Document Type : Review Article

Authors

1 Dept. of Pathology, Transplant Research Center, Shiraz University of Medical Sciences, Shiraz, Iran

2 University of British Columbia, Vancouver, BC, Canada

3 Dept. of Pathology, Vancouver General Hospital and University of British Columbia, Vancouver , BC, Canada

Abstract

Background: Solitary fibrous tumor (SFT) is a mesenchymal tumor which is most commonly seen in the pleura; however it can be seen in other organs such as the meninge, gastrointestinal tract, soft tissue, bone, and skin. SFT should be differentiated from other mesenchymal tumors in these organs. Immunohistochemistry plays a pivotal role for the histopathologic diagnosis of this tumor. Currently, new markers have been introduced which has been very useful for definite diagnosis of SFT along with other markers in each specific location which are negative in SFT. Methods: Here we review the reported positive and negative immunohistochemical markers of SFT in the English literature with the emphasis on the useful markers in each specific organ. We explored the English literature from 1990 through 2015 via PubMed, Google, and Google scholar using the following search keywords: Solitary fibrous tumor, Solitary fibrous tumor and immunohistochemistry, Solitary fibrous tumor and diagnosis, Solitary fibrous tumor and histogenesis, Solitary fibrous tumor and prognosis, Solitary fibrous tumor and hemangiopericytoma, Solitary fibrous tumor and differential diagnosis, Solitary fibrous tumor and markers. Results: The most important and valuable positive markers in SFT are CD34, CD99, Bcl-2 and STAT-6.There are consistently negative markers in this tumor as well, used according to the tumor location, such as EMA and S100 Conclusion: Immunohistochemistry is very useful for the diagnosis of solitary fibrous tumor and for its differentiation with other spindle cell mesenchymal tumor in different locations.
 
How to cite this article:
Geramizadeh B, Marzban M, Churg A.  Role of Immunohistochemistry in the Diagnosis of Solitary Fibrous Tumor, a Review. Iran J Pathol. 2016; 11(3):195-293.
 

Keywords

Introduction

Solitary fibrous tumor (SFT) is a spindle cell mesenchymal tumor of poorly understood origin. It was first mentioned in pleura in 1870 (1), however the first description of this tumor was in 1931 by Klemperer, who called it “localized fibrous mesothelioma” (2). Although initially regarded as a pleural tumor, it is now recognized that SFT occur in, skin, nervous system, soft tissue, liver, lung, kidney, and thyroid (3).

The usual histomorphology of SFT is variable, ranging  from  a  paucicellular  to  a  moderate to highly cellular tumor, composed of round to spindle-shaped cells with little cytoplasm, between prominent eosinophilic bands of collagen often arranged in a short storiform pattern, along with thin-walled branching vessels showing a staghorn hemangiopericytoma-like configuration (Fig. 1). Hypocellular and hypercellular areas can be seen (1-3).

 

Fig. 1 Sections show a moderately cellular SFT composed of bland spindle-shaped cells with little cytoplasm, running between bands of collagen arranged in a short storiform pattern. (H&E X 250)

Fig. 1 Sections show a moderately cellular SFT composed of bland spindle-shaped cells with little cytoplasm, running between bands of collagen arranged in a short storiform pattern. (H&E X 250)

 

SFT and hemangiopericytoma (HPC) have been originally regarded as separate entities, but according to the 2013 WHO classification of soft tissue tumors, they are now considered as one neoplasm, except for the central nervous system where meningeal HPC is still considered a separate entity (4).

This tumor is the most common in the middle- aged adults (20-70 yr). Rare cases in paediatric age groups have also been reported (5).

Clinical manifestations are highly variable according to the location of the tumor (6). Clinical behavior, can often be predicted by features, such as hypercellularity, high mitotic figures (>4/10HPF), cytologic atypia, tumor necrosis, infiltrative margins (4). Absence of these criteria is not a definite predictor of benign behavior and some SFTs with completely bland histomorphologic findings can have an aggressive course.  Immunohistochemistry is not widely accepted to be predictive of malignancy (6).

Data Acquisition

  In this review, we explored the English literature from 1990 through 2015 via PubMed, Google, and Google scholar using the following search keywords:

1) Solitary fibrous tumor

2) Solitary fibrous tumor and immunohistochem- istry

3) Solitary fibrous tumor and diagnosis

4) Solitary fibrous tumor and histogenesis

5) Solitary fibrous tumor and prognosis

6)Solitaryfibroustumorandhemangiopericytoma

7)  Solitary  fibrous  tumor  and  differential diagnosis

8) Solitary fibrous tumor and markers

 

 Positive Markers for SFT

  CD34 and Bcl-2

The most important and consistent positive immunohistochemical markers useful for the first line of diagnosis in SFT are CD34 and Bcl-2 (Fig. 2).

 

Fig. 2 CD34 and Bcl-2 are positive in the tumor shown in Figure 1. (X 400)

Fig. 2 CD34 and Bcl-2 are positive in the tumor shown in Figure 1. (X 400)

A combination of positive CD34 and Bcl-2 is highly characteristics of SFT. CD34 positivity has been reported in 95 to 100% of the cases. Therefore to call a tumor “SFT” CD34 should be positive. The only exception to this is malignant and dedifferentiated cases of SFT in which the percentage of CD34 positivity is lower, but still significant (83%) (7-10).In such cases, cytokeratin (CK) will be positive and CK positivity accompanied with negative CD34 is an indication for this tumor to be dedifferentiated or malignant and to behave aggressively, in which the tumor is still recognizable as SFT but has cytologically malignant features (11).

In various locations of the body, Bcl-2 has been reported positive in 50-100% of the SFTs (11, 12). A double negative CD34, and Bcl-2 makes the diagnosis of SFT highly unlikely (9).

  STAT-6

NAB2-STAT6 fusion genes are specific for SFTs and the detection of the fusion gene can be helpful in diagnostically challenging cases. However, the molecular tests are costly, and are not available in every laboratory. Recently, the use of immunohistochemistry for STAT6, as a surrogate for detecting the fusion gene has been introduced. It has been showed a strong nuclear STAT6 immunoreactivity that was highly sensitive and specific for SFTs (13, 14) (Fig. 3).

By using this marker, SFT can be accurately differentiated from other histologic mimics such as meningeal hemangiopericytoma. Intense and diffuse nuclear staining of STAT-6 is highly characteristics of SFT, seen in more than 90% of the cases (15, 16). Less than 10% of other spindle cell tumors in different locations of the body have been positive with STAT-6, most of which do not show as diffuse and intense staining as SFT (16, 17).

Useful Immunohistochemical Markers according to the specific location: (Table-1)

Fig. 2 SFT with diffuse nuclear positivity for STAT6 (inset) 

Fig. 3 SFT with diffuse nuclear positivity for STAT6 (inset)   

   

Table 1

Percentage of positivity of different markers in benign SFTs in different locations of the body

 

Marker

Pleura 18-26

Meninges 27-35

Soft tissue 36-41

Skin 20,42, 43           GI tract 44,46

STAT-6

95-100%

91%

99-100%

NR

NR

CD34

90-100%

92-100%

85-100%

80%-1005

100%

CD99

88.6%

100%

89-100%

60-100%

NR

Bcl-2

94.3-100%

89-100%

85-100%

60-100%

NR

Beta-catenin

77-100%

100%

22-67%

NR

24%

Vimentin

100%

NR

NR

NR

NR

Calretinin

0-13%

NR

NR

NR

NR

Desmin

0

NR

NR

NR

NR

cytokeratin

0-3.5%

0

NR

0

NR

EMA

0

0-29%

NR

0

NR

CK5/6

NR

0

NR

NR

NR

D2-40

NR

NR

NR

NR

NR

Claudin-1

NR

0

NR

NR

NR

SMA

0

NR

NR

30%

0

CD117

3.4%

NR

NR

NR

0

S100

0

0-26%

NR

0

0

P53

0-79.6

NR

NR

NR

NR

Ki-67

0-2%

NR

NR

NR

NR

 

Pleuropulmonary SFT

The first report of SFT was from the pleura and overall the most common site of this tumor is pleura. However, SFT is not a common tumor in the pleura and comprises less than 5% of pleural neoplasms, so it should be differentiated from other more common pleural tumors (3). It most commonly arises from the visceral pleura and very rarely from the parietal pleura. The most common neoplasm that must be differentiated from SFT in the pleura is localized malignant mesothelioma   especially   the   desmoplastic subtype (18, 19).

The best positive markers in mesothelioma that are mostly negative in SFT are cytokeratin (CK), calretinin, WT-1, CK5/6 (20). Cytokeratin is mostly negative in SFT (21, 22). Calretinin is also mostly negative in SFTs, and it’s uncommon to be positive for calretinin (up to 13%) (23).

D2-40 is another marker which has been reported to be helpful in the diagnosis of pleural mesothelioma, which is mostly negative in SFT, however very rare reports of focal reactivity has been reported in SFT (24).

Intrapulmonary SFT is very rare and immunohistochemical findings are very similar to those in pleural SFT. Intrapulmonary SFT are keratin and TTF-1 negative (25, 26).

  Meningeal SFT

Another common location of SFT is the nervous system i.e. meningeal SFT, which are most commonly intracranial, however less than 20% are intraspinal. The two most important differential diagnoses in the meninges are hemangiopericytoma (HPC) and fibroblastic meningioma (27).

Hemangiopericytoma   is   an   aggressive tumor which, according to the 2007 WHO classification of CNS tumors, is still viewed as a separate tumor from SFT of the meninges (28). However, the presence of NAB2-STAT6 fusion gene and STAT6 protein expression by immunohistochemistry in both SFT and HPC suggest that these are probably the same entity. STAT6 reactivity has been reported in 95 to

100% of meningeal HPC and 100% of SFTs (29). Bcl-2, CD34 and CD99 are frequently positive in meningeal HPC, similar to SFT (80-100%) (30,

31). Many of the previously diagnosed meningeal HPC has in fact been SFT and that HPC cases represent malignant or aggressive SFTs (32).

Another important differential diagnosis of SFT in the nervous system is meningioma (fibroblastic type). Immunohistochemistry plays a pivotal role for this differential diagnosis, because in all of the previous studies, EMA and  S100  have  been  consistently  negative in SFT, as opposed to meningioma which is consistently  reactive  with  S100  and  EMA. Meanwhile meningiomas are reported to be consistently nonreactive for CD34, CD99 and Bcl-2. Claudin-1 has been also reactive in more than 70% of the meningiomas and consistently negative in meningeal SFTs (34).

The MIB-1 index has been proposed as an acceptable criterion for prediction of aggressive behavior in CNS SFTs (35).

  Soft tissue and bone SFT

As it has been mentioned above, according to the WHO classification (2013) (4), HPC and SFT are considered to be the same entity. Immunohistochemistry of soft tissue SFT is fairly similar to meningeal SFT i.e. both are consistently positive with CD34, CD99 and Bcl-2, although the average Ki67 positivity is higher in meningeal SFT (36, 37).

STAT6 is both a sensitive and specific marker in soft tissue SFTs as is true in other locations (13, 38, 39). In other studies, this marker was completely negative in many of the soft tissue tumors with spindle cell morphology (13). Table-2 shows some of the soft tissue tumors with reported percentage of nuclear positivity of STAT6 (13, 38, 39). There are a number of other genes that are up-regulated in SFTs in comparison with other histological mimics in soft tissue. The most frequently and highly over expressed is GRIA2, which encodes an AMPA selective ionotropic glutamate receptor subunit thought to mediate increased cell proliferation. GRIA2 has been absent in normal fibroblasts. Vivero et al. have investigated GRIA2 expression in some soft tissue tumors by immunohistochemical analysis. The marker was positive in 89% of SFTs, but more than 99% of all other histologic mimics mentioned in Table 2 has been nonreactive with this marker (40).

Another important issue in differential diagnosis of this tumor is fibromatosis, because of the probability of SFT to show nuclear positivity with β-catenin which should be interpreted cautiously. However, presence of nuclear STAT-6 in SFT and consistenly negative STAT-6 in fibromatosis is very helpful for this differential diagnosis in equivocal cases (41).

  Cutaneous SFT

There are a group of spindle cells in the dermis that are CD34 positive called “dermal dendrocytes”. Proliferation of these cells will cause different types of tumors including SFT. These tumors consist of dermatofibrosarcoma protuberans (DFSP), and spindle cell lipoma, which show great histopathologic overlap (42).  These CD34 positive tumors must be differentiated from SFT when it arises from the dermis (20). Both of these tumors are consistently non-reactive with CD99 and Bcl-2 (43). Another dermal tumor which shows histologic overlap with SFT is fibrous histiocytoma. This tumor is most commonly CD34 negative, as opposed to SFT (20). Neural tumors such as Schwannoma can be easily differentiated by positivity with S100 which is non-reactive with tumor cells in SFT (20).

  Gastrointestinal SFT

There  are  four  main  tumors  in  the gastrointestinal  tract  (GI)  which  can  be differentiated  by  using  immunohistochemical markers;    i.e.,  gastrointestinal stromal tumor  (GIST),  desmoid  type  fibromatosis, leiomyosarcoma and schwannoma (44). CD-117 is the best marker for the diagnosis of GIST and exclusion of SFT, because most of the GISTs are both CD34 and CD99 positive (45). Desmoid type fibromatoses are mostly positive with smooth muscle actin which is rarely positive in SFT; this is the opposite of CD34 which is consistently negative in desmoid type fibromatosis (46). Leiomyosarcoma and schwannoma in the GI tract can be differentiated from SFT by being positive with SMA and S100 respectively (44).

 

  Table 2

STAT-6 nuclear positivity in different spindle cell tumors

 

Tumor type

Percentage of positive nuclear staining

Solitary fibrous tumor, benign 9,13

100%

Cellular angiofibroma 13,38

0

Myofibroblastoma 13, 38

0

Spindle cell lipoma 13,38

0

Benign fibrous histiocytoma 13,38

0

DFSP 13, 38                                                                        0

Desmoid type fibromatosis 13,38, 39

0-7.6%

Monophasic synovial sarcoma 13,38

0

Mesenchymal chondrosarcoma 13,38

0

High grade fibromyxoid sarcoma 13

28.5%

Lieomyoma 13

0

Leiomyosarcoma 13

0

Schwannoma 13

0

Neurofibroma 13

0

MPNSD 13

0

Dedifferentiated liposarcoma 13, 39

0-12%

Ewing’s sarcoma 13

0

Nodular fasciitis 13

0

Unclassfied sarcoma 39

12.3%

Other locations

SFTs have been reported from salivary gland especially as a parotid gland tumor, which should be differentiated from other mesenchymal tumors of this organ such as schwannoma, desmoid tumor, DFSP, and leiomyosarcoma using the three most important markers that have been mentioned before i.e. CD34, CD99 and Bcl-2 (15, 47). O’regan et al. have reported the same experience in 21 cases of SFT in the oral cavity i.e. all were reactive with CD34, CD99 and Bcl-2 but nonreactive with EMA, CK, S-100 and SMA (48) Blandamura et al. (49) have reported similar results for eye and peri-ocular SFT (49).

Role of Immunohistochemistry for prediction of the behavior and prognosis in SFT

Malignant SFT is rare and malignancy has been reported in 12% to 37% of the cases. Several histomorphologic findings were reported to be important for prediction of malignancy and disease free survival, including high cellularity, mitotic  activity  (Some  studies  report  that presence of mitosis per se is a poor prognostic indicator however most of the previous studies have emphasized that >4 mitosis /10 HPF is predictor of malignant and aggressive behaviour), with hemorrhage and necrosis (50). There are reports about the role of immunohistochemical biomarkers in prediction of behaviour in SFTs such as P53, and Ki67, however it has not been widely accepted (21, 50).

Dedifferentiation has also been reported as a poor prognostic factor. It means that in a tumor, in addition to typical features of benign- appearing SFT there is an abrupt transition to nondistinctive high-grade sarcoma.  This can be round or spindle shaped cells or epithelioid (51). There are reports of CD34 loss and P53 expression in these dedifferentiated SFTs (52). Besides, Ki67 shows a significant increase in dedifferentiated SFTs (51, 52).

 

Conclusion

 SFTisamesenchymalspindlecelltumorwhich is most commonly seen in the pleura; however it can be seen in various extrapleural organs and should be differentiated from other spindle cell mesenchymal tumors. Immunohistochemical markers are very important for the histopathologic diagnosis of this tumor; especially CD34, Bcl-2 and STAT-6.There are also consistently negative markers in this tumor which can be used according to the location.

 

Acknowledgements

 There has been no financial source for this study. The authors declare that there is no conflict of interests.

  1. Wagner E. Das tuberkelähnliche Lymphadenom. (Der cytogene oder reticulirte Tuberkel). Leipzig: O. Wigand; 1871.
  2. Klemperer P, Coleman BR. Primary neoplasms of the pleura. A report of five cases. Am J Ind Med 1992; 22(1):1-31.
  3. Guo W, Xiao HL, Jiang YG, Wang RW, Zhao YP, Ma Z, et al. Retrospective analysis for thirty-nine patients with solitary fibrous tumor of pleura and review of the literature. World J Surg Oncol 2011;9: 134-140.
  4. Fletcher C DM, Bridge JA, Lee JC. Extrapleural solitary fibrous tumor. World Health Organization Classification of Tumors of Soft Tissue and Bone. Lyon, France: IARC Press; 2013; 81.
  5. Geramizadeh B, Banani A, Moradi A, Hosseini SMV. Intrapulmonary solitary fibrous tumor with bronchial involvement: a rare case report in a child. J Pediat Surg 2010; 45(1): 249–251.
  6. DeVito N, Henderson E, Han G,Reed D, Bui MM, Lavey R, et al. Clinical characteristics and outcomes for solitary fibrous tumor (SFT): A Single center experience. PLoS One 10(10): e0140362
  7. Hsieh TY, Chang Chien YC, Chen WH, Chen SC, Chang LC, Hwang CC, Chein HP, Chen JR. De novo malignant solitary fibrous tumor of the kidney. Diagn Pathol 2011;6: 96-102.
  8. Rakheis D, Molberg KH, Roberts CA, Jaiswal VR. Immunohistochemical Expression of β-Catenin in Solitary Fibrous Tumors. Arch Pathol Lab Med 2005; 129 (6):776–779.
  9. Vogels RJ, Vlenterie M, Versleijen-Jonkers YMH, Ruijter E, Bekers EM,Verdijk MAJ, et al. Solitary fibrous tumor – clinicopathologic, immunohistochemical and molecular analysis of 28 cases. Diagn Pathol 2014;9:224-33.
  10. Dagrada GP, Spagnuolo RD, Mauro V, Tamborini E, Cesana L, Gronchi A, et al. Solitary fibrous tumors: loss of chimeric protein expression and genomic instability mark dedifferentiation. Mod Pathol 2015; 28(8): 1074–1083.
  11. Akaike K, Kurisaki-Arakawa A, Hara K, Suehara Y, Takagi T, MT KM, et al.Distinct clinicopathological features of NAB2-STAT6 fusion gene variants in solitary fibrous tumor with emphasis on the acquisition of highly malignant potential. Hum Pathol 2015; 46(3): 347–356.
  12. Wang H, Chen P, Zhao W, Shi L, Gu X, Xu Q. Clinicopathological findings in a case series of abdominopelvic solitary fibrous tumors. Oncol Lett 2014; 7(4): 1067-1072.
  13. Yoshida A, Tsuta k, Ohno M, Yoshida M, Narita y, Kawai A, et al. STAT6 Immunohistochemistry Is Helpful in the Diagnosis of Solitary Fibrous Tumors. Am J Surg Pathol 2014;38(4): 552–559.
  14. Koelsche C, Schweizer L, Renner M, Warth A, Jones DTW, Sahm F, et al. Nuclear relocation of STAT6 reliably predicts NAB2–STAT6 fusion for the diagnosis of solitary fibrous tumour. Histopathology 2014; 65(5):613-622.
  15. Bauer JL, Miklos AZ, Thompson LDR. Parotid Gland Solitary Fibrous Tumor: A Case Report and Clinicopathologic Review of 22 Cases from the Literature. Head and Neck Pathol 2012; 6(1):21–31.
  16. Mohajeri A,Tayebwa J, Collin A,Nilsson j,Magnusson l,Vult von Steyern F, et al. Comprehensive Genetic Analysis Identifies a Pathognomonic NAB2/STAT6 Fusion Gene, Nonrandom Secondary Genomic Imbalances, and a Characteristic Gene Expression Profile in Solitary Fibrous Tumor. Genes Chromosomes Cancer 2013;52 (10):873–886.
  17. Barthelme S,Geddert H, Boltze C, Moskalev EA, Bieg M, Sirbu H, et al.Solitary Fibrous tumors/hemangiopericytomas with different variants of the NAB2-STAT6 gene fusion are characterized by specific histomorphology and distinct clinicopathological features. Am J Pathol 2014;184(4): 1209-18.
  18. Jadczak P,Guz W, Kaznowska E,Ramotowski R,Szalacha-Tarała,Górecki A, Samojedny A. Solitary Fibrous Tumour of the Pleura – Cases Analysis. Pol J Radiol 2014;79: 368-373 .
  19. Karpathiou G, Stefanou D, Froudarakis ME. Pleural neoplastic pathology. Respir Med 2015; 109 (8) :931-43.
  20. Morgab MB, Smoller BR. Solitary fibrous tumors are immunophenotypically distinct from mesothelioma(s). J Cutan Pathol 2000;27(9):451-54.
  21. Yokoi T, Tsuzuki T, Yatabe y, Suzuki M, Kurumaya H, Koshikawa T, et al. Solitary fibrous tumor: Significance of P53 and CD34 immunoreactivity in its malignant transformation. Histopathology 1998;32(5):423-32.
  22. Schirosi L, Lantuejoul S, Cavazza A, Murer B, Brichon PY, Migaldi M,et al. Pleuro-pulmonary solitary fibrous tumors. A clinicopathologic, immunohistochemical, and molecular study of 88 cases confirming the prognostic value of de Perrot staging system and p53 expression, and evaluating the role of c-kit, BRAF, PDGFRs (a/b), c-met, and EGFR. Am J Surg Pathol 2008;32(11):1627-1642.
  23. Barak S, Wang Z Miettinen M. Immunoreactivity for calretinin and keratins in desmoid fibromatosis and other myofibroblastic tumors. A diagnostic pitfall. Am J Surg Pathol 2012;36(9):1404–1409.
  24. Naito Y, Ishii G, Kawai O, Hasebe T, Nishiwaki Y, Nagai K and et al. D2-40-positive solitary fibrous tumors of the pleura: Diagnostic pitfall of biopsy specimen. Pathol Int 2007;57:618-21.
  25. Rao N, Colby TV, Falconieri G, Cohen H, Moran CA, Suster S.Intrapulmonary Solitary Fibrous Tumors Clinicopathologic and Immunohistochemical Study of 24 Cases. Am J Surg Pathol 2013;37(2):155-166.
  26. Kouki HS, Koletsis EN, Zolota V, Prokakis C, Apostolakis E, Dougenis D. Solitary fibrous tumor of the lung. Gen Thorac Cardiovasc Surg 2008;56(5):249-251.
  27. Suzuki SO, Fukul M, Nlshlo S, Iwakl T. Clinicopathological features of solitary fibrous tumor of the meninges: An immunohistochemical reappraisal of cases previously diagnosed to be fibrous meningioma or hemangiopericytoma. Pathol Int 2000;50(10):808-817.
  28. Bosman F, Jaffe E, Lakhani S, Ohgaki H. WHO classification of tumors of central nervous system. IARC Press, Lyon , 2013.
  29. Schweizer L, Koelsche C, Sahm F,Piro RM,Capper D, Reuss DE, et al. Meningeal hemangiopericytoma and solitary fibrous tumors carry the NAB2-STAT6 fusion and can be diagnosed by nuclear expression of STAT6 protein. Acta Neuropath 2013;125(5):651-8.
  30. Bouvier C, Métellus P, de Paula AM, Vasiljevic A, Jouvet A, Guyotat J, et al.Solitary Fibrous Tumors and Hemangiopericytomas of the Meninges: Overlapping Pathological Features and Common Prognostic Factors Suggest the Same Spectrum of Tumors. Brain Pathol 2012;22(4):511-521.
  31. Mekni A, Kourda J, Ben Hammouda K, Tangour M, Kchir N, Zitouna M, et al. Solitary fibrous tumour of the central nervous system: pathological study of eight cases and review of the literature. Pathology 2009;41(7):649-54.
  32. Hayashia Y,Uchiyamaa N, Hayashia Y, Nakadaa M, Iwatoa M. A re-evaluation of the primary diagnosis of hemangiopericytoma and the clinical importance of differential diagnosis from solitary fibrous tumor of the central nervous system. Clin Neurol Neurosurg 2009;111(1):34-8
  33. Bisceglia M, Galliani C, Giannatempo G, Lauriola W, Bianco M, D’Angelo V, et al .Solitary Fibrous Tumor of the Central Nervous System:A 15-year Literature Survey of 220 Cases. Adv Anat pathol 2011; 18(5):356-92.
  34. Hah HP, Bundock EA, Hornick JL, .Immunohistochemical Staining for Claudin-1 Can Help Distinguish Meningiomas from Histologic Mimics. Am J Clin Pathol 2006; 125(2):203-208.
  35. Chen H, Zeng XW, Wu JS, Dou YF, Wang Y, Zhong P, et al. Solitary fibrous tumor of the central nervous system: a clinicopathologic study of 24 cases. Acta Neurochir (Wien). 2012;154(2):237-48
  36. Ambrosini-Spaltro A, Eusebi V. Meningeal hemangiopericytomas and hemangiopericytoma /solitary fibrous tumors of extracranial soft tissues: a comparison. Virchows Arch 2010;456 (4): 343-354.
  37. Verbeke SL, Fletcher CD, Alberghini M, Daugaard S, Flamagan AM, Hogendoom CW, et al. A Reappraisal of Hemangiopericytoma of Bone; Analysis of Cases Reclassified as Synovial Sarcoma and Solitary Fibrous Tumor of Bone. Am J Surg Pathol 2010;34(6):777-783.
  38. Cheah AL, Billings SD, Goldblum JR, Carver P, Tanas MZ, Rubin BP. STAT6 rabbit monoclonal antibody is a robust diagnostic tool for the distinction of solitary fibrous tumour from its mimics. Pathology 2014;46(5): 389-95.
  39. Demicco EG, Harms PW, Patel RM, Smith SC, Ingram D, Torres K, et al. Extensive Survey of STAT6 Expression in a Large Series of Mesenchymal Tumors. Am J Clin Pathol 2015;143(5):672-82.
  40. Vivero M, Doyle LA, Fletcher CD, Mertens F, Hornick JL. GRIA2 is a novel diagnostic marker for solitary fibrous tumour identified through gene expression profiling. Histopathology 2014;65(7):71-80.
  41. Erday G, Qureshi HS, Patterson JW, Wick MR. Solitary fibrous tumors of the skin: a clinicopathologic study of 10 cases and review of the literature. J Cut Pathol 2007;34(11):844-850.
  42. Carlson JW, Fletcher CDM. Immunohistochemistry for β-catenin in the differential diagnosis of spindle cell lesions: analysis of a series and review of the literature. Histopathology 2007;51(4):509-14.
  43. Wood L, Fountaine TJ, Rosamilia L, Helm KF, Clarke LE. Cutaneous CD34+ Spindle Cell Neoplasms: Histopathologic Features Distinguish Spindle Cell Lipoma, Solitary Fibrous Tumor, and Dermatofibrosarcoma Protuberans. Am J Dematopathol 2010;32(8):764-768.
  44. Turner MS, Goldsmith JD. Best Practices in Diagnostic Immunohistochemistry. Spindle Cell Neoplasms of the Gastrointestinal Tract. Arch Pathol Lab Med 2009;133(9):1370-74.
  45. Shidham VB, Chivukula M, Gupta D, Nagarjun R, Komorowski R. Immunohistochemical comparison of gastrointestinal stromal tumor and solitary fibrous tumor. Arch Pathol Lab Med 2002;126(10):1189-92.
  46. Yamaguchi U, Hasegawa T, Masuda T, Sekine · Akira Kawai S, Chuman H, et al.Differential diagnosis of gastrointestinal stromal tumor and other spindle cell tumors in the gastrointestinal tract based on immunohistochemical analysis. Virchows Arch 2004;445(2):142-150.
  47. Cho KJ, Ro JY, Choi SH, Nam SY, Kim SY. Mesenchymal neoplasms of the major salivary glands:clinicopathological features of 18 cases. Eur Arch Otorhinolaryngol 2008;265 (Suppl 1) S47-S56.
  48. O’regan EM, Vanguri V, Allen CM, Eversole LR, Wright JM, Woo SB. Solitary Fibrous Tumor of the Oral Cavity: Clinicopathologic and Immunohistochemical Study of 21 Cases. Head and Neck Pathol 2009;3(2):106-115.
  49. Blandamura S, Alaggio R, Bettini G, Guzzardo V, Valentini E, Bedogin A. Four cases of solitary fibrous tumour of the eye and orbit: one with sarcomatous transformation after radiotherapy and one in a 5-year-old child’s eyelid. J Clin Pathol 2014;67(3):263-67.
  50. Mosquera JM, Fletcher CD. Expanding the Spectrum of Malignant Progression in Solitary Fibrous Tumors. A Study of 8 Cases With a Discrete Anaplastic Component— Is This Dedifferentiated SFT? Am J Surg Pathol 2009;33(9): 1314-1321.
  51. Demicco EG, Park MS, Araujo DM, Fox PS, Bassetts RL, Pollock RE, et al.Solitary fibrous tumor: a clinicopathological study of 110 cases and proposed risk assessment model. Mod Pathol 2012;25 (9): 1298-1306.
  52. Subramaniam MM, Lim XY, Venkateswaran K, Shuen CS, Soong R, Petersson F. Dedifferentiated solitary fibrous tumour of the nasal cavity: the first case reported with molecular characterization of a TP53 mutation. Histopathology 2011;59(6):1269-79.
  53. Collini P, Negri T, Barisella M, Palassini E, Tarantino E, Pastorino U, et al. High-grade Sarcomatous Overgrowth in Solitary Fibrous Tumors.A Clinicopathologic Study of 10 Cases. Am J Surg Pathol 2012;36 (8):1202-1215.