Overexpression of SOCS3 is associated with decreased survival in a cohort of patients with de novo follicular lymphoma

Abstract

SummaryThe prognostic significance of SOCS3 protein expression was determined in de novo follicular lymphomas (FL) with t(14;18) and bcl-2 overexpression. Presentation lymph nodes from 82 FL patients for whom clinical information was available were immunohistochemically segregated into SOCS3-positive (n ¼ 42) or -negative (n ¼ 40) cohorts, and overall survival (OS) was analysed. SOCS3-positive FL patients had a median OS of 10 years compared with 22 years in SOCS3-negative patients (P ¼ 0AE001, log rank test). After adjusting for Follicular Lymphoma International Prognostic Index subgroups, SOCS3 overexpression remained an independent predictor of decreased OS (P < 0AE001). These findings suggest that overexpression of SOCS3 may be an independent poor prognostic variable in patients with de novo FL.

Loss of SOCS3 expression is associated with an increased risk of recurrent disease in breast carcinoma

“…Methylation silencing of SOCS3 is one of the most important mechanisms of constitutive activation of JAK-STAT pathway in cancer pathogenesis. It has been identified that the methylation of SOCS3 promoter may be involved in the pathogenesis of glioblastoma multiforme (GBM) (Martini et al 2008), follicular lymphoma (Krishnadasan et al 2006), neck and head squamous cell carcinoma (Weber et al 2005), cholangiocarcinoma (Isomoto et al 2007), malignant melanoma (Tokita et al 2007) and hepatocellular carcinoma (Yang et al 2008). SOCS3 itself may function as an important tumor suppressor gene and may be involved in the resistance of these neoplasms to conventional treatment.…”

Immunohistochemical Analysis of IL-6, IL-8/CXCR2 Axis, Tyrp-STAT-3, and SOCS-3 in Lymph Nodes from Patients with Chronic Lymphocytic Leukemia: Correlation between Microvascular Characteristics and Prognostic Significance

“…This is strengthened by the inverse correlation between SOCS-3 and FasL expression within PCs, the latter being a mechanism adopted by CLL cells to avoid immunosurveillance [26]. In support of this role, SOCS-3 overexpression reportedly diminishes proliferation of classical Hodgkin lymphoma cell lines [40], whereas its loss has been postulated to predispose for the emergence of a more aggressive disease [39, 41]. …”

Phosphorylation of signal transducer and activator of transcription 3 in soft tissue leiomyosarcoma is associated with a better prognosis

“…SOCS family members have mechanisms that inhibit JAK/STAT signaling 23, 24. SOCS3 is generally recognized as a tumor suppressor reflecting its inhibition of STAT3 tumorigenesis; however, follicular lymphomas have been reported to show more aggressive behaviors when expressing SOCS3 25. Some studies have also revealed that SOCS3 contributes to cell proliferation in some conditions by suppressing STAT families 26–28…”