期刊
COLD SPRING HARBOR PERSPECTIVES IN MEDICINE
卷 7, 期 8, 页码 -出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/cshperspect.a026617
关键词
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资金
- Stand Up 2 Cancer
- CRICK PhD studentship
- Francis Crick Institute from Cancer Research UK [FC001169]
- UK Medical Research Council [FC001169, MR/FC001169 /1]
- Wellcome Trust [FC001169]
- Cancer Research UK (TRACERx)
- CRUK Lung Cancer Centre of Excellence
- Stand Up 2 Cancer (SU2C)
- Rosetrees Trust
- NovoNordisk Foundation [16584]
- Prostate Cancer Foundation
- Breast Cancer Research Foundation
- European Research Council (THESEUS)
- National Institute for Health Research
- University College London Hospitals Biomedical Research Centre
- Cancer Research UK University College London Experimental Cancer Medicine Centre
- Sontag Foundation
- Josie Robertson Foundation
- Cycle for Survival
- American Cancer Society [127350-RSG-15-067-01-TBG]
- National Institutes of Health (NIH) [R01CA207244, U54OD202355]
- Sloan Kettering Institute for Cancer Research Cancer Center Support Grant [P30CA008748]
- Dabbiere family
- National Institutes of Health [R01CA169316, P01CA118816]
- Hana Jabsheh Research Initiative
- Cancer Research UK [20466] Funding Source: researchfish
- Novo Nordisk Fonden [NNF15OC0016584] Funding Source: researchfish
- The Francis Crick Institute [10169] Funding Source: researchfish
Despite the great progress in our understanding of the molecular basis of human cancer, the heterogeneity of individual tumors and the evolutionary pressures imposed by therapy have hampered our ability to effectively eradicate and control this disease. How, therefore, do cancers evolve under the selective pressures of cancer therapy? Recent studies have linked both primary (or de novo) and acquired treatment resistance to intratumor heterogeneity and clonal evolution. Resistance to targeted therapies often includes mutation of the drug target itself and aberrations of pathways upstream of, downstream from, or parallel to the drug target. For systemic chemotherapies, discrete and recurrent resistance-conferring genetic aberrations have eluded the community, due in part to their wide-ranging mutagenic effects. In this review, we discuss different patterns of clonal evolution during treatment-specific selective pressures and focus on the genetic mechanisms of treatment resistance that have emerged to both targeted therapies and chemotherapies.
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