop Med Public Health. 2007;38(3):519.
5
AHMADI SA, Boroumand M-A, GOUHARI MK, Tajik P, Dibaj S-M. The impact of low serum triglyceride on LDL-cholesterol estimation. Arch Iran Med .2008.
6
McPherson RA, Pincus MR. Henry's Clinical Diagnosis and Management by Laboratory Methods E-Book: Elsevier Health Sciences; 2017.
7
Martin SS, Blaha MJ, Elshazly MB, Toth PP, Kwiterovich PO, Blumenthal RS, Jones SR. Comparison of a novel method vs the Friedewald equation for estimating low-density lipoprotein cholesterol levels from the standard lipid profile. Jama. 2013 Nov 20;310(19):2061-8. [DOI:10.1001/jama.2013.280532] [PMID] [PMCID]
8
Choukem S-P, Manases T, Nda-Mefoo J-P, Dimala CA, Mboue-Djieka Y, Sobngwi E, et al. Validation of the Friedewald formula for the estimation of low density lipoprotein cholesterol in a sub-Saharan African population. Clin Biochem. 2018;53:25-30. [DOI:10.1016/j.clinbiochem.2017.12.008] [PMID]
9
Tighe DA, Ockene IS, Reed G, Nicolosi R. Calculated low density lipoprotein cholesterol levels frequently underestimate directly measured low density lipoprotein cholesterol determinations in patients with serum triglyceride levels≤ 4.52 mmol/l: An analysis comparing the LipiDirect® magnetic LDL assay with the Friedewald calculation. Clin Chim Act. 2006;365(1-2):236-42. [DOI:10.1016/j.cca.2005.08.026] [PMID]
10
Choi H, Shim J-S, Lee MH, Yoon YM, Choi DP, Kim HC. Comparison of formulas for calculating low-density lipoprotein cholesterol in general population and high-risk patients with cardiovascular disease. Korean Circ J. 2016;46(5):688-98. [DOI:10.4070/kcj.2016.46.5.688] [PMID] [PMCID]
11
Bairaktari E, Elisaf M, Tzallas C, Karabina SA, Tselepis AD, Siamopoulos KC, et al. Evaluation of five methods for determining low-density lipoprotein cholesterol (LDL-C) in hemodialysis patients. Clin Biochem. 2001;34(8):593-602. [DOI:10.1016/S0009-9120(01)00274-0]
12
Tremblay AJ, Morrissette H, Gagné J-M, Bergeron J, Gagné C, Couture P. Validation of the Friedewald formula for the determination of low-density lipoprotein cholesterol compared with β-quantification in a large population. Clin Biochem. 2004;37(9):785-90. [DOI:10.1016/j.clinbiochem.2004.03.008] [PMID]
13
DeLong DM, DeLong ER, Wood PD, Lippel K, Rifkind BM. A comparison of methods for the estimation of plasma low-and very low-density lipoprotein cholesterol: the Lipid Research Clinics Prevalence Study. Jama. 1986 Nov 7;256(17):2372-7. [DOI:10.1001/jama.256.17.2372] [PMID]
14
Warnick GR, Kimberly MM, Waymack PP, Leary ET, Myers GL. Standardization of measurements for cholesterol, triglycerides, and major lipoproteins. Lab Med. 2008;39(8):481-90. [DOI:10.1309/6UL9RHJH1JFFU4PY]
15
Mullins E. Statistics for the quality control chemistry laboratory: Royal Soc Chem; 2007.
16
Chen Y, Zhang X, Pan B, Jin X, Yao H, Chen B, et al. A modified formula for calculating low-density lipoprotein cholesterol values. Lipids Health Dis. 2010 Dec;9(1):1-5.. [DOI:10.1186/1476-511X-9-52] [PMID] [PMCID]
17
Boshtam M, Ramezani MA, Naderi G, Sarrafzadegan N. Is Friedewald formula a good estimation for low density lipoprotein level in Iranian population? J Res Med Sci. 2012 Jun;17(6):519.
18
Hichem B, Hanane B, Mouna Z, Radia S. The best formula for estimating the low density lipoprotein cholesterol on a North African population. bioRxiv. 2016 Jan 1:083790. [DOI:10.1101/083790]
19
Azam Karkhaneh, Molood Bagherieh, Solmaz Sadeghi and Asma Kheirollahi. Evaluation of eight formulas for LDL-Cestimation in Iranian subjects with different metabolic health statuses: Lip Health Dis. 2019; 18:231. [DOI:10.1186/s12944-019-1178-1] [PMID] [PMCID]
20
Knopfholz J, Disserol CCD, Pierin AJ, Schirr FL, Streisky L, Takito LL, et al. Validation of the friedewald formula in patients with metabolic syndrome. Cholesterol. 2014;2014. [DOI:10.1155/2014/261878] [PMID] [PMCID]
21
Molavi F, Namazi N, Asadi M, Sanjari M, Motlagh ME, Shafiee G, et al. Comparison common equations for LDL-C calculation with direct assay and developing a novel formula in Iranian children and adolescents: the CASPIAN V study. Lipids in Health and Disease. 2020;19(1):1-8. [DOI:10.1186/s12944-020-01306-7] [PMID] [PMCID]
22
Krishnaveni P, Gowda VM. Assessing the validity of Friedewald's formula and Anandraja's formula for serum LDL-cholesterol calculation. Journal of clinical and diagnostic research: JCDR. 2015;9(12):BC01. [DOI:10.7860/JCDR/2015/16850.6870] [PMID] [PMCID]
23
Brownstein AJ, Martin SS. More accurate LDL-C calculation: Externally validated, guideline endorsed. Clinica Chimica Acta. 2020. [DOI:10.1016/j.cca.2020.03.030] [PMID]
24
Ephraim RK, Acheampong E, Swaray SM, Odame Anto E, Agbodzakey H, Adoba P, et al. Developing a modified low-density lipoprotein (M-LDL-C) Friedewald's equation as a substitute for direct LDL-C measure in a Ghanaian population: a comparative study. Journal of lipids. 2018;2018. [DOI:10.1155/2018/7078409] [PMID] [PMCID]
25
Martins J, Olorunju SA, Murray L, Pillay TS. Comparison of equations for the calculation of LDL-cholesterol in hospitalized patients. Clinica Chimica Acta. 2015;444:137-42. [DOI:10.1016/j.cca.2015.01.037] [PMID]
26
Mehta R, Reyes-Rodríguez E, Bello-Chavolla OY, Guerrero-Díaz AC, Vargas-Vázquez A, Cruz-Bautista I, et al. Performance of LDL-C calculated with Martin's formula compared to the Friedewald equation in familial combined hyperlipidemia. Atherosclerosis. 2018;277:204-10. [DOI:10.1016/j.atherosclerosis.2018.06.868] [PMID]
27
Mendes de Cordova CM, de Santa Helena ET, Galgowski C, Figueira VH, Setter GB, Markus MRP, et al. Evaluation of a new equation for LDL-c estimation and prediction of death by cardiovascular related events in a German population-based study cohort. Scandinavian journal of clinical and laboratory investigation. 2018;78(3):187-96. [DOI:10.1080/00365513.2018.1432070] [PMID]
28
Rasouli M, Mokhtari H. Calculation of LDL‐Cholesterol vs. Direct Homogenous Assay. Journal of clinical laboratory analysis. 2017;31(3):e22057. [DOI:10.1002/jcla.22057] [PMID] [PMCID]
29
Anwar M, Khan DA, Khan FA. Comparison of Friedewald formula and modified Friedewald formula with direct homogeneous assay for low density lipoprotein cholesterol estimation. J Coll Physicians Surg Pak. 2014;24(1):8-12.
30
ORIGINAL_ARTICLE
Assessment of p16 and Ki67 Immunohistochemistry Expression in Squamous Intraepithelial Lesion with Cytohistomorphological Correlation
Background & Objective: Cervical cancer is the most common cancer in women worldwide with high mortality, necessitating quicker diagnostic methods. We wish to enhance the existing cervical biopsies of Squamous Intraepithelial Lesions (SIL) using p16 and Ki67 as surrogate markers to assess correlation between its positivity and histological grade of the lesion. Methods: Analysis of p16 and Ki67 expression was done on 31 histopathologically diagnosed cases of SILs. Positive expression of p16 was assessed based on a scoring system and compared with histology and cytology. Ki67 expression was studied and the correlation was observed with degree of dysplasia. Twenty cases of chronic cervicitis was assigned to the control group for comparison. Result: Cases of HSIL showed greater expression of p16 as compared to LSIL. Sensitivity of p16 for HSIL was higher than that for LSIL. The specificity for HSIL and LSIL was 100%. Ki67 expression correlated well with the degree and level of dysplasia with a significant P-value of 0.002. Conclusion: p16 and Ki67 positivity of SILs should point towards further evaluation. The expressions of p16 and Ki67 are useful markers for confirmation of SILs and in predicting HPV infection which can be further confirmed by HPV DNA testing.
https://ijp.iranpath.org/article_43484_c582b5579250228a546c0506f10592b0.pdf
2020-10-01
268
273
10.30699/ijp.2020.112421.2208
Squamous intraepithelial lesion
HSIL
LSIL
Apurv
Ghosh
apurvghosh@gmail.com
1
Department of Pathology, Kasturba Medical College, Mangalore, Manipal Academy of Higher Education, Manipal, India
AUTHOR
M
Nirupama
deptofpath@gmail.com
2
Department of Pathology, Kasturba Medical College, Mangalore, Manipal Academy of Higher Education, Manipal, India
LEAD_AUTHOR
Nandan
Padmanabha
nandanp0@gmail.com
3
Department of Pathology, Kasturba Medical College, Mangalore, Manipal Academy of Higher Education, Manipal, India
AUTHOR
Hema
Kini
hema.kini@manipal.edu
4
Department of Pathology, Kasturba Medical College, Mangalore, Manipal Academy of Higher Education, Manipal, India
AUTHOR
Bruni L, Barrionuevo-Rosas L, Albero G, Serrano B, Mena M, Gómez D, Muñoz J, Bosch FX, De Sanjosé S. ICO information centre on HPV and cancer (HPV information centre). Human papillomavirus and related diseases in the world. Summary Report. 2015 Mar;4(08).
1
Sreedevi A, Javed R, Dinesh A. Epidemiology of cervical cancer with special focus on India. Int J Womens Health. 2015;7:405-14. [DOI:10.2147/IJWH.S50001] [PMID] [PMCID]
2
Musa J, Achenbach CJ, O'Dwyer LC, et al. Effect of cervical cancer education and provider recommendation for screening on screening rates: A systematic review and meta-analysis [published correction appears in PLoS One. 2017 Dec 29;12 (12 ):e0190661]. PLoS One. 2017;12(9):e0183924. [DOI:10.1371/journal.pone.0183924] [PMID] [PMCID]
3
Khazaei S, Izadi B, Mirbahari SG, Madani SH, Malek Khosravi Sh, Emami Alagha M, Sajadimajd S. Comparison Between Two Detection Methods for HPV16, HPV18 and P16Ink4a Biomarkers in Diagnosis of Abnormal Cervical Cytology. Asian Pac J Cancer Prev. 2016 Dec 1;17(12):5223-7.
4
Solomon D, Nayar R. The Bethesda System for Reporting Cervical Cytology. Nayar R, Wilbur DC, editors. Cham: Springer International Publishing; 2015. 342.
5
Genovés J, Alameda F, Mancebo G, Solé JM, Bellosillo B, Lloveras B, et al. Human papillomavirus detection and p16INK4a expression in cervical lesions: A comparative study. Hum Pathol. 2014;45(4):826-33. [DOI:10.1016/j.humpath.2013.10.035] [PMID]
6
Galgano MT, Castle PE, Atkins KA, Brix WK, Nassau SR, Stoler MH. Using biomarkers as objective standards in the diagnosis of cervical biopsies. Am J Surg Pathol. 2010;34(8):1077-87. [DOI:10.1097/PAS.0b013e3181e8b2c4] [PMID] [PMCID]
7
van Baars R, Griffin H, Wu Z, et al. Investigating Diagnostic Problems of CIN1 and CIN2 Associated With High-risk HPV by Combining the Novel Molecular Biomarker PanHPVE4 With P16INK4a. Am J Surg Pathol. 2015;39(11):1518-28. [DOI:10.1097/PAS.0000000000000498] [PMID] [PMCID]
8
de Freitas AC, Coimbra EC, Leitão MDCG. Molecular targets of HPV oncoproteins: Potential biomarkers for cervical carcinogenesis. Biochim Biophys Acta. 2014;1845(2):91-103. [DOI:10.1016/j.bbcan.2013.12.004] [PMID]
9
Wentzensen N, von Knebel Doeberitz M. Biomarkers in cervical cancer screening. Dis Markers. 2007;23(4):315-30. [DOI:10.1155/2007/678793] [PMID] [PMCID]
10
Rk M, Su V, Sk M, Nagger S, Shrivastava K, Mishra RK, et al. The use of molecular markers ( Ki67 & p53 ) in premalignant and malignant cervical neoplasms. Trop J Pathol Microbiol. 2016;2(1):3-8. [DOI:10.17511/jopm.2016.i01.02]
11
Alshenawy HAS. Evaluation of p16, human papillomavirus capsid protein L1 and Ki-67 in cervical intraepithelial lesions: Potential utility in diagnosis and prognosis. Pathol Res Pract. 2014;210(12):916-21. [DOI:10.1016/j.prp.2014.07.007] [PMID]
12
Volgareva G, Zavalishina L, Andreeva Y, et al. Protein p16 as a marker of dysplastic and neoplastic alterations in cervical epithelial cells. BMC Cancer. 2004;4:58. [DOI:10.1186/1471-2407-4-58] [PMID] [PMCID]
13
Krishnappa P, Mohamad IB, Lin YJ, Barua A. Expression of P16 in high-risk human papillomavirus related lesions of the uterine cervix in a government hospital, Malaysia. Diagn Pathol. 2014;9:202. [DOI:10.1186/s13000-014-0202-z] [PMID] [PMCID]
14
Sangwaiya A, Gill M, Bairwa S, Chaudhry M, Sen R, Prakash Kataria S. Utility of P16/INK4a and Ki-67 in Preneoplasticand Neoplastic Lesions of Cervix. Iran J Pathol. 2018;13(3):308-16.
15
Lee H, Lee H, Cho YK. Cytokeratin7 and cytokeratin19 expression in high grade cervical intraepithelial neoplasm and squamous cell carcinoma and their possible association in cervical carcinogenesis [published correction appears in Diagn Pathol. 2017 May 22;12 (1):40]. Diagn Pathol. 2017;12(1):18. [DOI:10.1186/s13000-017-0609-4] [PMID] [PMCID]
16
Kong J, Li Y, Liu S, et al. High expression of ezrin predicts poor prognosis in uterine cervical cancer. BMC Cancer. 2013;13:520. Published 2013 Nov 4. doi:10.1186/1471-2407-13-520. [DOI:10.1186/1471-2407-13-520] [PMID] [PMCID]
17
Zhang W, Ou J, Lei F, et al. C14ORF166 overexpression is associated with pelvic lymph node metastasis and poor prognosis in uterine cervical cancer. Tumour Biol. 2016;37(1):369-379. [DOI:10.1007/s13277-015-3806-3] [PMID] [PMCID]
18
Lim S, Lee MJ, Cho I, Hong R, Lim SC. Efficacy of p16 and Ki-67 immunostaining in the detection of squamous intraepithelial lesions in a high-risk HPV group. Oncol Lett. 2016;11(2):1447-52. [DOI:10.3892/ol.2015.4071] [PMID] [PMCID]
19
Vinyuvat S, Karalak A, Suthipintawong C, Kleebkaow P, Trivijitsilp P, Triratanachat S, et al. Interobserver Reproducibility in Determining p16 Overexpression in Cervical Lesions : Use of a Combined Scoring Method. Asian Pac J Cancer Prev. 2008;9:653-7.
20
Schwarz JK, Lewis JS, Pfeifer J, Huettner P, Grigsby P. Prognostic Significance of p16 Expression in Advanced Cervical Cancer Treated With Definitive Radiotherapy. Int J Radiat Oncol. 2012 ;84(1):153-7. [DOI:10.1016/j.ijrobp.2011.11.032] [PMID]
21
Srivastava S. P16INK4A and MIB-1: An immunohistochemical expression in preneoplasia and neoplasia of the cervix. Indian J Pathol Microbiol. 2010;53(3):524. [DOI:10.4103/0377-4929.68301] [PMID]
22
Hebbar A, Murthy V. Role of p16/INK4a and Ki-67 as specific biomarkers for cervical intraepithelial neoplasia: An institutional study. J Lab Physicians. 2017;9(2):104. [DOI:10.4103/0974-2727.199630] [PMID] [PMCID]
23
Galgano MT, Castle PE, Atkins K a, Brix WK, Nassau SR, Stoler MH. Using Biomarkers as Objective Standards in the Diagnosis of Cervical Biopsies. Am J Surg Pathol. 2010 ;34(8):1077-87. [DOI:10.1097/PAS.0b013e3181e8b2c4] [PMID] [PMCID]
24
Eleutério Jr J, Lima T, Cunha M, Cavalcante D, Silva A. Immunohistochemical Expression of the Tumor Suppressor Protein p16INK4a in Cervical Adenocarcinoma. Rev Bras Ginecol e Obs / RBGO Gynecol Obstet. 2017;39(01):21-5. [DOI:10.1055/s-0037-1598042] [PMID]
25
Kanthiya K, Khunnarong J, Tangjitgamol S, Puripat N, Tanvanich S. Expression of the p16 and Ki67 in cervical squamous intraepithelial lesions and cancer. Asian Pacific J Cancer Prev. 2016;17(7):3201-6.
26
Eleutério Jr J, Giraldo PC, Gonçalves AK, Cavalcante DIM, Ferreira FVDA, Mesquita SM, et al. Prognostic markers of high-grade squamous intraepithelial lesions: the role of p16 INK4a and high-risk human papillomavirus. Acta Obstet Gynecol Scand. 2007 ;86(1):94-8. [DOI:10.1080/00016340601089727] [PMID]
27
Eleutério J, Cavalcante D, Linhares I, Pompeu M., Giraldo P. The utility of p16 INK4a and Ki-67 to identify high-grade squamous intraepithelial lesion in adolescents and young women. Indian J Pathol Microbiol. 2012;55(3):339. [DOI:10.4103/0377-4929.101740] [PMID]
28
Xing Y, Wang C, Wu J. Expression of geminin, p16, and Ki67 in cervical intraepithelial neoplasm and normal tissues. Medicine (Baltimore). 2017 ;96(26):e7302. [DOI:10.1097/MD.0000000000007302] [PMID] [PMCID]
29
Leite P, Tafuri L, Costa M, Lima M, Simões R, Leite PM de O, et al. Evaluation of the p16 and Ki-67 Biomarkers as Predictors of the Recurrence of Premalignant Cervical Cancer Lesions after LEEP Conization. Rev Bras Ginecol e Obs / RBGO Gynecol Obstet. 2017;39(06):288-93. [DOI:10.1055/s-0037-1598643] [PMID]
30
ORIGINAL_ARTICLE
Investigation of HER-2 expression and its Correlation with clinicopathological parameters and overall survival of esophageal squamous cell carcinoma patients
Background & Objective: Human epidermal growth factor receptor 2 (HER-2) exhibits a vast range of expression in esophageal squamous cell carcinoma (ESCC) patients as a biomarker. This paper aimed to investigate HER-2 expression and clinicopathological parameters of esophageal SCC. Methods: HER-2 expression was assessed in 102 ESCC patients by immunohistochemistry. The HER-2 staining intensity , according to the Gastric HER2 Biomarker1.0.0.1 version of the college of American pathologists (CAP) protocol for gastric and gastroesophageal junction cancers, was graded as 0 (no reactivity in any of the cancer cells’ membranes); 1+ (pale or hardly noticeable reactivity in the membrane of cancer cells’ cluster [≥ 5 neoplastic cells] regardless of the positive cancer cells’ percentage); 2+ (weak-to-moderate complete, basolateral, or lateral membranous reactivity regardless of the positive cancer cells’ percentage); and 3+ ( strong complete, basolateral, or lateral reactivity in the membrane of the cancer cell cluster regardless of the positive cancer cells’ percentage).In this regard, 3+ scored samples were considered as positive. If HER-2 expression was scored 2+, an additional fluorescence in situ hybridization (FISH) was performed. Fisher's exact test was employed for investigating the correlation of HER-2 expression status with patients’ clinicopathological characteristics (including age, gender, tumor location, stage, grade, infiltration level, venous invasion, lymphatic invasion, and tumor recurrence). Kaplan-Meier analysis was done for the patients’ survival assessments. Result: Five patients (~5%) were HER-2 positive and no significant association was observed between HER-2 expression and clinicopathological properties. In addition, HER-2 expression status exhibited no significant association with the patients’ overall survival (p =0.9299). Conclusion: HER-2 is not a suitable prognostic biomarker for Iranian ESCC patients.
https://ijp.iranpath.org/article_43485_75bef0daae6230c679a7180cc7eb0e46.pdf
2020-10-01
274
281
10.30699/ijp.2020.113829.2235
HER-2 receptor
Esophageal cancer
Squamous cell carcinoma
Mitra
Heidarpour
mitraheidarpour@gmail.com
1
Department of Pathology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Mehran
Taheri
mehran.drtaher@gmail.com
2
Department of Pathology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Ali
Akhavan
ali52akhavan@yahoo.com
3
Department of Radiation Oncology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Parvin
Goli
parvin_goli@yahoo.com
4
Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Amirhosein
Kefayat
ahkefayat@yahoo.com
5
Department of Oncology, Cancer Prevention Research Center, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
LEAD_AUTHOR
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Sato-Kuwabara Y, Neves JI, Fregnani JH, Sallum RA, Soares FA. Evaluation of gene amplification and protein expression of HER-2/neu in esophageal squamous cell carcinoma using Fluorescence in situ Hybridization (FISH) and immunohistochemistry. BMC cancer. 2009 Dec 1;9(1):6. [DOI:10.1186/1471-2407-9-6] [PMID] [PMCID]
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21
Roskoski Jr RJPr. The ErbB/HER family of protein-tyrosine kinases and cancer. 2014;79:34-74. [DOI:10.1016/j.phrs.2013.11.002] [PMID]
22
Cretella D. Combined use of tyrosine kinase inhibitors (TKIs) and monoclonal antibodies (mAbs) as target therapy in non-small cell lung cancer (NSCLC) (Doctoral dissertation, Università di Parma. Dipartimento di Scienze Biomediche, Biotecnologiche e Traslazionali).
23
Jørgensen JT, Nielsen KB, Kjærsgaard G, Jepsen A, Mollerup J. Gene signal distribution and HER2 amplification in gastroesophageal cancer. J Cancer. 2017;8(9):1517. [DOI:10.7150/jca.17878] [PMID] [PMCID]
24
Feng Y, Spezia M, Huang S, Yuan C, Zeng Z, Zhang L, Ji X, Liu W, Huang B, Luo W, Liu B. Breast cancer development and progression: Risk factors, cancer stem cells, signaling pathways, genomics, and molecular pathogenesis. Genes Dis. 2018 Jun 1;5(2):77-106. [DOI:10.1016/j.gendis.2018.05.001] [PMID] [PMCID]
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26
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27
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35
Gibault L, Metges JP, Conan-Charlet V, Lozac'h P, Robaszkiewicz M, Bessaguet C, Lagarde N, Volant A. Diffuse EGFR staining is associated with reduced overall survival in locally advanced oesophageal squamous cell cancer. Br J Cancer. 2005 Jul;93(1):107-15. [DOI:10.1038/sj.bjc.6602625] [PMID] [PMCID]
36
Reichelt U, Duesedau P, Tsourlakis MC, Quaas A, Link BC, Schurr PG, Kaifi JT, Gros SJ, Yekebas EF, Marx A, Simon R. Frequent homogeneous HER-2 amplification in primary and metastatic adenocarcinoma of the esophagus. Modern Pathol. 2007 Jan;20(1):120-9. [DOI:10.1038/modpathol.3800712] [PMID]
37
Wu D, Xu J, Yu G, Zhang B, Wang H, Wang C, Ru G, Sun A, Shen L, Wei Q. Expression status of fatty acid synthase (FAS) but not HER2 is correlated with the differentiation grade and prognosis of esophageal carcinoma. Hepato-gastroenterology. 2013 Jan 1;60(121):99-106. [DOI:10.5754/hge122415]
38
Yoon HH, Shi Q, Sukov WR, Wiktor AE, Khan M, Sattler CA, Grothey A, Wu TT, Diasio RB, Jenkins RB, Sinicrope FA. Association of HER2/ErbB2 expression and gene amplification with pathologic features and prognosis in esophageal adenocarcinomas. Clin Cancer Res. 2012 Jan 15;18(2):546-54. [DOI:10.1158/1078-0432.CCR-11-2272] [PMID] [PMCID]
39
Huang JX, Zhao K, Lin M, Wang Q, Xiao W, Lin MS, et al. HER2 gene amplification in esophageal squamous cell carcinoma is less than in gastroesophageal junction and gastric adenocarcinoma. 2013;6(1):13-8. [DOI:10.3892/ol.2013.1348] [PMID] [PMCID]
40
Barros-Silva JD, Leitao D, Afonso L, Vieira J, Dinis-Ribeiro M, Fragoso M, Bento MJ, Santos L, Ferreira P, Rêgo S, Brandão C. Association of ERBB2 gene status with histopathological parameters and disease-specific survival in gastric carcinoma patients. Br J Cancer. 2009 Feb;100(3):487-93. [DOI:10.1038/sj.bjc.6604885] [PMID] [PMCID]
41
ORIGINAL_ARTICLE
Overexpression of MicroRNA-506 in Jurkat (acute T Cell Leukemia) Cell Line
Background & Objective: Acute lymphoblastic leukemia (ALL) is a malignant disease that arises from various mutations in B or T-lymphoid progenitors. MicroRNAs (miRNAs) regulate gene expression by binding to the 3' untranslated region of protein-coding genes. Dysregulation of miRNA expression may result in the development of cancerous phenotypes. Therefore, for the first time in this field, the present study aims to investigate the effect of overexpression of miR-506 in Jurkat (acute T cell leukemia) cell line. Methods: In this study, Jurkat cell lines were cultured in RPMI-1640 medium. Next, miR-506 was transfected with concentrations of 50 and 100 nM with Lipofectamine 2000. The accuracy of the transfection was confirmed by the transfection of siRNA conjugated with FITC. 48 h after transfection, the cells were prepared for other tests (flow cytometry, MTT assay, and RNA extraction). The expression level of miR-506 in the cells was analyzed using the quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). Finally, SPSS 21 software was used for the data analysis. Results: According to our results, the viability of cells in concentrations of 50 and 100 nM was significantly higher than the control group. By overexpression of miR-506, the expressions of pro-apoptotic genes (p53, p21) and anti-apoptotic gene B-cell lymphoma-2 (BCL-2) are decreased and increased, respectively. Conclusion: This study showed that miR-506 may function as an oncogenic miRNA in the T- ALL cell line. In conclusion, overexpression of miR-506 leads to an increase in viable cancer cells.
https://ijp.iranpath.org/article_43486_cb0d59ecacb5cfbd59787f7fa9d481ad.pdf
2020-10-01
282
291
10.30699/ijp.2020.119627.2298
Keywords: MicroRNA
miR-506
Jurkat cell
p53 Genes
Acute Lymphoid Leukemia
Apoptosis
Shaghayegh
Rostami Yasuj
sh.rostami.lab.70@gmail.com
1
Department of Hematology, School of Para Medicine, Bushehr University of Medical Sciences, Bushehr, Iran
AUTHOR
Narges
Obeidi
nobeidi@yahoo.com
2
Department of Hematology, School of Para Medicine, Bushehr University of Medical Sciences, Bushehr, Iran
LEAD_AUTHOR
Gholamreza
Khamisipour
ghr.khamisi@gmail.com
3
Department of Hematology, School of Para Medicine, Bushehr University of Medical Sciences, Bushehr, Iran
AUTHOR
Zeynab
Gharehdaghi
z.gharehdaghi1993@gmail.com
4
Department of Hematology, School of Para Medicine, Bushehr University of Medical Sciences, Bushehr, Iran
AUTHOR
Zivar
Zangeneh
zangeneh@yahoo.com
5
Department of Hematology, School of Para Medicine, Bushehr University of Medical Sciences, Bushehr, Iran
AUTHOR
Pui C-H. Acute lymphoblastic leukemia: Springer; 2011. [DOI:10.1007/978-3-642-16483-5_57]
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Shi C, Zhang X, Li X, Zhang L, Li L, Sun Z, et al. Effects of microRNA-21 on the biological functions of T-cell acute lymphoblastic lymphoma/leukemia. Oncology letters. 2016;12(5):4173-80. [DOI:10.3892/ol.2016.5163] [PMID] [PMCID]
2
Passaro D, Quang CT, Ghysdael J. Microenvironmental cues for T‐cell acute lymphoblastic leukemia development. Immunological reviews. 2016;271(1):156-72. [DOI:10.1111/imr.12402] [PMID]
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Xu Y, Yang J, Li X. MicroRNA-25 promotes T-cell acute lymphoblastic leukemia cell proliferation and invasion by directly targeting EphA8. Int J Clin Exp Pathol. 2016;9(5):5292-8.
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5
Alizadeh S, Kaviani S, Soleimani M, Abroun S, Kashani-Khatib Z, Asgharzadeh A, et al. Mir-55 inhibition can reduce cell proliferation and induce apoptosis in Jurkat (Acute T cell Leukemia) cell line. Iranian journal of pediatric hematology and oncology. 2014;4(4):141.
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9
Lv M, Zhang X, Jia H, Li D, Zhang B, Zhang H, et al. An oncogenic role of miR-142-3p in human T-cell acute lymphoblastic leukemia (T-ALL) by targeting glucocorticoid receptor-α and cAMP/PKA pathways. Leukemia. 2012;26(4):769-77. [DOI:10.1038/leu.2011.273] [PMID]
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29
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30
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36
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37
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38
ORIGINAL_ARTICLE
Association of Human Papilloma Virus and Epstein-Barr Virus with Ovarian Cancer in Shiraz, Southwestern Iran
Background & Objective: Ovarian cancer is one of the most common cancers amongst women. The association of Human papillomavirus (HPV) and Epstein-Barr virus (EBV) with ovarian cancer is inconclusive; therefore, the aims of this study were to evaluate the frequency of HPV and EBV in malignant, borderline, benign and normal ovarian tissues. Methods: In this case-control study, 205 Paraffin-embedded ovarian tissue specimens including 68 malignant, 27 borderline, 65 benign, and 45 normal tissues were included from December 2014 to January 2018 and subjected to DNA extraction. The β-globin gene was amplified using PCR to confirm the quality of the extracted DNA. The genomes of HPV (genotypes 16 and 18) and EBV were identified, using specific primers by PCR. Results: The mean age of participants was 43.42 ± 15.4 years. The frequency of HPV was statistically significant between malignant versus benign (p =0.02) and control groups (p =0.002), but not with borderline tumor group (p =0.78). Amongst HPV infected samples, 1 (4.5%) and 14 (63.6%) samples were infected with types 16 and 18, respectively. Also 4 (18.2 %) samples were infected with both genotypes. Eleven samples including 7(10.3%) malignant, 1 (3.7%) borderline, 3 (4.6%) benign and none (0%) of normal control groups were infected with EBV, which was statistically different between malignant and the normal control group (p =0.03). Conclusion: The results of our study showed the possible role of high risk HPVs as well as EBV in pathogenesis of ovarian cancer, and further studies are recommended to confirm these findings.
https://ijp.iranpath.org/article_43601_e26f297d95a22b93c9327e6285eed0fc.pdf
2020-10-01
292
298
10.30699/ijp.2020.119681.2306
Epstein-Barr virus
Human papillomavirus
Ovarian Cancer
Mohammad Reza
Shokouh
mrshg1372@gmail.com
1
Department of Bacteriology and Virology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Akbar
Safaie
safaeia@sums.ac.ir
2
Pathology Department, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Afagh
Moattari
moattaria@sums.ac.ir
3
Department of Bacteriology & Virology, School of Medicine, Shiraz University of Medical Sciences Shiraz, Iran
AUTHOR
Jamal
Sarvari
sarvarij@sums.ac.ir
4
Department of Bacteriology and Virology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
LEAD_AUTHOR
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39
ORIGINAL_ARTICLE
Thiopurine S-methyltransferase and Pemphigus Vulgaris: A Phenotype-Genotype Study
Background & Objective: Thiopurine drugs are considered as a treatment modality in various autoimmune disorders including pemphigus vulgaris (PV). These drugs are metabolized by an enzyme “Thiopurine S-methyl transferase” (TPMT). Various variants of this enzyme may have decreased activity leading to serious drug side effects. To investigate the phenotype and genotype of TPMT in PV patients receiving thiopurine drugs. Methods: 50 patients (29 women and 21 men) with pemphigus vulgaris treating with standard dose of Thiopurine drugs were selected. Sex, age, result of liver function test and complete blood count were recorded. Genotyping of two common non-functional allele (TPMT*2 and TPMT*3C) by Allele-specific and RFLP-PCR was performed. TPMT enzymatic level was determined by an ELISA based method. Results: Of patients, 36 (72%) were found to have normal TPMT level; and 12, (24%) had higher level of enzyme and 2, 4% had low TPMT enzyme, but none of the patients showed mutant TPMT*2 and TPMT*3C alleles. None of the patients showed hepatotoxicity and bone marrow suppression. Conclusion: The phenotypic assay based on ELISA method may have false positive and misleading results but genotyping using PCR-RFLP and allele specific PCR is accurate, simple and cost-effective and can be used in patients decided to undergo thiopurine treatment.
https://ijp.iranpath.org/article_43602_a1b48f225df1e1fa9f755c885065579f.pdf
2020-10-01
299
305
10.30699/ijp.2020.121365.2320
Allele specific PCR
PCR-RFLP
Thiopurine S- methyl transferase
Thiopurine drugs
ELISA test
Maral
Mokhtari
maral_mokhtari@yahoo.com
1
Pathology Department, Shahid Faghihi Hospital, Shiraz University of Medical Sciences, Shiraz, Iran
LEAD_AUTHOR
Farzaneh
Mostanbet
farzanehmostanbet@yahoo.com
2
Pathology Department, Shahid Faghihi Hospital, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Saideh
Nekooee Fard
s.nekooee@gmail.com
3
Pathology Department, Shahid Faghihi Hospital, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Golsa
Shekarkhar
g.shekarkhar@gmail.com
4
Pathology Department, Shahid Faghihi Hospital, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Mozhdeh
Sepaskhah
sepaskhah_m@yahoo.com
5
Dermatology Department, Shahid Faghihi Hospital, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Maryam Sadat
Sadati
msadati63@yahoo.com
6
Dermatology Department, Shahid Faghihi Hospital, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Diaz LA, Giudice GJ. End of the century overview of skin blisters. Arch Dermatol. 2000;136(1):106-12. [DOI:10.1001/archderm.136.1.106] [PMID]
1
Broussard KC, Leung TG, Moradi A, Thorne JE, Fine JD. Autoimmune bullous diseases with skin and eye involvement: Cicatricial pemphigoid, pemphigus vulgaris, and pemphigus paraneoplastica. Clin Dermatol. 2016;34(2):205-13. [DOI:10.1016/j.clindermatol.2015.11.006] [PMID]
2
Gregoriou S, Efthymiou O, Stefanaki C, Rigopoulos D. Management of pemphigus vulgaris: challenges and solutions. Clin Cosmet Investig Dermatol. 2015;8(1):521-7. [DOI:10.2147/CCID.S75908] [PMID] [PMCID]
3
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4
Gordon M, Taylor K, Akobeng AK, Thomas AG. Azathioprine and 6-mercaptopurine for maintenance of surgically-induced remission in Crohn's disease. Cochrane Database Syst Rev. 2014(8):Cd010233. [DOI:10.1002/14651858.CD010233.pub2] [PMCID]
5
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6
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8
Zhang B, Xu XW, Zeng XJ, Li DK. Correlation of thiopurine methyltransferase activity and 6-thioguanine nucleotide concentration in Han Chinese patients treated with azathioprine 25 to 100 mg: A 1-year, single-center, prospective study. Curr Ther Res Clin Exp. 2006;67(4):270-82. [DOI:10.1016/j.curtheres.2006.07.002] [PMID] [PMCID]
9
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14
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15
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16
Sanderson JD. TPMT Testing Before Starting Azathioprine or Mercaptopurine: Surely Just Do It?. Gastroenterology. 2015;149(4):850-3. [DOI:10.1053/j.gastro.2015.08.040] [PMID]
17
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18
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20
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21
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22
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23
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24
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25
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26
Fong WY, Ho CC, Poon WT. Comparison of direct sequencing, real-time PCR-high resolution melt (PCR-HRM) and PCR-restriction fragment length polymorphism (PCR-RFLP) analysis for genotyping of common Thiopurine intolerant variant alleles NUDT15 c. 415C> T and TPMT c. 719A> G (TPMT* 3C). Diagnostics. 2017;7(2): E27. [DOI:10.3390/diagnostics7020027] [PMID] [PMCID]
27
Ho CC, Fong WY, Lee YH, Poon WT. Novel Tetra-Primer ARMS-PCR Assays for Thiopurine Intolerance Susceptibility Mutations NUDT15 c. 415C> T and TPMT c. 719A> G (TPMT* 3C) in East Asians. Genes. 2017;8(10):E285. [DOI:10.3390/genes8100285] [PMID] [PMCID]
28
Gisbert JP, Gomollon F. Thiopurine-induced myelotoxicity in patients with inflammatory bowel disease: a review. Am J Gastroenterol. 2008;103(7):1783-800. [DOI:10.1111/j.1572-0241.2008.01848.x] [PMID]
29
Shipkova M, Niedmann PD, Armstrong VW, Oellerich M, Wieland E. Determination of thiopurine methyltransferase activity in isolated human erythrocytes does not reflect putative in vivo enzyme inhibition by sulfasalazine. Clin Chem. 2004;50(2):438-41. [DOI:10.1373/clinchem.2003.026096] [PMID]
30
Brouwer C, De Abreu RA, Keizer-Garritsen JJ, Lambooy LH, Ament K, ter Riet PG, et al. Thiopurine methyltransferase in acute lymphoblastic leukaemia: biochemical and molecular biological aspects. Eur J Cancer. 2005;41(4):613-23. [DOI:10.1016/j.ejca.2004.10.027] [PMID]
31
ORIGINAL_ARTICLE
The Association of FLT3-ITD Gene Mutation with Bone Marrow Blast Cell Count, CD34, Cyclin D1, Bcl-xL and hENT1 Expression in Acute Myeloid Leukemia Patients
Background & Objective: FLT3-ITD has been recently used as a molecular prognostic marker for risk classification in acute myeloid leukemia (AML) therapy. In this study we aimed to investigate the association of FLT3-ITD gene mutation with bone marrow blast cell count, CD34 expression as malignant cell burden, cyclin D1 and Bcl-xL expressions as indexes of cell proliferation and anti-apoptosis and human equilibrative nucleoside transporter 1 (hENT1) expression as cytarabine transporter during AML treatment. Methods: We investigated FLT3-ITD mutations, bone marrow blast cell count, CD34, cyclin D1, Bcl-xL and hENT1 expression in bone marrow aspirates from 22 de novo AML patients in a cross sectional study. Results: FLT3-ITD mutations were observed in 5 out of 22 de novo AML patients (22.7%). Patient with FLT3-ITD mutations had higher blast cell counts (79.5% vs 56.1%, p =0.004). In patients with FLT3-ITD mutations, CD34 and cyclin D1 expressions were higher (MFI 328.80 vs 25.78, p =0.003 and MFI 74.51 vs 57.15 p =0.005) than the patients without mutations. hENT1 expression in AML with FLT3-ITD mutation was lower (MFI 29.64 versus 56.32, p =0.0000) than in mutation-free AML. There was no significant difference in Bcl-xL expression between patients with and without mutations (p =0.61). Conclusion: A significant association was found between FLT3-ITD gene mutations in AML patients with bone marrow blast cell count, CD34, cyclin D1 and hENT1 expressions, however no association was obtained with Bcl-xL expression. These findings support the role of such mutation in pathogenesis of AMLand its contribution in rearrangement of standard therapy with cytarabine in management of AML.
https://ijp.iranpath.org/article_43603_91746cc84a69ce7653423b137e55c0b0.pdf
2020-10-01
306
312
10.30699/ijp.2020.122579.2328
AML
Bcl-xL
Blast cell count
CD34
Cyclin D1
FLT3-ITD
hENT1
Paulus
Notopuro
paulusbudiono@yahoo.com
1
Faculty of Medicine, Airlangga University, Jawa, Indonesia
LEAD_AUTHOR
Jusak
Nugraha
jusakn.nugraha@yahoo.com
2
Department of Clinical Pathology, Faculty of Medicine, Airlangga University, Jawa, Indonesia
AUTHOR
Budi
Utomo
plsbn2010@yahoo.co.id
3
Department of Public Health, Faculty of Medicine, Airlangga University, Jawa, Indonesia
AUTHOR
Harianto
Notopuro
paulusbudiono77@gmail.com
4
4. Department of Biochemistry and Molecular Biology, Faculty of Medicine, Airlangga University, Jawa, Indonesia
AUTHOR
Seer cancer statistic review (CSR) 1975 - 2014 [Internet]. National Cancer Institute. 2017 [cited September 29, 2017]. Available from: http://seer.cancer.gov/csr/1975-2014/.
1
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Wang L, Xu Wl, Meng Ht, Qian Wb, Mai Wy, Tong Hy, et al. FLT3 and NPM1 mutations in Chinese patients with acute myeloid leukemia and normal cytogenetics. J Zhejiang Univ-Sci B ( Biomed & Biotechnol ). 2010;11(10):762-70. [DOI:10.1631/jzus.B1000052] [PMID] [PMCID]
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Thiede C, Steudel C, Mohr B, Schaich M, Schakel U, Platzbecker U, et al. Analysis of FLT3-activating mutations in 979 patients with acute myelogenous leukemia : association with FAB subtypes and identification of subgroups with poor prognosis. Blood 2002;99:4326-35. [DOI:10.1182/blood.V99.12.4326] [PMID]
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25
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35
ORIGINAL_ARTICLE
Comparison of patient-collected and lab technician-collected nasopharyngeal and oropharyngeal swabs for detection of COVID-19 by RT-PCR
Background & Objective: A simple approach to prevent close contact in healthcare settings during the COVID-19 outbreak is to train patients to collect their own nasopharyngeal and oropharyngeal swabs and deliver them to medical laboratories to have them processed. The aim of our study was to compare lab technician- with patient- collected oropharyngeal and nasopharyngeal samples for detection of the coronavirus disease 2019 (COVID 19) using rapid real-time polymerase chain reaction (rRT-PCR). Methods: Fifty adult patients with flu-like symptoms and radiologic findings compatible with atypical pneumonia who were admitted to the infectious diseases ward of Imam Khomeini Hospital Complex, Tehran, Iran, with a clinical diagnosis of COVID-19 from February 28 to April 27 of 2020 were randomly selected and entered in our study. Two sets of naso- and oropharyngeal swabs were collected, one set by a lab technician and the other by the patients, and the COVID-19 rRT-PCR test was performed. Results: Of 50 selected cases, in seven patients all collected naso- and oropharyngeal swabs tested positive, and in 22 patients all samples tested negative for COVID-19 in rRT-PCR. Discrepancies between rRT-PCR results of lab technician- and patient-collected swabs were observed in 12 nasopharyngeal and 13 oropharyngeal specimens. Positive lab technician-collected and negative patient-collected samples were observed in 10 and 5 nasopharyngeal and oropharyngeal specimens, respectively. Negative lab technician-collected and positive patient-collected samples were observed in two and seven nasopharyngeal and oropharyngeal specimens, respectively. The overall percentage of agreement among both nasopharyngeal and oropharyngeal swabs taken by a lab technician and patients was 76% with a kappa value of 0.49 (p =0.001). Conclusion: Based on our findings, lab technician-collected naso- and oropharyngeal swabs cannot be replaced by patient-collected ones with regard to COVID-19 rRT-PCR.
https://ijp.iranpath.org/article_43604_61451c8f2eab4980ad5b46444f8366a2.pdf
2020-10-01
313
319
10.30699/ijp.2020.127312.2387
COVID-19
Oropharynx
Nasopharynx
Real-Time Polymerase Chain Reaction
Specimen collection
Alireza
Abdollahi
dr_p_abdollahi@yahoo.com
1
Department of Pathology, Imam Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Abbas
Shakoori
shakoori@yahoo.com
2
Medical Genetic Ward, Imam Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Hoda
Khoshnevis
h.khoshnevis@yahoo.com
3
Supervisor of Genetic Ward, Imam Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Mohammad
Arabzadeh
m.arabzadeh@yahoo.com
4
Laboratory Senior Technical Associate of Genetic Ward, Imam Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Seyed Ali
Dehghan Manshadi
sa.dmanshadi@yahoo.com
5
Department of Infectious Diseases and Tropical Medicine, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Esmaeil
Mohammadnejad
emohammadnejad@yahoo.com
6
Department of Medical-Surgical Nursing, School of Nursing and Midwifery, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Dorsa
Ghasemi
dorsa.gh@yahoo.com
7
Department of Pathology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Maryam
Safari Aboksari
m.safariab@yahoo.com
8
Department of Pathology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Shaban
Alizadeh
sh.alizadeh@yahoo.com
9
Hematology Department, Allied medical school, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Vahid
Mehrtash
vahidmehrtash@gmail.com
10
Department of Pathology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Arezoo
Eftekhar-javadi
e_eftekhar@tums.ac.ir
11
Department of Pathology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Masoomeh
Safaei
safaeima32@gmail.com
12
Department of Pathology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Buddhisha Udugama, Pranav Kadhireson, Hannah N. Kozlowski ,et al. Diagnosing COVID-19 :The disease and tools for detection. March 2020;10.1021/acsnano.oco2624 [DOI:10.1021/acsnano.0c02624] [PMID] [PMCID]
1
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2
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3
Huang C, Wang Y, Li X, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet. 2020;396:497-506. [DOI:10.1016/S0140-6736(20)30183-5]
4
Dhiman N, Miller RM, Finley JL, Sztajnkrycer MD, Nestler DM, Boggust AJ, Jenkins SM, Smith TF, Wilson JW, Cockerill III FR, Pritt BS. Effectiveness of patient-collected swabs for influenza testing. InMayo Clinic Proceedings 2012 Jun 1 (Vol. 87, No. 6, pp. 548-554). Elsevier. [DOI:10.1016/j.mayocp.2012.02.011] [PMID] [PMCID]
5
Shantanu Nundy, MD, Kavitak Patel, MD. Self-service Diagnosis of COVID-19-Ready for prime time? .March 2020;PA19462
6
Centers for Disease Control and Prevention, Corona Virus (COVID-2019), Last reviewed: March 20, 2020, https://www.cdc.gov/coronavirus/2019-ncov/symptoms-testing/
7
Lambert SB, Allen KM, Druce JD, Birch CJ, Mackay IM, Carlin JB, Carapetis JR, Sloots TP, Nissen MD, Nolan TM. Community epidemiology of human metapneumovirus, human coronavirus NL63, and other respiratory viruses in healthy preschool-aged children using parent-collected specimens. Pediatrics. 2007 Oct 1;120(4):e929-37. [DOI:10.1542/peds.2006-3703] [PMID]
8
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9
Esposito S, Molteni CG, Daleno C, et al. Collection by trained pediatricians or parents of mid-turbinate nasal flocked swabs for the detection of influenza viruses in childhood. Virol J. 2010;7:85 [DOI:10.1186/1743-422X-7-85] [PMID] [PMCID]
10
Seaman CP, Tran LT, Cowling BJ, Sullivan SG. Self-collected compared with professional-collected swabbing in the diagnosis of influenza in symptomatic individuals: A meta-analysis and assessment of validity. J Clin Virol. 2019 Sep 1;118:28-35. [DOI:10.1016/j.jcv.2019.07.010] [PMID]
11
Jackson ML, Nguyen M, Kirlin B, Madziwa L. Self-collected nasal swabs for respiratory virus surveillance. InOpen forum infectious diseases 2015 Dec 1 (Vol. 2, No. 4). Oxford University Press. [DOI:10.1093/ofid/ofv152] [PMID] [PMCID]
12
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13
Chunqin Longb, Huaxiang Xuc, Qinglin Shend , Xianghai Zhangb , Bing Fana, Chuanhong Wang. Diagnosis of the Coronavirus disease (COVID-19): rRT-PCR or CT? Europ J Radiol. 126 (2020) 108961 [DOI:10.1016/j.ejrad.2020.108961] [PMID] [PMCID]
14
Udugama B, Kadhiresan P, Kozlowski HN, Malekjahani A, Osborne M, Li VY, Chen H, Mubareka S, Gubbay JB, Chan WC. Diagnosing COVID-19: the disease and tools for detection. ACS nano. 2020 Mar 30;14(4):3822-35. [DOI:10.1021/acsnano.0c02624] [PMID] [PMCID]
15
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Serology testing for COVID-19. Johns Hopkins Center for Health Security, centerforhealthsecurity.org, 02/28/2020
17
Gilsenan-Reed C, Higgins G, Langlois N. Determining a sampling regime for PCR detection of respiratory tract viral infection at coronial post-mortem examinations. Forensic Sci Med Pathol 2020 Jun 23. [DOI:10.1007/s12024-020-00273-w] [PMID] [PMCID]
18
Rahmani AR, Leili M, Azarian G, Poormohammadi A. Sampling and detection of corona viruses in air: A mini review. Sci Total Environ 2020 Jun 15;740:140207. [DOI:10.1016/j.scitotenv.2020.140207] [PMID] [PMCID]
19
Waghmare A, Krantz EM, Baral S, Vasquez E, Loeffelholz T, Chung EL, et al. Reliability of self-sampling for accurate assessment of respiratory virus viral and immunologic kinetics. medRxiv 2020 Apr 6. [DOI:10.1101/2020.04.03.20051706]
20
.Mohammadi A, Esmaeilzadeh E, Li Y, Bosch RJ, Li J. SARS-CoV-2 Detection in Different Respiratory Sites: A Systematic Review and Meta-Analysis. medRxiv 2020 May 19. [DOI:10.1101/2020.05.14.20102038]
21
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22
Piras A, Rizzo D, Longoni E, Turra N, Urru S, Saba PP,et al. Nasopharyngeal swab collection in the suspicion of Covid-19. Am J Otolaryngol 2020 May 27:102551. [DOI:10.1016/j.amjoto.2020.102551] [PMID] [PMCID]
23
Mavian C, Pond SK, Marini S, Magalis BR, Vandamme AM, Dellicour S, et al. Sampling bias and incorrect rooting make phylogenetic network tracing of SARS-COV-2 infections unreliable. Proc Natl Acad Sci U S A 2020 Jun 9;117(23):12522-12523. [DOI:10.1073/pnas.2007295117] [PMID] [PMCID]
24
Petruzzi G, De Virgilio A, Pichi B, Mazzola F, Zocchi J, Mercante G, et al. COVID-19: Nasal and oropharyngeal swab. Head Neck 2020 Jun;42(6):1303-1304. [DOI:10.1002/hed.26212] [PMID] [PMCID]
25
Mawaddah A, Gendeh HS, Lum SG, Marina MB. Upper respiratory tract sampling in COVID-19. Malays J Pathol 2020 Apr;42(1):23-35.
26
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27
Péré H, Podglajen I, Wack M, Flamarion E, Mirault T, Goudot G,et al. Nasal Swab Sampling for SARS-CoV-2: a Convenient Alternative in Times of Nasopharyngeal Swab Shortage. J Clin Microbiol 2020 May 26;58(6). [DOI:10.1128/JCM.00721-20] [PMID] [PMCID]
28
Ye G, Li Y, Lu M, Chen S, Luo Y, Wang S, et al. Experience of different upper respiratory tract sampling strategies for detection of COVID-19. J Hosp Infect 2020 May;105(1):1-2. [DOI:10.1016/j.jhin.2020.03.012] [PMID] [PMCID]
29
ORIGINAL_ARTICLE
Genetic Diversity of ctxB Gene Among Classical O1 and El Tor Strains of Vibrio cholerae using High-Resolution Melting Curve Analysis
Background & Objective: Vibrio cholerae is a natural inhabitant of the environment and causes severe diarrhea ailments (cholera) that affects thousands of people each year worldwide. The most important virulence factors of this pathogen are cholera toxin (cholera toxin CT) and Type IV pili (toxin co-regulated pili TCP), which are encoded within the genome of the filamentous bacteriophage CTXφ. In the present study, according to researchers’ report on genotypic variations of cholera toxin, we evaluated the sequence of ctxB subunit obtained from 100 strains of patients infected with cholera in Iran. Methods: The evaluation of genotype variations of cholera toxin was made by high-resolution melting curve analysis illustrating a single nucleotide change. Then, ctxB gene sequencing was performed. Through this analysis and the sequencing process, two standard samples were studied. Results: Using serologic tests, all the strains analyzed in this study were identified to be in O1 serotype. However, there have been differences in sequences of ctxB as some were similar to V. cholerae O1 biovar El Tor str. N16961 while others were similar to the genotype of V. cholerae ATCC 14035. We did not observe any particular pattern within the process of mutation. Conclusion: The analysis of the new samples of ctxB showed that they were potentially different. It seems that these complicated species were affected by a new genetic exchange of El Tor and classic genotypes.
https://ijp.iranpath.org/article_43605_2d91f7412fc010515c8f2ea38e3ef7cc.pdf
2020-10-01
320
325
10.30699/ijp.2020.127793.2393
ctxB
Vibrio cholerae
High-resolution melt analysis
Genotyping Techniques
Mahdieh
Mahboobi
mahdiehmahboobi@gmail.com
1
Applied Microbiology Research Center, Systems Biology and Poisonings Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran
AUTHOR
Reza
Mirnejad
rmirnejad@yahoo.com
2
Molecular Biology Research Center Systems Biology and Poisonings Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Hamid
Sedighian
osedighian@gmail.com
3
Applied Microbiology Research Center, Systems Biology and Poisonings Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran
AUTHOR
Vahhab
Piranfar
vahab.p@gmail.com
4
Research and Development Department, Farname Inc, Thornhill, Canada
AUTHOR
Abbas Ali
Imani Fooladi
imanifouladi.a@gmail.com
5
Applied Microbiology Research Center, Systems Biology and Poisonings Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Hun Yoon S, Waters CM. Vibrio cholerae. Trends Microbiol. 2019;27(9):806-7. [DOI:10.1016/j.tim.2019.03.005] [PMID]
1
Mandal S, Mandal MD, Pal NK. Cholera: a great global concern. Asian Pac J Trop Med.. 2011;4(7):573-80. [DOI:10.1016/S1995-7645(11)60149-1]
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3
Muanprasat C, Chatsudthipong V. Cholera: pathophysiology and emerging therapeutic targets. Future Med Chem. 2013;5(7):781-98. [DOI:10.4155/fmc.13.42] [PMID]
4
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5
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6
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9
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10
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Safa A, Sultana J, Dac Cam P, Mwansa JC, KONG YCR. Vibrio cholerae O1 hybrid El Tor strains, Asia and Africa. Emerg Infect Dis. 2008. [DOI:10.3201/eid1406.080129] [PMID] [PMCID]
12
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13
Nair GB, Qadri F, Holmgren J, Svennerholm A-M, Safa A, Bhuiyan NA, et al. Cholera due to altered El Tor strains of Vibrio cholerae O1 in Bangladesh. J of clin microbiol. 2006;44(11):4211-3. [DOI:10.1128/JCM.01304-06] [PMID] [PMCID]
14
Son MS, Megli CJ, Kovacikova G, Qadri F, Taylor RK. Characterization of Vibrio cholerae O1 El Tor biotype variant clinical isolates from Bangladesh and Haiti, including a molecular genetic analysis of virulence genes. J Clin microbiol. 2011;49(11):3739-49. [DOI:10.1128/JCM.01286-11] [PMID] [PMCID]
15
Marashi SMA, Rajabnia R, Fooladi AAI, Hojati Z, Moghim S, Esfahani BN. Determination of ctxAB expression in Vibrio cholerae Classical and El Tor strains using Real-Time PCR. International journal of molecular and cellular medicine. 2013;2(1):9.
16
Tehrani FHE, Moradi M, Ghorbani N. Bacterial Etiology and Antibiotic Resistance Patterns in Neonatal Sepsis in Tehran during 2006-2014. Iran J Pathol. 2017;12(4):356. [PMCID] [DOI:10.30699/IJP.2017.27992]
17
Nusrin S, Khan GY, Bhuiyan N, Ansaruzzaman M, Hossain M, Safa A, et al. Diverse CTX phages among toxigenic Vibrio cholerae O1 and O139 strains isolated between 1994 and 2002 in an area where cholera is endemic in Bangladesh. J clin microbiol. 2004;42(12):5854-6. [DOI:10.1128/JCM.42. 12.5854-5856.2004] [PMID] [PMCID]
18
van der Stoep N, van Paridon CD, Janssens T, Krenkova P, Stambergova A, Macek M, et al. Diagnostic guidelines for high‐resolution melting curve (HRM) analysis: An interlaboratory validation of BRCA1 mutation scanning using the 96‐well LightScanner™. Human mutation. 2009;30(6):899-909. [DOI:10.1002/humu.21004] [PMID]
19
Giannopoulos A, Rougkala N, Loupis T, Mantzourani M, Viniou N-A, Variami E, et al. Detection of CALR mutations using high resolution melting curve analysis (HRM-A); application on a large cohort of greek et and mf patients. Mediterr J Hematol Infect Dis. 2019;11(1). [DOI:10.4084/mjhid.2019.009] [PMID] [PMCID]
20
Cruz TD, Publow AJ, University VC, America USo. qPCR Genotype Determination and Mixture Detection Using High Resolution Melting Curve Analysis of STR Loci. 2019.
21
Mehrabadi JF, Morsali P, Nejad HR, Fooladi AAI. Detection of toxigenic Vibrio cholerae with new multiplex PCR. J Infect Public Health. 2012;5(3):263-7. [DOI:10.1016/j.jiph.201 2.02.004] [PMID]
22
Sedighian H, Halabian R, Amani J, Heiat M, Taheri RA, Fooladi AAI. Manufacturing of a novel double-function ssDNA aptamer for sensitive diagnosis and efficient neutralization of SEA. Analytical biochemistry. 2018;548:69-77. [DOI:10.1016/j.ab.2018.02.017] [PMID]
23
Rad HS, Mousavi SL, Rasooli I, Amani J, Nadooshan MRJ. EspA-Intimin chimeric protein, a candidate vaccine against Escherichia coli O157: H7. Iran J Microbiol. 2013;5(3):244.
24
Habibian R, Khayyat Khameneie M, Sedighian H, Daneshi F, Bagheri Moghadam M, Mahboobi M. Virulence factor diversity between imipenem resistant and imipenem susceptible strains of Escherichia coli isolated from hospitalized patients with severe urinary tract infections. Biosciences Biotech Res Asia. 2014;11(2):469-77. [DOI:10.13005/bbra/1297]
25
Xi D, Li Y, Yan J, Li Y, Wang X, Cao B. Small RNA coaR contributes to intestinal colonization in Vibrio cholerae via the two‐component system EnvZ/OmpR. Env Microbiol. 2019.
26
Taylor C. Mutation scanning using high-resolution melting. Biochemical Society Transactions. 2009;37(2):433. [DOI:10.1042/BST0370433] [PMID]
27
Fazil MT, Bhanumathi R, Pandey H, Singh D. Characterization of Vibrio cholerae O139 belonging to multiple ribotypes and isolated from diarrhoeal patients in Kerala, southern India. Infection, Genetics and Evolution. 2011;11(2):454-9. [DOI:10.1016/j.meegid.2010.12.008] [PMID]
28
Choi SY, Lee JH, Jeon Y-S, Lee HR, Kim EJ, Ansaruzzaman M, et al. Multilocus variable-number tandem repeat analysis of Vibrio cholerae O1 El Tor strains harbouring classical toxin B. J med microbiol 2010;59(7):763-9. [DOI:10.1099/jmm.0.017939-0] [PMID]
29
Le Roux WJ, Van Blerk GN. Use of a high resolution melt real-time polymerase chain reaction (PCR) assay for the environmental monitoring of Vibrio cholerae. 2011.
30
Jin D, Luo Y, Zhang Z, Fang W, Ye J, Wu F, et al. Rapid molecular identification of Listeria species by use of real-time PCR and high-resolution melting analysis. FEMS Microbiol Lett. 2012;330(1):72-80. [DOI:10.1111/j.1574-6968.2012.02535.x] [PMID]
31
Piranfar V, Sharif M, Hashemi M, Vahdati AR, Mirnejad R. Detection and discrimination of two Brucella species by multiplex real-time PCR and high-resolution melt analysis curve from human blood and comparison of results using RFLP. Iran J Basic Med Sci. 2015;18(9):909.
32
Masjedian Jazi F, Mirnejad R, Piranfar V, Amir Mozafari N, Zahraei Salehi T, Khormali M, et al. Real-time PCR and high-resolution melt analysis methods for detection of pathogenic species of Brucella. Journal of Laboratory Medicine. 2017;41(6):325-31. [DOI:10.1515/labmed-2017-0030]
33
ORIGINAL_ARTICLE
Matrix metalloproteinase-9 (MMP-9) Expression in Non-Small Cell Lung Carcinoma and Its Association with Clinicopathologic Factors
Background & Objective: Matrix metalloproteinases-9 (MMP-9) is one of the most important enzymes to breakdown extracellular matrix which plays a major role in tumor invasion and metastasis. This study aimed to determine tumor MMP-9 expression in non-small-cell lung carcinoma (NSCLC) and whether it is associated with histopathologic factors and has prognostic value to affect overall survival (OS). Methods: The specimens of 92 patients with NSCLC diagnosis were included. Tumor sections were stained by immunohistochemistry method. Using scores for the percentage of cells positively stained and the intensity of staining, MMP-9 expression total score was classified as low-score (scores of 0 to 2), moderate-score (scores of 3 to 5), or high-score (scores of 6 or 7). OS was defined as the time interval since the diagnosis of NSCLC to the status at the last follow-up (dead or alive). The follow up period was up to 70 months. Results: About 74% of undifferentiated specimens (grade III tumors) showed high scores for MMP-9 expression which was significantly higher than moderately differentiated tumors (25% had high scores for MMP-9 expression) and well differentiated ones which did not have high scores (p <0.001). A total of 74 patients (80.4%) died during the follow-up period. Of this, 36% had high scores for MMP-9 expression. In contrast, none of the patients who were alive at the last follow-up had high scores for MMP-9 expression (p <0.001). Median OS was significantly lower in high score group (6 months) compared to moderate score (9 months) and high score group (15 months) (p <0.001). Conclusion: MMP-9 expression may serve as a significant prognostic factor for mortality and overall survival in NSCLC. Undifferentiated tumors significantly express higher MMP-9 immunohistochemically.
https://ijp.iranpath.org/article_43606_8466358de55ee98b8c858b8174cad5d9.pdf
2020-10-01
326
333
10.30699/ijp.2020.95177.1940
Immunohistochemistry
Matrix metalloproteinase 9
Non-small-cell lung carcinoma
Amir Hossein
Jafarian
jafarianah@mums.ac.ir
1
Pathology Department, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Melika
Kooshki forooshani
melika_k90@yahoo.com
2
Pathology Department, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Hossein
Reisi
reisih881@mums.ac.ir
3
Pathology Department, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Nema
Mohamadian roshan
roshann@mums.ac.ir
4
Pathology Department, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
Siegel R, Naishadham D, Jemal A. Cancer statistics, 2013. CA Cancer J Clin 2013;63(1):11-30. [DOI:10.3322/caac.21166] [PMID]
1
Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D. Global cancer statistics. CA Cancer J Clin 2011;61(2):69-90. [DOI:10.3322/caac.20107] [PMID]
2
Cooke DT, Nguyen DV, Yang Y, Chen SL, Yu C, Calhoun RF. Survival comparison of adenosquamous, squamous cell, and adenocarcinoma of the lung after lobectomy. Ann Thorac Surg 2010;90(3):943-8. [DOI:10.1016/j.athoracsur.2010.05.025] [PMID]
3
Hubbard MO, Fu P, Margevicius S, Dowlati A, Linden PA. Five-year survival does not equal cure in non-small cell lung cancer: a Surveillance, Epidemiology, and End Results-based analysis of variables affecting 10- to 18-year survival. J Thorac Cardiovasc Surg 2012;143(6):1307-13. [DOI:10.1016/j.jtcvs.2012.01.078] [PMID]
4
Han JY, Kim HS, Lee SH, Park WS, Lee JY, Yoo NJ. Immunohistochemical expression of integrins and extracellular matrix proteins in non-small cell lung cancer: correlation with lymph node metastasis. Lung Cancer 2003;41(1):65-70. [DOI:10.1016/S0169-5002(03)00146-6]
5
Cox G, Jones JL, O'Byrne KJ. Matrix metalloproteinase 9 and the epidermal growth factor signal pathway in operable non-small cell lung cancer. Clin Cancer Res 2000;6(6):2349-55.
6
Willumsen N, Bager CL, Leeming DJ, Smith V, Christiansen C, Karsdal MA, et al. Serum biomarkers reflecting specific tumor tissue remodeling processes are valuable diagnostic tools for lung cancer. Cancer Med 2014;3(5):1136-45. [DOI:10.1002/cam4.303] [PMID] [PMCID]
7
Wen YL, Li L. Correlation between matrix metalloproteinase-9 and vascular endothelial growth factor expression in lung adenocarcinoma. Genet Mol Res 2015;14(4):19342-8. [DOI:10.4238/2015.December.29.44] [PMID]
8
Gong L, Wu D, Zou J, Chen J, Chen L, Chen Y, et al. Prognostic impact of serum and tissue MMP-9 in non-small cell lung cancer: a systematic review and meta-analysis. Oncotarget 2016;7(14):18458-68. [DOI:10.18632/oncotarget.7607] [PMID] [PMCID]
9
Hiratsuka S, Nakamura K, Iwai S, Murakami M, Itoh T, Kijima H, et al. MMP9 induction by vascular endothelial growth factor receptor-1 is involved in lung-specific metastasis. Cancer Cell 2002;2(4):289-300. [DOI:10.1016/S1535-6108(02)00153-8]
10
Vandooren J, Van den Steen PE, Opdenakker G. Biochemistry and molecular biology of gelatinase B or matrix metalloproteinase-9 (MMP-9): the next decade. Crit Rev Biochem Mol Biol 2013;48(3):222-72. [DOI:10.3109/10409238.2013.770819] [PMID]
11
Shao W, Wang W, Xiong XG, Cao C, Yan TD, Chen G, et al. Prognostic impact of MMP-2 and MMP-9 expression in pathologic stage IA non-small cell lung cancer. J Surg Oncol 2011;104(7):841-6. [DOI:10.1002/jso.22001] [PMID]
12
Lee CY, Shim HS, Lee S, Lee JG, Kim DJ, Chung KY. Prognostic effect of matrix metalloproteinase-9 in patients with resected Non small cell lung cancer. J Cardiothorac Surg 2015;10:44. [DOI:10.1186/s13019-015-0248-3] [PMID] [PMCID]
13
Stenvold H, Donnem T, Andersen S, Al-Saad S, Al-Shibli K, Busund LT, et al. Overexpression of matrix metalloproteinase-7 and -9 in NSCLC tumor and stromal cells: correlation with a favorable clinical outcome. Lung Cancer 2012;75(2):235-41. [DOI:10.1016/j.lungcan.2011.06.010] [PMID]
14
Shi M, Cao M, Song J, Liu Q, Li H, Meng F, et al. PinX1 inhibits the invasion and metastasis of human breast cancer via suppressing NF-kappaB/MMP-9 signaling pathway. Mol Cancer 2015;14:66. [DOI:10.1186/s12943-015-0332-2] [PMID] [PMCID]
15
Chee-Keong Toh. The Changing Epidemiology of Lung Cancer. 2009. 19: 397-411 [DOI:10.1007/978-1-60327-492-0_19] [PMID]
16
Wei Dong, Hong Li, Yan Zhang, et al. Matrix metalloproteinase 2 promotes cell growth and invasion in colorectal cancer. Acta Biochim Biophys Sin 2011, 43: 840-848. [DOI:10.1093/abbs/gmr085] [PMID]
17
Rydlova M, Holubec L, Jr., Ludvikova M, Jr., Kalfert D, Franekova J, Povysil C, et al. Biological activity and clinical implications of the matrix metalloproteinases. Anticancer Res 2008;28(2b):1389-97.
18
Mehner C, Hockla A, Miller E, Ran S, Radisky DC, Radisky ES. Tumor cell-produced matrix metalloproteinase 9 (MMP-9) drives malignant progression and metastasis of basal-like triple negative breast cancer. Oncotarget 2014;5(9):2736-49. [DOI:10.18632/oncotarget.1932] [PMID] [PMCID]
19
Safranek J, Pesta M, Holubec L, Kulda V, Dreslerova J, Vrzalova J, et al. Expression of MMP-7, MMP-9, TIMP-1 and TIMP-2 mRNA in lung tissue of patients with non-small cell lung cancer (NSCLC) and benign pulmonary disease. Anticancer Res 2009;29(7):2513-7.
20
El-Badrawy MK, Yousef AM, Shaalan D, Elsamanoudy AZ. Matrix metalloproteinase-9 expression in lung cancer patients and its relation to serum mmp-9 activity, pathologic type, and prognosis. J Bronchology Interv Pulmonol 2014;21(4):327-34. [DOI:10.1097/LBR.0000000000000094] [PMID]
21
Pinto CA, Carvalho PE, Antonangelo L, Garippo A, Da Silva AG, Soares F, et al. Morphometric evaluation of tumor matrix metalloproteinase 9 predicts survival after surgical resection of adenocarcinoma of the lung. Clin Cancer Res 2003;9(8):3098-104.
22
Zheng S, Chang Y, Hodges KB, Sun Y, Ma X, Xue Y, et al. Expression of KISS1 and MMP-9 in non-small cell lung cancer and their relations to metastasis and survival. Anticancer Res 2010;30(3):713-8.
23
Sienel W, Hellers J, Morresi-Hauf A, Lichtinghagen R, Mutschler W, Jochum M, et al. Prognostic impact of matrix metalloproteinase-9 in operable non-small cell lung cancer. Int J Cancer 2003;103(5):647-51. [DOI:10.1002/ijc.10841] [PMID]
24
Grossi F, Spizzo R, Bordo D, Cacitti V, Valent F, Rossetto C, et al. Prognostic stratification of stage IIIA pN2 non-small cell lung cancer by hierarchical clustering analysis of tissue microarray immunostaining data: an Alpe Adria Thoracic Oncology Multidisciplinary Group study (ATOM 014). J Thorac Oncol 2010;5(9):1354-60. [DOI:10.1097/JTO.0b013e3181e77a78] [PMID]
25
Weiling He , Hui Zhang , Yuefeng Wang , Yanbin Zhou , Yifeng Luo, et al. CTHRC1 induces non-small cell lung cancer (NSCLC) invasion through upregulating MMP-7/MMP-9. BMCCancer(2018)18:400 . [DOI:10.1186/s12885-018-4317-6] [PMID] [PMCID]
26
Vincenti MP. The matrix metalloproteinase (MMP) and tissue inhibitor of metalloproteinase (TIMP) genes. Transcriptional and posttranscriptional regulation, signal transduction and cell-type-specific expression. Methods Mol Biol. 2001;151:121-48. [DOI:10.1385/1-59259-046-2:121] [PMID]
27
A. Churg, R. Wang, X. Wang, P.O. Onnervik, K. Thim, et al. Effect of an MMP-9/MMP-12 inhibitor on smoke-induced emphysema and airway remodeling in guinea pigs. Thorax 62 (2007) 706-713. [DOI:10.1136/thx.2006.068353] [PMID] [PMCID]
28
Balla, M., Desai, S., Purwar, P. et al. Differential diagnosis of lung cancer, its metastasis and chronic obstructive pulmonary disease based on serum Vegf, Il-8 and MMP-9. Sci Rep 6, 36065 (2016). [DOI:10.1038/srep36065] [PMID] [PMCID]
29
Hao Huang, Matrix Metalloproteinase-9 (MMP-9) as a Cancer Biomarker and MMP-9 Biosensors: Recent Advances, Sensors 2018, 18(10), 3249 [DOI:10.3390/s18103249] [PMID] [PMCID]
30
ORIGINAL_ARTICLE
Coexistence of Benign Brenner Tumor with Mucinous Cystadenoma in an Ovarian Mass
Ovarian cancer is the most lethal gynecologic malignancy. The surface epithelial tumor is the most common type of ovarian cancer. Among these, the mucinous tumors account for 10-15% of ovarian tumors. Mucinous ovarian tumors are among the most difficult ovarian neoplasms for surgical pathologists to interpret. Mucinous tumors sometimes coexist with other surface epithelial tumors. Therefore, making the accurate diagnosis of the mucinous tumors is essential. On the other hand, association of Brenner tumors with other neoplasms is rare. Ovarian Brenner tumor has always been discussed by pathologists as an enigmatic tumor, because of its rarity and disputed histogenesis. Here, we reported a case of large mucinous cystadenoma with Brenner component.
https://ijp.iranpath.org/article_43581_20ea32773c0dca9cba8cdf3507b839d9.pdf
2020-10-01
334
337
10.30699/ijp.2020.104017.2052
Brenner tumor
Mucinous tumor
Ovarian Cancer
Farzaneh
Nazari
nazarif78@yahoo.com
1
Department of Gynecology and Obstetrics, School of medicine, Bushehr university of medical sciences, Bushehr, Iran
LEAD_AUTHOR
Zahra
Dehghani
zahradehghani111070@yahoo.com
2
Department of Pathology, School of Medicine, Bushehr University of Medical Sciences, Bushehr, Iran
AUTHOR
Alan H.D, Lauren N, Neri L, Ashley S.R. Current Diagnosis and Treatment Obstetrics and Gynecology. 11th ed. Under the united states copyright: McGraw Hill; 2013. p. 848-9.
1
J S. Berek. Berek & Novak's Gynecology. 15th ed. Lippincott Williams and Wilkins. Philadelphia. USA; 2012. P. 1350-60.
2
Chen VW, Ruiz B, Killeen JL, Cote TR, Wu XC, Correa CN. Pathology and classification of ovarian tumors. Cancer. 2003; 97:2631‑42. [DOI:10.1002/cncr.11345] [PMID]
3
Hemalatha AL, Konanahalli P. Bilateral malignant Brenner tumor of ovary. J Obstet Gynecol India. 2005;55:81-2.
4
Sridevi S, Rao V Manmadha, Kumar S. Satish, Bhagyalakshmi A. Mucinous cystadenoma with Brenner tumor: A Case Report. J Evid-based Med Healthcare. 2015;2(4): 455-458 [DOI:10.18410/jebmh/2015/64]
5
Clement PB, Young RH. Ovarian Surface Epithelial-Stromal Tumors. In,Mills SE (editor). Sternberg's Diagnostic Surgical Pathology, 5th ed. Philadelphia, Lippincott Williams and Wilkins, A.Wolters Kluwer business. 2010, 2278-2308
6
Choudhury ND, Kadri MS, Reshi R, Besina S, Laharwal MA, Tasleem R, et al. Bilateral malignant Brenner tumor. JK Sci 2002; 4:215-7
7
Joh K, Aizawa S, Ohkawa K, Dohzono H, Aida S, Ohgoshi E. Case report of a malignant Brenner tumor with hyperestrogenism. Pathol Int. 1995; 45:75-84. [DOI:10.1111/j.1440-1827.1995.tb03382.x] [PMID]
8
Berge T, Borglin N.E. Brenner tumors. Histogenetic and clinical studies. Cancer 1967; 20:308-13 https://doi.org/10.1002/1097-0142(1967)20:23.0.CO;2-W [DOI:10.1002/1097-0142(1967)20:23.0.CO;2-W]
9
Yoonessi M, Abell MR. Brenner tumor of the ovary. Obstetric Gynecol. 1979; 54:90-96 [DOI:10.1097/00006250-197907000-00021] [PMID]
10
Pradhan P, Mohanty L, Pradhan D, Pujari S, Kar A. Benign brenner tumor of ovary with mucinous cystadenoma: A case report. Asia J Pharmaceutic Health Sci. 2017; 7:1643-6.
11
Tafe LJ, Muller KE, Ananda G, et al. Molecular Genetic Analysis of Ovarian Brenner Tumors and Associated Mucinous Epithelial Neoplasms: High Variant Concordance and Identification of Mutually Exclusive RAS Driver Mutations and MYC Amplification. Am J Pathol. 2016;186(3):671-677. doi:10.1016/j.ajpath.2015.11.008 [DOI:10.1016/j.ajpath.2015.11.008] [PMID] [PMCID]
12
Gaur JH, Hassan MJ, Elahi AA, Khetrapal S, Khan S, Jetley S. Synchronous benign Brenner's tumor of ovary with leiomyoma and endometrial adenocarcinoma in a postmenopausal female. J Can Res Ther 2019;15:1418-20 [DOI:10.4103/jcrt.JCRT_109_18] [PMID]
13
Sharma M, Khangar B, Mallya V, Khurana N, Gupta S. Coexisting Brenner tumor and endometrial carcinoma. J Midlife Health 2017;8:89-91. [DOI:10.4103/jmh.JMH_3_17] [PMID] [PMCID]
14
Borah T, Mahanta RK, Bora BD, Saikia S. Brenner tumor of ovary: An incidental finding. J Midlife Health 2011;2:40-1 [DOI:10.4103/0976-7800.83273] [PMID] [PMCID]
15
ORIGINAL_ARTICLE
Orthotopic Liver Transplantation for Etanercept-Induced Acute Hepatic Failure; a case report
The occurrence of hepatotoxicity following etanercept (tumor necrosis factor-alpha antagonist) prescription, has been studied well. However, an acute hepatic failure leading to liver transplant as an adverse effect of this drug has not been reported in the literature. In this article, we are going to present a case of acute liver failure followed by liver transplantation, in a 32 years old man with a previous history of ankylosing spondylitis after etanercept administration. On pathologic examination of the explanted liver, extensive confluent necrosis in all liver segments, as well as prominent infiltration of a mixed population of inflammatory cells in portal tracts, were noted. This study urges the importance of close follow-up of patients receiving etanercept regarding liver complications. Further studies are required to assess the prevalence, risk factors, and outcome of these cases.
https://ijp.iranpath.org/article_43628_8ccb99be9f68916aafa72460adc37a8b.pdf
2020-10-01
338
341
10.30699/ijp.2020.117000.2269
Etanercept
liver Transplantation
Hepatitis
Autoimmunity
Hepatic failure
Dorsay
Sadeghian
dorsay.sadeghian@gmail.com
1
Department of Pathology, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Farid
Azmoudeh-Ardalan
azmoudeh@gmail.com
2
Department of Pathology, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Simin
Dashti-Khavidaki
dashtis@sina.tums.ac.ir
3
Department of Clinical Pharmacy, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Nasir
Fakhar
n-fakhar@tums.ac.ir
4
Liver Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
French JB, Bonacini M, Ghabril M, Foureau D, Bonkovsky HL. Hepatotoxicity associated with the use of anti-TNF-α agents. Drug Safety. 2016;39(3):199-208. [DOI:10.1007/s40264-015-0366-9] [PMID] [PMCID]
1
Björnsson ES, Gunnarsson BI, Gröndal G, Jonasson JG, Einarsdottir R, Ludviksson BR, et al. Risk of drug-induced liver injury from tumor necrosis factor antagonists. Clin Gastroenterol Hepatol. 2015;13(3):602-8. [DOI:10.1016/j.cgh.2014.07.062] [PMID]
2
Shelton E, Chaudrey K, Sauk J, Khalili H, Masia R, Nguyen D, et al. New onset idiosyncratic liver enzyme elevations with biological therapy in inflammatory bowel disease. Aliment Pharmacol Therapeut. 2015;41(10):972-9. [DOI:10.1111/apt.13159] [PMID]
3
Ghabril M, Bonkovsky HL, Kum C, Davern T, Hayashi PH, Kleiner DE, et al. Liver injury from tumor necrosis factor-α antagonists: analysis of thirty-four cases. Clin Gastroenterol Hepatol. 2013;11(5):558-64. e3. [DOI:10.1016/j.cgh.2012.12.025] [PMID] [PMCID]
4
Aparicio AMG, Rey JR, Sanz AH, Alvarez JS. Successful treatment with etanercept in a patient with hepatotoxicity closely related to infliximab. Clin Rheumatol. 2007;26(5):811-3. [DOI:10.1007/s10067-006-0253-y] [PMID]
5
Thiéfin G, Morelet A, Heurgué A, Diebold M-D, Eschard J-P. Infliximab-induced hepatitis: absence of cross-toxicity with etanercept. Joint Bone Spine. 2008;75(6):737-9. [DOI:10.1016/j.jbspin.2007.12.009] [PMID]
6
Massarotti M, Marasini B. Successful treatment with etanercept of a patient with psoriatic arthritis after adalimumab-related hepatotoxicity. Int J Immunopathol Pharmacol. 2009;22(2):547-9. [DOI:10.1177/039463200902200234] [PMID]
7
De Rycke L, Baeten D, Kruithof E, Van den Bosch F, Veys E, De Keyser F. The effect of TNFalpha blockade on the antinuclear antibody profile in patients with chronic arthritis: biological and clinical implications. Lupus. 2005;14(12):931-7. [DOI:10.1191/0961203305lu2240rr] [PMID]
8
Danan G, Benichou C. Causality assessment of adverse reactions to drugs-I. A novel method based on the conclusions of international consensus meetings: application to drug-induced liver injuries. J Clin Epidemiol. 1993;46(11):1323-30. [DOI:10.1016/0895-4356(93)90101-6]
9
Organization WH. The use of the WHO-UMC system for standardized case causality assessment. Uppsala: The Uppsala Monitoring Centre. 2005:2-7.
10
Van Lümig P, Driessen R, Roelofs‐Thijssen M, Boezeman J, Van de Kerkhof P, De Jong E. Relevance of laboratory investigations in monitoring patients with psoriasis on etanercept or adalimumab. Br J Dermatol. 2011;165(2):375-82. [DOI:10.1111/j.1365-2133.2011.10329.x] [PMID]
11
Farah M, Al Rashidi A, Owen DA, Yoshida EM, Reid GD. Granulomatous hepatitis associated with etanercept therapy. J Rheumatol. 2008;35(2):349-51.
12
Leak AM, Rincon-Aznar B. Hepatotoxicity associated with etanercept in psoriatic arthritis. J Rheumatol . 2008;35(11):2286-8. [DOI:10.3899/jrheum.080521] [PMID]
13
Li Z, Xiao S, Ren J, Zhang Y, Tu C, Ji F. Hepatotoxicity due to etanercept abated after dose reduction in a patient with pustular psoriasis and without compromised efficacy. Revista espanola de enfermedades digestivas: organo oficial de la Sociedad Espanola de Patologia Digestiva. 2014;106(7):492-3.
14
Iwamoto M, Minota S. Successful treatment with very low-dose etanercept in a patient with etanercept-induced liver dysfunction. Rheumatol Int. 2011;31(4):561-2. [DOI:10.1007/s00296-010-1456-8] [PMID]
15
Titos AJ, Hallal H, Robles M, Andrade RJ. Recurrent hepatotoxicity associated with etanercept and adalimumab but not with infliximab in a patient with rheumatoid arthritis. Revista española de enfermedades digestivas: organo oficial de la Sociedad Española de Patología Digestiva. 2012;104(5):282. [DOI:10.4321/S1130-01082012000500014] [PMID]
16
Van Denderen J, Blom G, Van der Horst-Bruinsma I, Dijkmans B, Nurmohamed M. Elevated liver enzymes in patients with ankylosing spondylitis treated with etanercept. Clin Rheumatol. 2012;31(12):1677-82. [DOI:10.1007/s10067-012-2072-7] [PMID]
17
Sokolove J, Strand V, Greenberg JD, Curtis JR, Kavanaugh A, Kremer JM, et al. Risk of elevated liver enzymes associated with TNF inhibitor utilisation in patients with rheumatoid arthritis. Annal Rheumat Dis. 2010;69(9):1612-7. [DOI:10.1136/ard.2009.112136] [PMID]
18
Ozorio G, McGarity B, Bak H, Jordan AS, Lau H, Marshall C. Autoimmune hepatitis following infliximab therapy for ankylosing spondylitis. The Medical Journal of Australia. 2007;187(9):524-6. [DOI:10.5694/j.1326-5377.2007.tb01396.x] [PMID]
19
ORIGINAL_ARTICLE
A Rare Case of Metastasis of Renal Clear Cell Carcinoma to the Thyroid Gland, Presenting as a Goiter Nodule, Three Years After Nephrectomy
Thyroid gland metastatic tumors are rare in clinical practice. Clear cell RCC is one of common metastatic tumors to thyroid. We here reported a case of incidentally found clear cell renal carcinoma metastasis to the thyroid gland 3 years after nephrectomy, in the thyroidectomy procedure performed for the patient due to the thyroid enlargement caused by multinodular goiter. A 65-year-old Iranian man with a history of multinodular goiter referred to our surgery clinic for thyroidectomy because of compressive effects on the trachea. Patient had a history of nephrectomy due to clear cell RCC 3 years ago. After thyroidectomy, gross and histological examination of thyroid revealed clear cell renal carcinoma metastasis to the thyroid gland in the setting of a multinodular goiter. The diagnosis was confirmed by immunohistochemistry staining. Patients with multinodular goiter are more prone to present with metastasis to thyroid gland if they have a history of malignancy, especially renal cell carcinoma.
https://ijp.iranpath.org/article_43630_77e389356c1c045a63b9002a4f28aa60.pdf
2020-10-01
342
345
10.30699/ijp.2020.117839.2282
Renal cell carcinoma
Thyroid gland
Metastasis
Multinodular Goiter
Hedieh
Moradi Tabriz
hmoradi@tums.ac.ir
1
Department of Anatomical and Surgical Pathology and Laboratory Medicine, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Arezoo
Eftekhar-Javadi
a_eftekhar@tums.ac.ir
2
Department of Anatomical and Surgical Pathology and Laboratory Medicine, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Atiieh
Zandnejadi
atiiiieh@gmail.com
3
Department of Anatomical and Surgical Pathology and Laboratory Medicine, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Mohammadi A, Toomatari S, Ghasemi-Rad M. Metastasis from renal cell carcinoma to thyroid presenting as rapidly growing neck mass. Int J Surg Case Rep 2014;5(12):1110-1112. [DOI:10.1016/j.ijscr.2014.09.010] [PMID] [PMCID]
1
Jackson G, Fino N, Bitting R. Clinical Characteristics of Patients with Renal Cell Carcinoma and Metastasis to the Thyroid Gland. Clin Med Insights Oncol 2017; 11:117955491774398. [DOI:10.1177/1179554917743981] [PMID] [PMCID]
2
Riaz K, Tunio M, AlAsiri M, Elbagir Mohammad A, Fareed M. Renal Cell Carcinoma Metastatic to Thyroid Gland, Presenting Like Anaplastic Carcinoma of Thyroid. Case Rep Urol 2013;2013:1-4. [DOI:10.1155/2013/651081] [PMID] [PMCID]
3
Valdez C, Rezaei M, Hendricks F, Knoll S. Metastatic Renal Cell Carcinoma to the Thyroid 23 Years After Nephrectomy. Urol Case Rep 2014;2(4):129-130. [DOI:10.1016/j.eucr.2014.04.002] [PMID] [PMCID]
4
Lee J, Yang Y, Kim K, Hyun C, Lee J, Koh G et al. A Case of Metastatic Renal Cell Carcinoma to Thyroid Gland. Chonnam Med J 2011;47(2), p.130. [DOI:10.4068/cmj.2011.47.2.130] [PMID] [PMCID]
5
Sayad S, Ahmadi SA, Moradi M, Nekouian R, Anbari K, Shahsavar F. A meta-analysis on diagnostic accuracy of serum HLA-G level in breast cancer. Expert Review of Precision Medicine and Drug Development. 2020 Mar 3;5(2):109-14. [DOI:10.1080/23808993.2020.1735936]
6
Khan M, Iyer V, Varshney N. A Rare Case of Metastasis to the Thyroid Gland from Renal Clear Cell Carcinoma 11 Years after Nephrectomy and Concurrent Primary Esophageal Carcinoma. Case Rep Oncol Med 2018; 2018:1-4. [DOI:10.1155/2018/3790106] [PMID] [PMCID]
7
Villumsen A, Mevik K, Fjøsne H, Brekke M, Haugen O. Late onset metastases to the thyroid gland from renal carcinoma. Tidsskr Nor Laegeforen 2013;133(21):2262-2265. [DOI:10.4045/tidsskr.12.0884] [PMID]
8
Macedo-Alves D, Koch P, Soares V, Gouveia P, Honavar M, Taveira-Gomes A. Thyroid metastasis from renal cell carcinoma-A case report after 9 years. Int J Surg Case Rep 2015; 16:59-63. [DOI:10.1016/j.ijscr.2015.09.004] [PMID] [PMCID]
9
Kihara M, Yokomise H, Yamauchi A. Metastasis of renal cell carcinoma to the thyroid gland 19 years after nephrectomy: a case report. Auris Nasus Larynx 2004;31(1):95-100. [DOI:10.1016/j.anl.2003.09.002] [PMID]
10
Cilengir A, Kalayci T, Duygulu G, Atasever Rezanko T, İnci M. Metastasis of Renal Clear Cell Carcinoma to Thyroid Gland Mimicking Adenomatous Goiter. Pol J Radiol. 2016; 81: 618-621. [DOI:10.12659/PJR.899459] [PMID] [PMCID]
11
Khairul-Asri MG, Sidhu S, Raja Gopal NS, Azli S, Badawi MA, Hadi S, Fahmy O. Thyrotoxic goiter and asymptomatic thyroid nodule as an initial presentation of clear cell renal cell carcinoma: A report of two cases. Urol Sci 2019;30:238-40
12
Connolly C. Renal cell metastasis to the thyroid gland: An emerging phenomenon. Int J Surg Case Rep. 2018; 45: 104-106. [DOI:10.1016/j.ijscr.2018.03.032] [PMID] [PMCID]
13
Kobayashi K, Hirokawa M, Yabuta T, Fukushima M, Masuoka H, Higashiyama T et al. Metastatic carcinoma to the thyroid gland from renal cell carcinoma: role of ultrasonography in preoperative diagnosis. Thyroid Res 8, 4 (2015). [DOI:10.1186/s13044-015-0016-4] [PMID] [PMCID]
14
Abara, E., Chivulescu, I., Clerk, N., Cano, P. and Goth, A. Recurrent renal cell cancer: 10 years or more after nephrectomy. Can Urol Assoc J 2010; 4(2), p.45. [DOI:10.5489/cuaj.829] [PMID] [PMCID]
15
ORIGINAL_ARTICLE
Intravascular Large B-cell Lymphoma: A Report of Two Cases
One of the rare variants of extranodal large B-cell lymphoma is intravascular large B-cell lymphoma (IVLBCL). Characteristics of IVLBCL include intraluminal selective proliferation of atypical lymphoid cells in small to medium-sized vessels. The etiologic of IVLBCL is unknown, but due to the growth pattern of this tumor, it is speculated that IVLBCL is caused by a defect in homing receptor of tumor cells. IVLBCL can involve any organ but central nervous system, lungs, and skin are the most involved sites. IVLBCL does not usually involve lymph nodes. IVLBCL mainly occurs in the middle aged to elderly population with a slight male predominance. Generally, IVLBCL is aggressive and rapidly fatal if left untreated. We here reported two cases of IVLBCL who succumbed to the disease at initial phase of treatment to emphasize the difficulty in diagnosis of IVLBCL due to its exclusive intravascular growth pattern and fulminant clinical course.
https://ijp.iranpath.org/article_43631_b175453dd5685ca37397bf8ba43fb628.pdf
2020-10-01
346
350
10.30699/ijp.2020.119590.2299
Extranodal large B-cell lymphoma
Intravascular lymphoma
Fever of Unknown Origin (FUO)
Fereshteh
Ameli
fereshtehameli@gmail.com
1
Department of Pathology, Cancer Institute, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Fatemeh
Nili
f_nili@yahoo.com
2
Department of Pathology, Cancer Institute, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Hana
Saffar
hana_saffar283@yahoo.com
3
Department of Pathology, Cancer Institute, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Swerdlow SH, et al. WHO classification of tumors of haematopoietic and lymphoid tissues. 2016
1
Jaffe ES, Arber DA, Campo E, Harris NL, Quintanilla-Fend L. Hematopathology e-book. Elsevier Health Sciences; 2016.
2
Kinoshita M, Izumoto S, Hashimoto N, Kishima H, Kagawa N, Hashiba T, et al. Immunohistochemical analysis of adhesion molecules and matrix metalloproteinases in malignant CNS lymphomas: a study comparing primary CNS malignant and CNS intravascular lymphomas. Brain Tumor Pathol. 2008 Nov;25(2):73. [DOI:10.1007/s10014-008-0232-x] [PMID]
3
Ponzoni M, Arrigoni G, Gould VE, Del Curto B, Maggioni M, Scapinello A, et al. Lack of CD 29 (β1 integrin) and CD 54 (ICAM-1) adhesion molecules in intravascular lymphomatosis. Hum Pathol. 2000;31(2):220-226. [DOI:10.1016/S0046-8177(00)80223-3]
4
Phoon YW, Lin X, Thirumoorthy T, Tan SY, Lee HY, Lim ST, et al. Intravascular large B-cell lymphoma presenting as panniculitis clinically: a case report. Singapore Med J. 2018 Mar;59(3):163. [DOI:10.11622/smedj.2018030] [PMID] [PMCID]
5
Shen Q, Duan X, Feng W, Nguyen N, Lapus A, Brown RE, et al. Intravascular large B-cell lymphoma: report of three cases and analysis of the mTOR pathway. Int J Clin Exp Pathol. 2011 Nov;4(8):782.
6
Fischer M, Iglseder S, Grams A, Matosevic B, Moser P, Stockhammer G, et al. Intravascular large B-cell lymphoma mimicking central nervous system vasculitis. Hum Pathol Case Rep. 2017 Jun;8:3-8. [DOI:10.1016/j.ehpc.2016.11.002]
7
Orwat DE, Batalis NI. Intravascular large B-cell lymphoma. Arch Pathol Lab Med. 2012 Mar;136(3):333-338. [DOI:10.5858/arpa.2010-0747-RS] [PMID]
8
Masaki Y, Dong L, Nakajima A, Iwao H, Miki M, Kurose N, et al. Intravascular large B cell lymphoma: proposed of the strategy for early diagnosis and treatment of patients with rapid deteriorating condition. Int J Hematol. 2009 Jun;89(5):600-610. [DOI:10.1007/s12185-009-0304-7] [PMID]
9
Murase T, Yamaguchi M, Suzuki R, Okamoto M, Sato Y, Tamaru J, et al. Intravascular large B-cell lymphoma (IVLBCL): a clinicopathologic study of 96 cases with special reference to the immunophenotypic heterogeneity of CD5. Blood. 2007 Jan;109(2):478-485. [DOI:10.1182/blood-2006-01-021253] [PMID]
10
Alizadeh AA, Eisen MB, Davis RE, Ma C, Lossos IS, Rosenwald A, Boldrick JC, Sabet H, Tran T, Yu X, Powell JI. Distinct types of diffuse large B-cell lymphoma identified by gene expression profiling. Nature. 2000 Feb;403(6769):503-11. [DOI:10.1038/35000501] [PMID]
11
Berglund M, Thunberg U, Amini RM, Book M, Roos G, Erlanson M, Linderoth J, Dictor M, Jerkeman M, Cavallin-Ståhl E, Sundström C. Evaluation of immunophenotype in diffuse large B-cell lymphoma and its impact on prognosis. Modern Pathol. 2005 Aug;18(8):1113-20. [DOI:10.1038/modpathol.3800396] [PMID]
12
De Paepe P, Achten R, Verhoef G, Wlodarska I, Stul M, Vanhentenrijk V, Praet M, De Wolf-Peeters C. Large cleaved and immunoblastic lymphoma may represent two distinct clinicopathologic entities within the group of diffuse large B-cell lymphomas. J Clin Oncol. 2005 Oct 1;23(28):7060-8. [DOI:10.1200/JCO.2005.15.503] [PMID]
13
Kanda M, Suzumiya J, Ohshima K, Tamura K, Kikuchi M. Intravascular large cell lymphoma: clinicopathological, immuno-histochemical and molecular genetic studies. Leukemia & lymphoma. 1999 Jan 1;34(5-6):569-80. [DOI:10.3109/10428199909058485] [PMID]
14
Yegappan S, Coupland R, Arber DA, Wang N, Miocinovic R, Tubbs RR, Hsi ED. Angiotropic lymphoma: an immunophenotypically and clinically heterogeneous lymphoma. Modern Pathology. 2001 Nov;14(11):1147-56. [DOI:10.1038/modpathol.3880450] [PMID]
15
ORIGINAL_ARTICLE
Is Micronucleus Assay Suitable for Cytogenetic Biomonitoring the Different Ways to Smoke?
The aim of the letter to editor is to provide some comments regarding the manuscript of DehghanNezhad et al.(1) recently published in the Iranian Journal of Pathology titled “Micronucleus Assay of Buccal Mucosa Cells in Waterpipe (Hookah) Smokers: A Cytologic Study.” In this article, the authors were able to detect high frequencies of micronucleus in buccal mucosa cells of waterpipe smokers when compared to non-smokers.
https://ijp.iranpath.org/article_43632_c98e8752919b080a8fa2c1b7421d99c8.pdf
2020-10-01
351
351
10.30699/ijp.2020.125206.2370
Micronucleus Assay
Waterpipe Smoke
Buccal Mucosa
Daniel
Ribeiro
daribeiro@unifesp.br
1
Department of Biosciences, Federal University of São Paulo, UNIFESP, Santos, SP, Brazil
LEAD_AUTHOR
Ingra
Malacarne
ingra_tais@hotmail.com
2
Department of Biosciences, Federal University of São Paulo, UNIFESP, Santos, SP, Brazil
AUTHOR
Daniel
Souza
danielvitor2006@hotmail.com
3
Department of Biosciences, Federal University of São Paulo, UNIFESP, Santos, SP, Brazil
AUTHOR
DehghanNezhad M, Jalayer Naderi N, Semyari H. Micronucleus Assay of Buccal Mucosa Cells in Waterpipe (Hookah) Smokers: A Cytologic Study. Iran J Pathol. 2020;15(2):75-80. [DOI:10.30699/ijp.2020.101701.2010] [PMID] [PMCID]
1
Torres-Bugarín O, Zavala-Cerna MG, Nava A, Flores-García A, Ramos-Ibarra ML. Potential uses, limitations, and basic procedures of micronuclei and nuclear abnormalities in buccal cells. Dis Markers. 2014 Feb 4;2014. [DOI:10.1155/2014/956835] [PMID] [PMCID]
2
Bonassi S, Coskun E, Ceppi M, Lando C, Bolognesi C, Burgaz S, Holland N, Kirsh-Volders M, Knasmueller S, Zeiger E, Carnesoltas D. The HUman MicroNucleus project on eXfoLiated buccal cells (HUMNXL): The role of life-style, host factors, occupational exposures, health status, and assay protocol. Mutation Research/Reviews in Mutation Research. 2011 Nov 1;728(3):88-97. [DOI:10.1016/j.mrrev.2011.06.005] [PMID]
3
ORIGINAL_ARTICLE
Response to letter to the editor:” Is micronucleus assay suitable for cytogenetic biomonitoring the different ways to smoke? ”
Dear Editor, I was very pleased to find that the article” Micronucleus Assay of Buccal Mucosa Cells in Waterpipe (Hookah) Smokers: A Cytologic Study “(1) has attracted the attention of some readers and has created a few points for them. In my opinion, these points are good bases to overcome some concerns regarding micronucleus assay.
https://ijp.iranpath.org/article_43633_cca93f0e10517429a2ded0c245cf91d5.pdf
2020-10-01
352
354
10.30699/ijp.2020.127517.2390
Micronucleus
Genotoxicity test
Buccal Mucosa
Noushin
Jalayer naderi
noushin_jly85@yahoo.com
1
Department of Oral and Maxillofacial Pathology, Faculty of Dentistry, Shahed University, Tehran, Iran
LEAD_AUTHOR
DehghanNezhad M, Jalayer Naderi N, Semyari H. Micronucleus Assay of Buccal Mucosa Cells in Waterpipe (Hookah) Smokers: A Cytologic Study. Iran J Pathol. 2020; 15:75-80. [DOI:10.30699/ijp.2020.101701.2010] [PMID] [PMCID]
1
Nanci A. Ten Cate's Oral Histology; Development, Structure, and Function. 9th ed, China: Elsevier; 2018.
2
Holbrook KA. Biologic structure and function: perspectives on morphologic approaches to the study of the granular layer keratinocyte. J Invest Dermatol. 1989 Apr 1;92(4):S84-104. [DOI:10.1111/1523-1747.ep13075079] [PMID]
3
El-Setouhy M, Loffredo CA, Radwan G, Rahman RA, Mahfouz E, Israel E, Mohamed MK, Ayyad SB. Genotoxic effects of waterpipe smoking on the buccal mucosa cells. Mut Res/Genetic Toxicology and Environmental Mutagenesis. 2008 Aug 1;655(1-2):36-40. [DOI:10.1016/j.mrgentox.2008.06.014] [PMID] [PMCID]
4
Farhadi S, Mohamadi M, Mohamadi M. Repair Index in Examination of Nuclear Changes in the Buccal Mucosa of Smokers: A Useful Method for Screening of Oral Cancer. Asian Pac J Cancer Prev. 2017; 18:3087-3090.
5
Grover S , Mujib A, Jahagirdar A, Telagi N, Kulkarni P. A comparative study for selectivity of micronuclei in oral exfoliated epithelial cells. J Cytol. 2012; 29:230-5. [DOI:10.4103/0970-9371.103940] [PMID] [PMCID]
6
Konopacka M. Effect of smoking and aging on micronucleus frequencies in human exfoliated buccal cells. Neoplasma. 2003; 50:380-2.
7
Martino-Roth MG, Viégas J, Amaral M , Oliveira L , Ferreira FLS , Erdtmann B. Evaluation of genotoxicity through micronuclei test in workers of car and battery repair garages. Genet Mol Biol. 2002; 25(4): 495-500. [DOI:10.1590/S1415-47572002000400021]
8
Ceppi M, Biasotti B, Fenech M, Bonassi S. Human population studies with the exfoliated buccal micronucleus assay: statistical and epidemiological issues. Mutat Res. 2010; 705:11-19. [DOI:10.1016/j.mrrev.2009.11.001] [PMID]
9
Thomas P, Holland N, Bolognesi C, Kirsch‑Volders M, Bonassi S, Zeiger E, et al. Buccal micronucleus cytome assay. Nat Protoc. 2009; 4(6):825‑37. [DOI:10.1038/nprot.2009.53] [PMID]
10
Bonassi S, Coskun E, Ceppi M, Lando C, Bolognesi C, Burgaz S , et al. The HUman MicroNucleus project on eXfoLiated buccal cells (HUMNXL): The role of life-style, host factors, occupational exposures, health status, and assay protocol. Mutat Res. 2011; 728(3):88-97. [DOI:10.1016/j.mrrev.2011.06.005] [PMID]
11