Inactivation of the cyclin-dependent kinase inhibitor p15INK4b by deletion and de novo methylation with independence of p16INK4a alterations in murine ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1997-03

AUTHORS

Marcos Malumbres, Ignacio Pérez de Castro, Javier Santos, Bárbara Meléndez, Ramon Mangues, Manuel Serrano, Angel Pellicer, José Fernández-Piqueras

ABSTRACT

A wide panel of murine induced T-cell lymphomas have been analysed for p16INK4a or p15INK4b alterations. Only one γ-radiation-induced lymphoma showed p16INK4a homozygous deletion and no other intragenic mutations were found in these INK4 genes. However, de novo methylation of the 5′ CpG islands of the murine p15INK4b and p16INK4a genes was found to be highly frequent. While p16INK4a hypermethylation was found in 36% of the neutron-radiation-induced lymphomas and 15% of the γ-radiation-induced lymphomas, de novo methylation of p15INK4b occurs in 88% and 42% of these tumors respectively, correlating with deficient expression of the corresponding mRNA and allelic losses in the p15INK4b and p16INK4a chromosome location. These data represent, to our knowledge, the first report on the significant involvement of hypermethylation of these INK4 genes in murine primary tumors. Moreover, they show the importance of allelic losses and CpG island methylation of p15INK4b gene inactivation and support a tumor suppressor role for p15INK4b in T-cell lymphomas independent of p16INK4a . More... »

PAGES

1361-1370

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1200969

DOI

http://dx.doi.org/10.1038/sj.onc.1200969

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1020004260

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9178896


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