Abstract

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...

Keywords

BiologyChromosomal translocationCell divisionSignal transductionCaenorhabditis elegansGeneticsLocus (genetics)Proto-OncogenesEnhancerCellCell growthFollicular lymphomaCell biologyLymphomaCancer researchOncogeneTranscription factorGeneCell cycleImmunology

Affiliated Institutions

Related Publications

Publication Info

Year
1994
Type
review
Volume
59
Issue
0
Pages
377-385
Citations
192
Access
Closed

External Links

Social Impact

Social media, news, blog, policy document mentions

Citation Metrics

192
OpenAlex

Cite This

H. Robert Horvitz, Shai Shaham, Michael O. Hengartner (1994). The Genetics of Programmed Cell Death in the Nematode Caenorhabditis elegans. Cold Spring Harbor Symposia on Quantitative Biology , 59 (0) , 377-385. https://doi.org/10.1101/sqb.1994.059.01.042

Identifiers

DOI
10.1101/sqb.1994.059.01.042