The bcl-2 oncogene: apoptosis and neoplasia.
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.
McDonnell
T J
TJ
Department of Molecular Pathology, University of Texas M. D. Anderson Cancer Center, Houston 77030.
Marin
M C
MC
Hsu
B
B
Brisbay
S M
SM
McConnell
K
K
Tu
S M
SM
Campbell
M L
ML
Rodriguez-Villanueva
J
J
D000818:Animals; D017209:Apoptosis; D006801:Humans; D009369:Neoplasms / Q000209:etiology*; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D019253:Proto-Oncogene Proteins c-bcl-2; D011519:Proto-Oncogenes
D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2