Ink4c is dispensable for tumor suppression in Myc-induced B-cell lymphomagenesis

Lisa Nilsson, U B Keller, C Yang, J A Nilsson, J L Cleveland, M F Roussel

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)2833-9
Number of pages7
Issue number20
Publication statusPublished - 3 May 2007


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