GWAS Meets TCGA to Illuminate Mechanisms of Cancer Predisposition | Zendy

Hyun Seok Kim | Zendy; John D. Minna | Zendy; Michael A. White | Zendy

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GWAS Meets TCGA to Illuminate Mechanisms of Cancer Predisposition

Author(s) -

Hyun Seok Kim,

John D. Minna,

Michael A. White

Publication year - 2013

Publication title -

cell

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 26.304

H-Index - 776

eISSN - 1097-4172

pISSN - 0092-8674

DOI - 10.1016/j.cell.2013.01.027

Subject(s) - biology , genome wide association study , germline , expression quantitative trait loci , genetics , genetic association , allele , breast cancer , gene , computational biology , cancer , single nucleotide polymorphism , genotype

Genome-wide association studies (GWASs) have unraveled a large number of cancer risk alleles. Understanding how these allelic variants predispose to disease is a major bottleneck confronting translational application. In this issue, Li and colleagues combine GWASs with The Cancer Genome Atlas (TCGA) to disambiguate the contributions of germline and somatic variants to tumorigenic gene expression programs. They find that close to half of the known risk alleles for estrogen receptor (ER)-positive breast cancer are expression quantitative trait loci (eQTLs) acting upon major determinants of gene expression in tumors.

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