Cloning of the t(14;18) translocation breakpoint resulted in the identification of a new putative oncogene, which mapped to 18q21, termed bcl-2. The t(14;18) resulted in inappropriately high levels of bcl-2 expression in follicular lymphoma. Prospective studies using mice transgenic for a human bcl-2-immunoglobulin minigene, intended to recreate the molecular features of the t(14;18), demonstrated that bcl-2 gene deregulation was oncogenic. Interestingly, overexpression of bcl-2 showed no demonstrable influence on rates of cellular proliferation. Rather, bcl-2 was found to extend cellular viability by blocking apoptosis. Recent studies with other oncogenes and tumor suppressor genes, such as c-myc and p53, have demonstrated that the deregulation of apoptosis may be of general significance in the development of multiple types of cancer and appears to be a critical event during multistep carcinogenesis. The selective induction of apoptosis in tumor cell populations is now being considered in the design of novel therapeutic interventions.
The bcl-2 Oncogene: Apoptosis and Neoplasia
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Timothy J. McDonnell, Maria C. Marin, Brenda Hsu, Shawn M. Brisbay, Kristina McConnell, Shi-Ming Tu, Martin L. Campbell, Julio Rodriguez-Villanueva; The bcl-2 Oncogene: Apoptosis and Neoplasia. Radiat Res 1 December 1993; 136 (3): 307–312. doi: https://doi.org/10.2307/3578541
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