Colon cancer: genomics and apoptotic events

C. Rupnarain, Z. Dlamini, S. Naicker, Kanti Bhoola

    Research output: Contribution to journalArticlepeer-review

    93 Citations (Scopus)

    Abstract

    Colon cancer is the third most common cancer globally. The risk of developing colon cancer is influenced by a number of factors that include age and diet, but is primarily a genetic disease, resulting from oncogene overexpression and tumour suppressor gene inactivation. The induction and progression of the disease is briefly outlined, as are the cellular changes that occur in its progression. While colon cancer is uniformly amenable to surgery if detected at the early stages, advanced carcinomas are usually lethal, with metastases to the liver being the most common cause of death. Oncogenes and genetic mutations that occur in colon cancer are featured. The molecules and signals that act to eradicate or initiate the apoptosis cascade in cancer cells, are elucidated, and these include caspases, Fas, Bax, Bid, APC, antisense hTERT PUMA, 15-LOX-1, ceramide, butyrate, tributyrin and PPARgamma, whereas the molecules which promote colon cancer cell survival are p53 mutants, Bcl-2, Neu3 and COX-2. Cancer therapies aimed at controlling colon cancer are reviewed briefly.
    Original languageEnglish
    Pages (from-to)449-464
    JournalBiological Chemistry
    Volume385
    Issue number6
    DOIs
    Publication statusPublished - 2004

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