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The Genetics of Programmed Cell Death in the Nematode Caenorhabditis elegans

Horvitz, H.R., Shaham, S., Hengartner, M.O.·1994·Cold Spring Harbor Symposia on Quantitative Biology

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...

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Metadata

Authors
Horvitz, H. R., Shaham, S., & Hengartner, M. O.
Venue
Cold Spring Harbor Symposia on Quantitative Biology
Published
1994-01-01
Volume
59
Issue
0
Pages
377-385
ISSN
  • 0091-7451 (ISSN-L)
  • 1943-4456
OpenAlex
W1994081180
Cited by
193
References
0
Type
posted content
Language
en
Open access
closed

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CoChat. (2026). Citation check: The Genetics of Programmed Cell Death in the Nematode Caenorhabditis elegans. https://app.cochat.ai/papers/10.1101/sqb.1994.059.01.042
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Horvitz, H. R., Shaham, S., & Hengartner, M. O. (1994). The Genetics of Programmed Cell Death in the Nematode Caenorhabditis elegans. Cold Spring Harbor Symposia on Quantitative Biology. https://doi.org/10.1101/sqb.1994.059.01.042

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