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Genome Biology | Full text | Cancer genomics just got personal

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Genome Biology | Full text | Cancer genomics just got personal



Cancer genomics just got personal

Rafal T Marszalek
Genome Biology, BioMed Central, 236 Gray’s Inn Road, London WC1X 8HB, UK
Genome Biology 2014, 15:464  doi:10.1186/s13059-014-0464-5

The electronic version of this article is the complete one and can be found online at:http://genomebiology.com/2014/15/9/464

Published:1 October 2014
© 2014 Marszalek; licensee BioMed Central Ltd. 
The licensee has exclusive rights to distribute this article, in any medium, for 12 months following its publication. After this time, the article is available under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Abstract

No abstract

Editorial

It was one Saturday morning in April when, after a 24-hour journey across half of the world, and a very early morning start to the 2014 AACR annual meeting marathon, I was sitting in a dark room in the San Diego Convention Center listening to Kornelia Polyak’s talk about the evolution of breast cancer. Polyak, an expert in breast cancer genomics, was reporting on some recent results from her group. Then, she made a statement that for many cancer researchers will perhaps seem obvious, but that was not yet obvious to me. Polyak noted that it is not uncommon that when several different clones of cancer are present in a patient, the clone that metastasizes is not the most aggressive one.
This does of course make a lot of sense: the clone that metastasizes doesn’t need to be aggressive at all. Rather, it needs to be resistant to therapy. And so it is quite logical that even if other, often more dominant and larger clones are destroyed by the treatment, the ones that were until then suppressed suddenly gain breathing space to grow and migrate. The idea resonated with me a lot, as it seemed to cover so many concepts and threads that we were already seeing in the submissions for the special issue: cancer heterogeneity, clonal diversity, therapy response and resistance, and progression of the disease. In one sentence Polyak unknowingly summarized the issue of Genome Biology that we now bring you.

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