| First Author | Nilsson LM | Year | 2007 |
| Journal | Oncogene | Volume | 26 |
| Issue | 20 | Pages | 2833-9 |
| PubMed ID | 17099725 | Mgi Jnum | J:122886 |
| Mgi Id | MGI:3715688 | Doi | 10.1038/sj.onc.1210104 |
| Citation | Nilsson LM, et al. (2007) Ink4c is dispensable for tumor suppression in Myc-induced B-cell lymphomagenesis. Oncogene 26(20):2833-9 |
| abstractText | p18(Ink4c) functions as a dedicated inhibitor of cyclin-D-dependent kinases. Loss of Ink4c predisposes mice to tumor development and, in a dose-dependent manner, complements the tumor-promoting effects of various oncogenes. We have now addressed whether Ink4c loss impacts B-cell tumor development in the Emu-Myc transgenic mouse, a model of human Burkitt lymphoma. Loss of one or both alleles did not influence the onset of lymphoma in Emu-Myc transgenics, and did not appreciably affect Myc's proliferative or apoptotic responses in precancerous B cells. Nevertheless, Ink4c loss modulated the effects of Myc-induced transformation by decreasing the frequency of Arf loss, an ordinarily common event in Emu-Myc-induced lymphomas. |
