Linked Life Data

7632929

Source:http://linkedlifedata.com/resource/pubmed/id/7632929

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pubmed-article:7632929pubmed:abstractTextt(14;18) is the most common translocation in human lymphoid malignancy and results in bcl-2 overexpression. Bcl-2 blocks apoptosis and constitutes the initial member of a new category of oncogenes, ie, regulators of cell death. Bcl-2-Ig transgenic mice develop follicular hyperplasia and progress to malignant B-cell lymphoma. To assess the oncogenic potential of bcl-2 in the T-cell lineage, a cohort of 68 lckpr-bcl-2 transgenic mice and 56 control littermates were monitored for signs of malignancy over a 24-month period. Eighteen (26%) lckpr-bcl-2 mice developed diffuse, predominantly large-cell lymphomas at a mean age of 18 months. In contrast, only one nontransgenic control mouse developed lymphoma. CD3 surface expression and clonal T-cell receptor beta rearrangements support the T-lineage classification of these neoplasms. lckpr-bcl-2-enforced lymphomas are predominantly CD4+CD8-, consistent with a mature peripheral T-cell phenotype. These data provide support for the thesis that violation of homeostasis through the repression of cell death can be a primary mechanism of tumorigenesis in multiple lineages.lld:pubmed
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pubmed-article:7632929pubmed:dateRevised2009-11-19lld:pubmed
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pubmed-article:7632929pubmed:articleTitlePeripheral T-cell lymphoma in lckpr-bcl-2 transgenic mice.lld:pubmed
pubmed-article:7632929pubmed:affiliationDepartment of Medicine, Howard Hughes Medical Institute at Washington University, St Louis, MO 63110, USA.lld:pubmed
pubmed-article:7632929pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:7632929pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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