EPHA7, a new target gene for 6q deletion in T-cell lymphoblastic lymphomas

29Citations
Citations of this article
24Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Cryptic deletions at chromosome 6q are common cytogenetic abnormalities in T-cell lymphoblastic leukemia/lymphoma (T-LBL), but the target genes have not been formally identified. Our results build on detection of specific chromosomal losses in a mouse model of γ-radiation-induced T-LBLs and provide interesting clues for new putative susceptibility genes in a region orthologous to human 6q15-6q16.3. Among these, Epha7 emerges as a bona fide candidate tumor suppressor gene because it is inactivated in practically all the T-LBLs analyzed (100% in mouse and 95.23% in human). We provide evidence showing that Epha7 downregulation may occur, at least in part, by loss of heterozygosity (19.35% in mouse and 12.5% in human) or promoter hypermethylation (51.61% in mouse and 43.75% in human) or a combination of both mechanisms (12.90% in mouse and 6.25% in human). These results indicate that EPHA7 might be considered a new tumor suppressor gene for 6q deletions in T-LBLs. Notably, this gene is located in 6q16.1 proximal to GRIK2 and CASP8AP2, other candidate genes identified in this region. Thus, del6q seems to be a complex region where inactivation of multiple genes may cooperatively contribute to the onset of T-cell lymphomas. © The Author 2011. Published by Oxford University Press. All rights reserved.

Cite

CITATION STYLE

APA

oĹpez-nieva, P., Vaquero, C., Fernández-navarro, P., González-sánchez, L., Villa-morales, M., Santos, J., … Fernández-piqueras, J. (2012). EPHA7, a new target gene for 6q deletion in T-cell lymphoblastic lymphomas. Carcinogenesis, 33(2), 452–458. https://doi.org/10.1093/carcin/bgr271

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free