Inhibin-α and synaptophysin immunoreactivity in synovial sarcoma with granular cell features

Setsu, Nokitaka; Kohashi, Kenichi; Yamamoto, Hidetaka; Ohishi, Yoshihiro; Sueyoshi, Kazunobu; Iwamoto, Yukihide; Tsuneyoshi, Masazumi; Motoi, Toru; Kumagai, Arisa

doi:10.1016/j.humpath.2011.07.012

Cited by 8 publications

(4 citation statements)

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“…Regarding the chromograninA labeling, our data as well as the data from literature revealed a striking dichotomy of synaptophysin and chromograninA expression. Synaptophysin-chromograninA co-expression was observed in 34% of our MN-NEs and in 5/92 (5%) neoplasms from the literature [ 2 – 4 , 12 , 15 , 18 , 19 , 23 , 30 , 33 , 34 , 36 , 38 – 42 , 44 , 46 , 47 , 49 , 50 , 54 ] (see Table 1 and 2 ), suggesting that the dichotomy in the synaptophysin-chromograninA expression is a common finding in these neoplasms and contrasts sharply with the expression rates in PanNETs, in which chromograninA labels 91% of the synaptophysin positive tumors [ 52 ]. Among our chromograninA, negative MN-NEs were SFT, ES, SMARCA4-deficient neoplasm, melanoma, and chordoma.…”

Section: Discussionmentioning

confidence: 85%

“…The other feature of MN-NEs, the patchy expression of synaptophysin and the absence or focality of chromograninA staining, are also rare in NECs, and particularly in NETs, which instead show a diffuse and usually intense staining. The complete absence of chromograninA should always arouse suspicion against the diagnosis of 40,49 0 (0/23) 0 (0/23) 0 (0/23) 0/0 unspecified 50 (1/2) 0 (0/2) 0 (0/2) 0/1 Soft tissue/retroperitoneum Alveolar soft part sarcoma 36,53,26,16,16,31,20 0 (0/7) NA NA NA Soft tissue 0 (0/5) 0 (0/4) 0 (0/4) 0/0 Case reports: soft tissue, head and neck, prostate, mediastinum Solitary fibrous tumor 30,33,19 17 (4/23) 0 (0/23) 0 (0/23) 0/4 Central nerve system 0 (0/28) 0 (0/28) 0 (0/28) 0/0 Mostly extrapleural soft tissue 0 (0/13) 0 (0/13) 0 (0/13) 0/0 Pleura Epithelioid sarcoma 23 60 In conclusion, MN-NEs represent only a small group among the various NEN mimickers, but have been increasingly noticed in recent years and are particularly found among new entities of mesenchymal tumors that share an epithelioid-mesenchymal morphology, show a variegated immunophenotype, are characterized by gene fusion alterations in the CREB family or mutations of SMARC genes, and can occur as pancreatic primaries. All these tumors may cause diagnostic problems in the distinction from NECs and to a minor degree also NETs.…”

Section: Discussionmentioning

confidence: 99%

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Mesenchymal/non-epithelial mimickers of neuroendocrine neoplasms with a focus on fusion gene-associated and SWI/SNF-deficient tumors

et al. 2021

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Mimickers of neuroendocrine neoplasms (NEN) include a number of important pitfall tumors. Here, we describe our experience with mesenchymal mimics of NENs to illustrate their spectrum and draw the attention particularly to a group of mesenchymal/non-epithelial neoplasms (MN) that combine epithelioid histology with neuroendocrine (NE-) features and peculiar genetic abnormalities. In a consultation series of 4498 cases collected between 2009 and 2021, 2099 neoplasms expressing synaptophysin and/or chromograninA were reviewed and analyzed. A total of 364 (18%) were diagnosed as non-NENs, while the remaining tumors were NEN. The group of mesenchymal/non-epithelial neoplasms with NE-features (MN-NE) included 31/364 (8%) cases. These mostly malignant neoplasms showed an epithelioid morphology. While all but one tumor expressed synaptophysin, mostly patchy, only 10/29 (34%) co-expressed chromograninA. A total of 13/31 (42%) of the MN-NE showed EWSR1-related gene fusions (6 Ewing sarcomas, 5 clear cell sarcomas, and 1 desmoplastic small round cell tumor, 1 neoplasm with FUS-CREM gene fusion) and 7 (23%) were SWI/SNF (SMARCB1 or SMARCA4)-deficient neoplasms. The remaining MN-NE included synovial sarcoma, sclerosing epithelioid mesenchymal neoplasm, melanoma, alveolar soft part sarcoma, solitary fibrous tumor, and chordoma. A total of 27/31 MN-NE were from the last 8 years, and 6 of them were located in the pancreas. Eleven MN-NE were initially diagnosed as neuroendocrine carcinomas (NECs). MN-NE with epithelioid features play an increasing role as mimickers of NECs. They mostly belong to tumors with gene fusions involving the EWSR1 gene, or with SWI/SNF complex deficiency. Synaptophysin expression is mostly patchy and chromograninA expression is infrequent in MN-NE of this series and data extracted from literature.

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Mesenchymal/non-epithelial mimickers of neuroendocrine neoplasms with a focus on fusion gene-associated and SWI/SNF-deficient tumors

et al. 2021

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“…Moreover, it is detected in virtually all epithelial NE tumors and the large majority of NE carcinomas including small cell carcinoma,12 as well as in non-NE tumors like adrenal cortical neoplasms13 and Sertoli-Leydig cell tumors 14. SYP has also anecdotally been identified in, for example, pancreatic cystic serous adenoma,15 basal cell carcinoma,16 thyroid adenoma,17 and malignant melanoma,18 as well as in various sarcomas, for example, synovial sarcoma 19…”

Section: Introductionmentioning

confidence: 99%

“…14 SYP has also anecdotally been identified in, for example, pancreatic cystic serous adenoma, 15 basal cell carcinoma, 16 thyroid adenoma, 17 and malignant melanoma, 18 as well as in various sarcomas, for example, synovial sarcoma. 19 SYP-positive NE cells occur as a minor component in many types of carcinomas, for example, in gastrointestinal epithelial malignancies, and are more extended in composite adenoneuroendocrine carcinoma, including amphicrine carcinoma. 20 The aim of this paper is to give an overview of the external quality assessment results for SYP tests in the 2 latest NordiQC runs: run 43 (2015) and run 52 (2018).…”

Section: Introductionmentioning

confidence: 99%

NordiQC Assessments of Synaptophysin Immunoassays

Vyberg

Nielsen

Bzorek

et al. 2021

Applied Immunohistochemistry &Amp; Molecular Morphology

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Solitary, multiple, benign, atypical, or malignant: the “Granular Cell Tumor” puzzle

et al. 2015

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The clinical evolution and biology of granular cell tumors (GCT) are poorly understood and treatment remains an issue of discussion. The majority of GCT are benign, although some display malignant behavior. The distinction between benign, atypical, and malignant GCT is controversial due to morphological and immunohistochemical overlap and lack of consistent histological and phenotypic criteria that predict behavior. Although histological criteria may indicate increased risk of malignant evolution, some GCT with evident benign appearance exceptionally progress towards metastatic disease. In this review, we discuss current knowledge on GCT, including histologic, immunophenotypic, and molecular characteristics and differential diagnosis. We focus on the following problematic items in GCT: (1) evolution of classification, (2) neural versus non-neural GCT, (3) neoplastic versus reactive disease, (4) malignant transformation of benign GCT, and (5) multiple versus metastatic GCT. We conclude that although a Ki-67 index >10 % and the presence of mitoses and/or of necrosis are frequently associated with malignant behavior, metastasis remains the only unequivocal sign of malignancy in GCT. An infiltrative growth pattern and vascular and/or perineural invasion are not indicative of malignancy. GCT with atypical/uncertain features almost never metastasize, and many of these tumors either behave in a benign fashion or only recur locally (similar to incompletely excised benign tumors). We therefore propose that classical and atypical histological variants form a single group of GCT. GCT with various unfavorable histological features might be labeled as "GCT with increased risk of metastasis" rather than malignant GCT.

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Inhibin-α and synaptophysin immunoreactivity in synovial sarcoma with granular cell features

Cited by 8 publications

References 28 publications

Mesenchymal/non-epithelial mimickers of neuroendocrine neoplasms with a focus on fusion gene-associated and SWI/SNF-deficient tumors

Mesenchymal/non-epithelial mimickers of neuroendocrine neoplasms with a focus on fusion gene-associated and SWI/SNF-deficient tumors

NordiQC Assessments of Synaptophysin Immunoassays

Solitary, multiple, benign, atypical, or malignant: the “Granular Cell Tumor” puzzle

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