The Genetics of Programmed Cell Death in the Nematode Caenorhabditis elegans

  1. H.R. Horvitz,
  2. S. Shaham, and
  3. M.O. Hengartner*
  1. Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139

This extract was created in the absence of an abstract.

Excerpt

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...

  • *

    * Present address: Cold Spring Harbor Laboratory, P.O. Box 100, Cold Spring Harbor, New York 11724.

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