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Tumour heterogeneity and the evolution of polyclonal drug resistance

Rebecca A. BurrellTranslational Cancer Therapeutics Laboratory, Cancer Research UK London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3L7, UK; UCL Cancer Institute, Paul O'Gorman Building University College London, 72 Huntley Street, London WC1E 6DD, UK. Electronic address: [email protected]Charles SwantonTranslational Cancer Therapeutics Laboratory, Cancer Research UK London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3L7, UK; UCL Cancer Institute, Paul O'Gorman Building University College London, 72 Huntley Street, London WC1E 6DD, UK. Electronic address: [email protected]

2014en

ABI

Аннотация

Cancer drug resistance is a major problem, with the majority of patients with metastatic disease ultimately developing multidrug resistance and succumbing to their disease. Our understanding of molecular events underpinning treatment failure has been enhanced by new genomic technologies and pre-clinical studies. Intratumour genetic heterogeneity (ITH) is a prominent contributor to therapeutic failure, and it is becoming increasingly apparent that individual tumours may achieve resistance via multiple routes simultaneously - termed polyclonal resistance. Efforts to target single resistance mechanisms to overcome therapeutic failure may therefore yield only limited success. Clinical studies with sequential analysis of tumour material are needed to enhance our understanding of inter-clonal functional relationships and tumour evolution during therapy, and to improve drug development strategies in cancer medicine.

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DOI: 10.1016/j.molonc.2014.06.005

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