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

Lisa Nilsson; U B Keller; C Yang; J A Nilsson; J L Cleveland; M F Roussel

doi:10.1038/sj.onc.1210104

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

Lisa Nilsson, U B Keller, C Yang, J A Nilsson, J L Cleveland, M F Roussel

UWA Centre for Medical Research (affiliated with the Harry Perkins Institute of Medical Research)

Research output: Contribution to journal › Article › peer-review

5 Citations (Scopus)

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 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.

Original language	English
Pages (from-to)	2833-9
Number of pages	7
Journal	Oncogene
Volume	26
Issue number	20
DOIs	https://doi.org/10.1038/sj.onc.1210104
Publication status	Published - 3 May 2007

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title = "Ink4c is dispensable for tumor suppression in Myc-induced B-cell lymphomagenesis",

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 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.",

keywords = "Animals, Apoptosis/genetics, Cell Proliferation, Cyclin-Dependent Kinase Inhibitor p16/genetics, Cyclin-Dependent Kinase Inhibitor p18/genetics, Disease Progression, Gene Expression Regulation, Neoplastic, Genes, Immunoglobulin Heavy Chain, Lymphoma, B-Cell/genetics, Mice, Mice, Inbred C57BL, Mice, Transgenic, Oncogene Proteins, Fusion/genetics, Proto-Oncogene Proteins c-myc/genetics",

author = "Lisa Nilsson and Keller, {U B} and C Yang and Nilsson, {J A} and Cleveland, {J L} and Roussel, {M F}",

year = "2007",

month = may,

day = "3",

doi = "10.1038/sj.onc.1210104",

language = "English",

volume = "26",

pages = "2833--9",

journal = "Oncogene",

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TY - JOUR

T1 - Ink4c is dispensable for tumor suppression in Myc-induced B-cell lymphomagenesis

AU - Nilsson, Lisa

AU - Keller, U B

AU - Yang, C

AU - Nilsson, J A

AU - Cleveland, J L

AU - Roussel, M F

PY - 2007/5/3

Y1 - 2007/5/3

N2 - 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.

AB - 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.

KW - Animals

KW - Apoptosis/genetics

KW - Cell Proliferation

KW - Cyclin-Dependent Kinase Inhibitor p16/genetics

KW - Cyclin-Dependent Kinase Inhibitor p18/genetics

KW - Disease Progression

KW - Gene Expression Regulation, Neoplastic

KW - Genes, Immunoglobulin Heavy Chain

KW - Lymphoma, B-Cell/genetics

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Transgenic

KW - Oncogene Proteins, Fusion/genetics

KW - Proto-Oncogene Proteins c-myc/genetics

U2 - 10.1038/sj.onc.1210104

DO - 10.1038/sj.onc.1210104

M3 - Article

C2 - 17099725

SN - 0950-9232

VL - 26

SP - 2833

EP - 2839

JO - Oncogene

JF - Oncogene

IS - 20

ER -

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

Abstract

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