Hypermethylation of the Ink4b locus in murine myeloid leukemia and increased susceptibility to leukemia in p15Ink4b-deficient mice View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2003-12-18

AUTHORS

Linda Wolff, Matthew T Garin, Richard Koller, Juraj Bies, Wei Liao, Marcos Malumbres, Lino Tessarollo, Douglas Powell, Christine Perella

ABSTRACT

The Ink4b gene (Cdkn2b) encodes p15Ink4b, a cyclin-dependent kinase inhibitor. It has been implicated in playing a role in the development of acute myeloid leukemia (AML) in man, since it is hypermethylated with high frequency. We provide evidence that the gene is a tumor suppressor for myeloid leukemia in mice. The evidence is twofold: (1) retrovirus-induced myeloid leukemias of the myelomonocytic phenotype were found to have hypermethylation of the 5′ CpG island of the Ink4b gene, and this could be correlated with reduced mRNA expression, as demonstrated by TaqMan real-time PCR. p15Ink4b mRNA expression in a leukemia cell line, with hypermethylation at the locus, was induced following treatment with 5-aza-2′-deoxycytidine. (2) Targeted deletion of one allele in mice by removal of exon 2 increases their susceptibility to retrovirus-induced myeloid leukemia. Mice deficient in both alleles were not more susceptible to myeloid disease than those deficient in one allele, raising the possibility that there are opposing forces related to the development of myeloid leukemia in Ink4b null mice. More... »

PAGES

9265-9274

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1207092

DOI

http://dx.doi.org/10.1038/sj.onc.1207092

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1033926090

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/14681685


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