Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7 Suppl
pubmed:dateCreated
1999-4-22
pubmed:abstractText
The chromosome translocations typifying Burkitt's lymphoma and follicular lymphoma deregulate very different oncogenes, myc and bcl-2. Transgenic mouse models have illuminated how each contributes to lymphomagenesis. Constitutive myc expression provokes sustained cell proliferation and retards differentiation. However, the resulting expansion in cell number is self-limiting, because the cells remain dependent on cytokines and undergo apoptosis when these become limiting. In contrast, bcl-2 is the prototype of a new class of oncogene that enhances cell survival but does not promote proliferation. Coexpression of these genes leads to the rapid transformation of lymphocytes, probably because each can counter an antioncogenic aspect of the other. Several close homologues of Bcl-2 also enhance cell survival and are thus potential oncogenes; each is essential for maintenance of particular major organs. More distant Bcl-2 relatives instead promote apoptosis and can be regarded as tumor suppressors. For many but not all apoptic signals, the balance between these competing activities determines cell survival. Learning how to adjust the apoptotic threshold in cancer cells should promote development of more effective therapeutic strategies.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
59
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1685s-1692s
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Insights from Bcl-2 and Myc: malignancy involves abrogation of apoptosis as well as sustained proliferation.
pubmed:affiliation
The Walter and Eliza Hall Institute of Medical Research, PO Royal Melbourne Hospital, Victoria, Australia.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't