Ink4c is dispensable for tumor suppression in Myc-induced B-cell lymphomagenesis
2007 (English)In: Oncogene, ISSN 0950-9232, Vol. 26, no 20, 2833-2839 p.Article in journal (Refereed) Published
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.
Place, publisher, year, edition, pages
Basingstoke: Macmillan Press , 2007. Vol. 26, no 20, 2833-2839 p.
Animals, Apoptosis/genetics, Cell Proliferation, Cyclin-Dependent Kinase Inhibitor p16/genetics, Cyclin-Dependent Kinase Inhibitor p18/genetics/*physiology, Disease Progression, Gene Expression Regulation; Neoplastic, Genes; Immunoglobulin Heavy Chain, Lymphoma; B-Cell/*genetics/pathology/*prevention & control, Mice, Mice; Inbred C57BL, Mice; Transgenic, Oncogene Proteins; Fusion/genetics/physiology, Proto-Oncogene Proteins c-myc/genetics/*physiology
IdentifiersURN: urn:nbn:se:umu:diva-16700DOI: 10.1038/sj.onc.1210104PubMedID: 17099725OAI: oai:DiVA.org:umu-16700DiVA: diva2:156373