The Genetics of Programmed Cell Death in the Nematode Caenorhabditis elegans

Cancerous growth often results from an increased rate of cell proliferation caused by the abnormal activation of a signal transduction pathway that normally stimulates cell division only in response to growth factor signals; many of the proto-oncogenes that have been characterized function in or respond to such intercellular signaling pathways (for review, see Cooper 1990). Recent findings indicate that cancerous growth also can result from a decreased rate of cell loss. The most striking example is provided by human B-cell follicular lymphomas. These cancers are often associated with t(14;18) chromosomal translocations that cause the proto-oncogene bcl-2 (bcl, B cell lymphoma), normally located on chromosome 18, to be adjacent to and regulated by an enhancer of the immunoglobulin heavy-chain locus, normally located on chromosome 14 (Bakhshi et al. 1985; Cleary and Sklar 1985; Tsujimoto et al. 1985). The resulting overexpression of a normal Bcl-2 protein in the B-cell lineage leads to...