Analysis of the p53/BAX pathway: Low BAX expression is a negative prognostic factor in patients with resected liver metastases of colorectal adenocarcinoma

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Abstract

The BCL-2 family with its anti-apoptotic members (BCL-2, BCL-XL, BCL-W, MCL-1, and A1) and the death promoting members (BAX, BCL-Xs, BAK, BAD, BIK/NBK, BID, BOK, HRK, and MTD) plays a central role in the regulation of cell death. The overexpression of anti-apoptotic factors of this gene family, such as BCL-2, contributes to cancer pathogenesis as in the case of follicular lymphoma and may be involved in the resistance to cancer therapy. In breast cancer, we previously described a defect in expression of the BAX protein, a key promoter of apoptosis [1]. Restoration of BAX expression in breast cancer cell lines inhibited tumorigenicity [2] and increased sensitivity to cytotoxic drug therapy [3]. In breast cancer patients, reduced BAX expression correlates with a poor response to chemotherapy and shorter overall survival. To further investigate the role of BAX in careinoma cells, we analysed the BAX mutational status and expression in patients with hepatic metastases of colorectal cancer.