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Cellular and molecular mechanisms of plasticity in cancer

Journal

TRENDS IN CANCER
Volume 8, Issue 9, Pages 735-746

Publisher

CELL PRESS
DOI: 10.1016/j.trecan.2022.04.007

Keywords

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Categories

Funding

  1. National Institutes of Health (NIH) /National Cancer Institute (NCI) [R37-CA244911]
  2. Cancer Center [P30-CA08748]
  3. NIH/NCI [F30-CA254120]
  4. Medical Scientist Training Program grant from the National Institute of General Medical Sciences of the National Institutes of Health [T32GM007739]
  5. Linn Fund from Cycle for Survival
  6. Josie Robertson, Rita Allen Foundation
  7. American Cancer Society
  8. V Foundation Scholarships

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Cancer cells have plasticity and can rapidly adapt to their environment and evade therapy. This article provides an overview of the fundamental mechanisms underlying cancer cell plasticity, and highlights the crucial role of high-plasticity cell states in cell state transitions and intra-tumoral heterogeneity.
Cancer cells are plastic - they can assume a wide range of distinct phenotypes. Plasticity is integral to cancer initiation and progression, as well as to the emer-gence and maintenance of intratumoral heterogeneity. Furthermore, plastic cells can rapidly adapt to and evade therapy, which poses a challenge for effec-tive cancer treatment. As such, targeting plasticity in cancer holds tremendous promise. Yet, the principles governing plasticity in cancer cells remain poorly understood. Here, we provide an overview of the fundamental molecular and cellular mechanisms that underlie plasticity in cancer and in other biological contexts, including development and regeneration. We propose a key role for high-plasticity cell states (HPCSs) as crucial nodes for cell state transitions and enablers of intra-tumoral heterogeneity.

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