| First Author | Kamimura K | Year | 2007 |
| Journal | Biochem Biophys Res Commun | Volume | 355 |
| Issue | 2 | Pages | 538-42 |
| PubMed ID | 17306224 | Mgi Jnum | J:118644 |
| Mgi Id | MGI:3700007 | Doi | 10.1016/j.bbrc.2007.02.003 |
| Citation | Kamimura K, et al. (2007) Haploinsufficiency of Bcl11b for suppression of lymphomagenesis and thymocyte development. Biochem Biophys Res Commun 355(2):538-42 |
| abstractText | Recurrent chromosomal rearrangements at BCL11B are found in human hematopoietic malignancies mostly of T-cell origin. However, it is unclear how this disruption contributes to oncogenesis, because the majority of leukemias express BCL11B from an undisrupted allele. Here, we show that Bcl11b(+/-)p53(+/-) mice exhibited greater susceptibility to lymphomas than Bcl11b(+/+)p53(+/-) mice but most lymphomas retained and expressed the wild-type Bcl11b allele. This strongly suggests that Bcl11b is haploinsufficient for suppression of thymic lymphoma development in mice of the p53(+/-) background, a situation in which functional loss of only one allele confers a selective advantage for tumor growth. The haploinsufficiency is further supported by that Bcl11b(+/-) mouse embryos were impaired in thymocyte development and survival. These results indicate relevance of BCL11B aberration to human leukemogenesis. |
