1. ¹Department of Biochemistry, St Jude Children's Research Hospital, Memphis, TN, USA
2. ²Department of Genetics and Tumor Cell Biology, St Jude Children's Research Hospital, Memphis, TN, USA
3. ³Department of Molecular Biology, Umeå University, Umeå, Sweden

Correspondence: Dr MF Roussel, Department of Genetics and Tumor Cell Biology, St Jude Children's Research Hospital, 332 N Lauderdale Street, Memphis, TN 38105, USA. E-mail: martine.roussel@stjude.org

Received 22 August 2006; Revised 27 September 2006; Accepted 27 September 2006; Published online 13 November 2006.

Abstract

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 E-Myc transgenic mouse, a model of human Burkitt lymphoma. Loss of one or both alleles did not influence the onset of lymphoma in E-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 E-Myc-induced lymphomas.