Somatic variation and cancer: therapies lost in the mix |
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Authors: | Andrew V Biankin Thomas J Hudson |
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Institution: | (1) Cancer Research Program, Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, Sydney, NSW, 2010, Australia;(2) Ontario Institute for Cancer Research, 101 College Street, Toronto, ON, M5G 0A3, Canada; |
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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. |
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