Evidence of a possible epigenetic inactivation mechanism operating on a region of mouse chromosome 19 in γ-radiation-induced thymic lymphomas View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2001-04

AUTHORS

Javier Santos, Michel Herranz, Mónica Fernández, Concepción Vaquero, Pilar López, José Fernández-Piqueras

ABSTRACT

Loss of heterozygosity (LOH) analysis, performed in 68 gamma-radiation-induced primary thymic lymphomas of F1 hybrid mice, provided evidence of significant LOH on chromosome 19 in a region defined by the D19Mit106 (22 cM) and D19Mit100 (27 cM) markers (Thymic Lymphoma Suppressor Region 8, TLSR8). Cd95 and Pten, two genes mapped at this region, were inactivated in a vast majority of these tumors (85.3% for Cd95 and 61.8% for Pten). Moreover, altered expression of Cd95 and Pten occurred concomitantly in 34 of 68 (50%) thymic lymphomas suggesting a coordinated mechanism of inactivation of these genes. Surprisingly, we also found that Jak2, a proto-oncogene located between Cd95 and Pten, was simultaneously inactivated in a significant fraction of the tumors analysed (24 of 34, 70.6%). Taken together these findings and the lack of mutations in the coding sequences of the mentioned genes clearly suggest a possible regional epigenetic inactivation mechanism on mouse chromosome 19 operating during the development of these tumors. More... »

PAGES

1204297

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1204297

DOI

http://dx.doi.org/10.1038/sj.onc.1204297

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1015331517

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11360203


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