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J Clin Pathol 2005;58:1046-1050 doi:10.1136/jcp.2004.024919
  • Original article

Suppressor of cytokine signalling 2 (SOCS-2) expression in breast carcinoma

  1. F Farabegoli1,
  2. C Ceccarelli2,
  3. D Santini2,
  4. M Taffurelli3
  1. 1Department of Experimental Pathology, University of Bologna, Via San Giacomo, 14, 40126 Bologna, Italy
  2. 2Institute of Anatomical and Pathological Histology, University of Bologna
  3. 3Breast Cancer Surgical Unit, First Surgical Clinic, University of Bologna
  1. Correspondence to:
 Dr F Farabegoli
 Department of Experimental Pathology, University of Bologna, Via San Giacomo, 14, 40126 Bologna, Italy; frbflalma.unibo.it
  • Accepted 14 February 2005

Abstract

Aims: To investigate SOCS-2 (suppressor of cytokine signalling 2) protein expression in breast carcinoma samples in relation to biopathological parameters and survival.

Methods: A polyclonal antibody against SOCS-2 was used to study 50 archival breast carcinoma samples, collected from 1993 to 1995. The presence of SOCS-2 protein was investigated in relation to clinical and biological parameters used in breast cancer pathology. Fluorescence in situ hybridisation (FISH) was used to study whether SOCS-2 expression was related to SOCS-2 gene copy number.

Results: SOCS-2 protein was expressed in 34 of 50 breast carcinoma samples and was positively associated with low grade, low nuclear grade, and p27 protein. SOCS-2 expression was inversely related to Ki-67, cyclin A, retinoblastoma protein (pRb), and the epidermal growth factor receptor (EGFR). No relation with overall survival was demonstrated. SOCS-2 amplification was found in three samples. No relation between the number of FISH signals and SOCS-2 expression was found.

Conclusions: The significant correlation seen between SOCS-2 expression, grade, nuclear grade, p27, Ki-67, cyclin A, pRb, and EGFR labelling strongly supports the hypothesis that SOCS-2 loss might be related to cell proliferation and tumour growth in breast carcinoma. Gene copy number changes did not seem to play a role in SOCS-2 regulation and expression; other mechanisms might be involved and deserve further study.

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