| Literature DB >> 19196996 |
Paul Bolitho1, Shayna E A Street, Jennifer A Westwood, Winfried Edelmann, Duncan Macgregor, Paul Waring, William K Murray, Dale I Godfrey, Joseph A Trapani, Ricky W Johnstone, Mark J Smyth.
Abstract
In the present study, we have examined the effect of perforin (pfp) deficiency in 4 models of mouse B-cell lymphomagenesis. We have examined pfp loss on the background of either Mlh1 tumor suppressor allele loss or oncogene expression [Ig heavy chain (Emu)-v-Abl, Emu-myc, and vav-bcl2]. Pfp was shown to act as a suppressor of B-cell malignancies characteristically driven by v-Abl or bcl-2, whereas Mlh loss cooperated in accelerating spontaneous B-cell lymphomas characteristic of pfp loss. No protective role for pfp was observed in the more aggressive Emu-myc model of B-cell lymphoma. These transgenic models have allowed us to distinguish the role of pfp in surveillance of B-cell lymphomagenesis, as opposed to its loss simply driving the onset of a spontaneous lymphoma characteristic of pfp deficiency.Entities:
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Year: 2009 PMID： 19196996 PMCID： PMC2650333 DOI： 10.1073/pnas.0809008106
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN： 0027-8424 Impact factor: 11.205