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Somatic variation and cancer: therapies lost in the mix

Abstract

Cancer arises as a consequence of mutations in genomes of cancer cells, which over time allow them to proliferate and spread to distant sites. Large-scale sequencing of cancer genomes is revealing an increasing number of potential driver mutations that may allow specific targeting of cancer genes, proteins, and pathways. Comprehensive views of cancer genomes are also revealing enormous heterogeneity of mutation profiles, even among tumours derived from the same organs and having similar pathological characteristics. There are now many examples where mutation profiles observed in tumours have been shown to correlate with clinical features of disease, drug response, and patient outcomes. When ignored, molecular heterogeneity can lead to failures in drug development, as drugs that may have efficacy in subgroups of patients with specific molecular phenotypes may show marginal response when tested in large groups of unselected patients. This article explores issues relevant to the clinical translation of sequence-based mutation profiles in the clinical development of targeted therapies and in the future management of cancer patients.

Type Journal
ISBN 1432-1203 (Electronic) 0340-6717 (Linking)
Authors Biankin, A. V.; Hudson, T. J.;
Publisher Name HUM GENET
Published Date 2011-01-01 00:00:00
Published Volume 130
Published Issue 1
Published Pages 79-91
URL http://www.ncbi.nlm.nih.gov/pubmed/21643984
Status Published In-print
OpenAccess Link https://publications.gimr.garvan.org.au/download.php?11079_11482/11 Biankin HG_.pdf