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Apoptosis

Edited by: Steven Benowitz A. Strasser, A.W. Harris, T. Jacks, S. Cory, "DNA damage can induce apoptosis in proliferating lymphoid cells via p53-independent mechanisms inhibitable by Bcl-2," Cell, 79:329-39, 1994. (Cited in more than 110 publications through October 1996) Comments by Tyler Jacks, Howard Hughes Medical Institute, Massachusetts Institute of Technology Center for Cancer Research; and Andreas Strasser, Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia CE

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Edited by: Steven Benowitz
A. Strasser, A.W. Harris, T. Jacks, S. Cory, "DNA damage can induce apoptosis in proliferating lymphoid cells via p53-independent mechanisms inhibitable by Bcl-2," Cell, 79:329-39, 1994. (Cited in more than 110 publications through October 1996) Comments by Tyler Jacks, Howard Hughes Medical Institute, Massachusetts Institute of Technology Center for Cancer Research; and Andreas Strasser, Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia

CELL SLEUTHING: From left, Suzanne Cory, Andreas Strasser, and Alan Harris of the Walter and Eliza Hall Institute of Medical Research study how cells die. The p53 tumor suppressor gene, which is mutated in as many as half of all human cancers, must be functioning for apoptosis-or programmed cell death-to occur when the DNA of immune system cells is damaged by radiation during cancer treatment. If p53 is missing or mutated, apoptosis is inhibited. The oncogene bcl-2, which also is mutated in ...

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