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

被引：0

作者：

L M Nilsson

U B Keller

C Yang

J A Nilsson

J L Cleveland

M F Roussel

机构：

[1] St Jude Children's Research Hospital,Department of Biochemistry

[2] St Jude Children's Research Hospital,Department of Genetics and Tumor Cell Biology

[3] Umeå University,Department of Molecular Biology

来源：

Oncogene | 2007年 / 26卷

关键词：

p18; Arf; Myc; lymphomagenesis;

D O I：

暂无

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学科分类号：

摘要：

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.

引用

页码：2833 / 2839

页数：6