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

• 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.

Nyckelord

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

Publikations- och innehållstyp

ref (ämneskategori)

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