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- Title
Ink4c is dispensable for tumor suppression in Myc-induced B-cell lymphomagenesis.
- Authors
Nilsson, L. M.; Keller, U. B.; Yang, C.; Nilsson, J. A.; Cleveland, J. L.; Roussel, M. F.
- Abstract
p18Ink4c 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 Eμ-Myc transgenic mouse, a model of human Burkitt lymphoma. Loss of one or both alleles did not influence the onset of lymphoma in Eμ-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 Eμ-Myc-induced lymphomas.Oncogene (2007) 26, 2833–2839. doi:10.1038/sj.onc.1210104; published online 13 November 2006
- Subjects
CYCLIN-dependent kinases; TUMORS; PROTEIN kinases; ONCOGENES; LYMPHOMAS; B cells
- Publication
Oncogene, 2007, Vol 26, Issue 20, p2833
- ISSN
0950-9232
- Publication type
Article
- DOI
10.1038/sj.onc.1210104