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pubmed-article:17099725pubmed:abstractTextp18(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.lld:pubmed
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pubmed-article:17099725pubmed:articleTitleInk4c is dispensable for tumor suppression in Myc-induced B-cell lymphomagenesis.lld:pubmed
pubmed-article:17099725pubmed:affiliationDepartment of Biochemistry, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.lld:pubmed
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