Abstract

Abstract Chromosome 7 copy gains are a recurrent genomic alteration in melanoma. Previous genomic studies identified a common peak of gain within 7p, highlighting it as a region likely to contain “driver” cancer genes. In this study, we identified several melanoma samples with focal amplification events located within this peak, and found that the overlapping region of these amplicons contained the locus of the ETS transcription factor and oncogene, ETV1. Fluorescent in situ hybridization analysis of a progressive melanoma tissue microarray revealed ETV1 amplification in 13% of the primary tumors and 18%of the metastatic melanomas, whereas no amplification in nevus samples. Silencing of ETV1 expression demonstrated dependency on ETV1 expression for proliferation and anchorage-independent growth in some melanoma cell lines. Moreover, over-expression of ETV1 in combination with oncogenic NRASG12D transformed primary melanocytes and promoted tumor formation in mice. Interestingly, overexpression of ETV1 increased MITF expression, a known oncogene in melanoma. Together, these observations suggest an oncogenic role for ETS transcription factors in general and ETV1 in particular in melanoma. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3111.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call