Linked Life Data

8278571

Source:http://linkedlifedata.com/resource/pubmed/id/8278571

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1994-2-10
pubmed:abstractText
Cloning of the t(14;18) translocation breakpoint resulted in the identification of a new putative oncogene, which mapped to 18q21, termed bcl-2. The t(14;18) resulted in inappropriately high levels of bcl-2 expression in follicular lymphoma. Prospective studies using mice transgenic for a human bcl-2-immunoglobulin minigene, intended to recreate the molecular features of the t(14;18), demonstrated that bcl-2 gene deregulation was oncogenic. Interestingly, overexpression of bcl-2 showed no demonstrable influence on rates of cellular proliferation. Rather, bcl-2 was found to extend cellular viability by blocking apoptosis. Recent studies with other oncogenes and tumor suppressor genes, such as c-myc and p53, have demonstrated that the deregulation of apoptosis may be of general significance in the development of multiple types of cancer and appears to be a critical event during multistep carcinogenesis. The selective induction of apoptosis in tumor cell populations is now being considered in the design of novel therapeutic interventions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0033-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
136
pubmed:geneSymbol
bcl-2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
307-12
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
The bcl-2 oncogene: apoptosis and neoplasia.
pubmed:affiliation
Department of Molecular Pathology, University of Texas M. D. Anderson Cancer Center, Houston 77030.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't