Extensive Survey of STAT6 Expression in a Large Series of Mesenchymal Tumors

Abstract

Objectives Expression of strong nuclear STAT6 is thought to be a specific marker for solitary fibrous tumors (SFT). Little is known about subtle expression patterns in other mesenchymal lesions. Methods We performed immunohistochemical studies against the C-terminus of STAT6 in tissue microarrays and whole sections, comprising 2366 mesenchymal lesions. Results Strong nuclear STAT6 was expressed in 285/2021 tumors, including 206/240 SFT, 49/408 well/dedifferentiated liposarcomas, 8/65 unclassified sarcomas, and 14/184 desmoids, among others. Expression in SFT was predominately limited to the nucleus. Other positive tumors typically expressed both nuclear and cytoplasmic STAT6. Complete absence of STAT6 was most common in pleomorphic liposarcoma and alveolar soft part sarcoma (60% and 72% cases negative, respectively). Conclusions Strong nuclear STAT6 is largely specific for SFT. Physiologic low-level cytoplasmic/nuclear expression is common in mesenchymal neoplasia, and is of uncertain significance.

Analysis of NAB2-STAT6 Gene Fusion in 17 Cases of Meningeal Solitary Fibrous Tumor/Hemangiopericytoma

“…Several studies have evaluated STAT6 IHC expression in SFT and other tumors and have reported high sensitivity and specificity (sensitivity: 86% to 100%, specificity: 96% to 100%). 13,[25][26][27][28][29] In our study, all 17 cases showed strong nuclear STAT6 expression by IHC, which was consistent with previous reports.…”

Update on Select Benign Mesenchymal and Meningothelial Sinonasal Tract Lesions

“…2d), bcl-2 and CD99, while the tumor cells are non-reactive with desmin, keratins, S100 protein, actins, and nuclear b-catenin [7,32,34]. The C-terminus of STAT6 yields a strong nuclear immunoreaction, considered specific and sensitive for SFT [48][49][50].…”

Immunoexpression analysis of selected JAK/STAT pathway molecules in non-small cell lung cancer patients

“…The most comprehensive studies focused on STAT3, the elevated level of which was found in blood malignancies and several solid neoplasms; the activation of STAT5 was found particularly in leukemias and lymphomas; and the activation of STAT6, which for a long time was studied for its role in immune function, tumor immunosurveillance, and lymphomagenesis, was also observed in solid tumors. [5][6][7] The role of STAT inhibitors was also evaluated in solid tumors, although to a limited extent. Regarding their involvement in lung tumorigenesis, they activate apoptotic genes, decrease lung cancer growth, and increase the antitumor effects of epidermal growth factor receptor inhibitors.…”