期刊
TRENDS IN CANCER
卷 7, 期 4, 页码 323-334出版社
CELL PRESS
DOI: 10.1016/j.trecan.2021.01.009
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资金
- Ramanujan Fellowship by SERB, DST, Government of India [SB/S2/RJN-049/2018]
- National Cancer Institute of the National Institutes of Health [NIH/NCI 5P30CA033572-34, NIH 1U54CA209978-01A1, NIH R01CA218545, NIH 1R01CA247471-01]
Drug resistance in cancer is caused by both genetic mutations and non-genetic mechanisms, with intermediate reversible phenotypes playing a crucial role in the emergence of resistant clones. Understanding the complex interplay of clonal groups and the surrounding microenvironment can help in designing more effective treatment strategies to delay or minimize drug resistance.
Drug resistance is a major impediment in cancer. Although it is generally thought that acquired drug resistance is due to genetic mutations, emerging evidence indicates that nongenetic mechanisms also play an important role. Resistance emerges through a complex interplay of clonal groups within a heterogeneous tumor and the surrounding microenvironment. Traits such as phenotypic plasticity, intercellular communication, and adaptive stress response, act in concert to ensure survival of intermediate reversible phenotypes, until permanent, resistant clones can emerge. Understanding the role of group behavior, and the underlying nongenetic mechanisms, can lead to more efficacious treatment designs and minimize or delay emergence of resistance.
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