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Arch Pathol Lab Med. 2006 Jun;130(6):792-8.

Beta-catenin nuclear expression correlates with cyclin D1 expression in primary and metastatic synovial sarcoma: a tissue microarray study.

Author information

1
Department of Pathology, University of California, San Francisco, CA 94114-1656, USA. andho@itsa.ucsf.edu

Abstract

CONTEXT:

The association between aberrant (nuclear) beta-catenin expression and cyclin D1 accumulation has been demonstrated in diverse neoplasms. In synovial sarcoma (SS), aberrant beta-catenin expression has prognostic relevance, but the association with cyclin D1 has not been established. The SYT-SSX fusion protein, unique to SS, may independently increase cyclin D1.

OBJECTIVE:

To determine whether nuclear beta-catenin is associated with cyclin D1 overexpression in SS and whether primary and metastatic SS differ in the expression of these markers.

DESIGN:

We incorporated 82 tumors initially diagnosed as SS into a tissue array. Fluorescence in situ hybridization with custom probes was used to select t(X;18) positive tumors. Clinical data, tumor type and outcome were tabulated. The tumors were tested for the association between nuclear beta-catenin and cyclin D1 immunostaining. Primary and metastatic tumors were compared.

RESULTS:

Fifty-one tumors (41 primary and 10 metastatic) from 43 patients demonstrated t(X;18). Cyclin D1 staining was identified in 21 (59%) primary and 8 (80%) metastatic tumors, respectively, and nuclear beta-catenin in 24 (41%) primary and 7 (70%) metastatic tumors, respectively. No significant difference was noted between primary and metastatic tumors with respect to the above markers. The presence of nuclear beta-catenin showed a significant association with cyclin D1 expression (P < .001). A small number of cyclin D1 cases were negative for nuclear beta-catenin but positive for phosphorylated Akt.

CONCLUSIONS:

Increased cyclin D1 in SS may be driven by abnormally expressed beta-catenin, similar to other neoplasms. The pattern of expression of these markers is established early during tumorigenesis.

[Indexed for MEDLINE]

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