The chromatin of cancer

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Science  26 Oct 2018:
Vol. 362, Issue 6413, pp. 401-402
DOI: 10.1126/science.aav3494

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Developments in modern genomics tools have led to rapid progress in our understanding of the genetic basis of cancer. Recent large-scale efforts have primarily focused on two types of analysis: mapping acquired somatic mutations by whole-exome and whole-genome sequencing (1, 2), and identification of common inherited variants that increase cancer risk using genome-wide association studies (GWAS) (3). Despite the power of these technologies, we are still far from understanding how the variants and mutations found in individual tumors precisely drive the oncogenic process. A large number of genetic variants increase risk for cancer, but most explain only a very small fraction of the risk. Furthermore, although acquired somatic mutations are found in almost all tumors, most do not carry complete sets of mutations that, according to our present mechanistic understanding, would be sufficient to cause cancer. On page 420 of this issue, Corces et al. (4) show how a third type of genomics approach—functional genomic analyses of primary human tumors—can begin to bridge this gap in our mechanistic understanding of the tumorigenic process.