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
中图分类号：
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.
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收藏
页码：2833 / 2839
页数：6
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