Cancer epigenetics: Tumor Heterogeneity, Plasticity of Stem-like States, and Drug Resistance
By Hariharan Easwaran, Hsing-Chen Tsai, S. Baylin. Molecules and Cells, 2014
836 citations recorded by the source corpus.
Summary The existence of sub-populations of cells in cancers with increased tumor initiating capacities and self-renewal potential, often termed ‘cancer stem cells’, is a much discussed and key area of cancer biology. Such cellular heterogeneity is very important due to its impact on therapy and especially states of treatment resistance. A major question is whether there is plasticity for evolution of these cell states during tumorigenesis which can involve movement between cell populations in a reversible fashion. In this review, we discuss the possible role of epigenetic abnormalities, as well as genetic alterations in such dynamics, and in the creation of cellular heterogeneity in cancers of all types.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/eddc0abcd7451e9ea9d1b8894108541e95386dbe
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In Cancer Research
In Molecular Biology
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- Bradley E. Bernstein
- William A. Flavahan
- Elizabeth Gaskell
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- C. Hill
- Bernhard Schmierer
Citations in the corpus
- Targeting MAPK Signaling in Cancer: Mechanisms of Drug Resistance and Sensitivity (2020, background): “Overall, both genetic and epigenetic factors contribute to the development of phenotypically distinct tumor cell clones and intratumoral heterogeneity [168,178,179].”
- Epigenetic plasticity and the hallmarks of cancer (2017, background): “We are optimistic that a fuller understanding of epigenetic plasticity and restriction in cancer will advance diagnostic tools for detection of early epigenetic lesions and for evaluation of tumor stage and heterogeneity (101, 102).”
- Epigenetic Determinants of Cancer. (2016, neutral): “6) (Easwaran et al. 2014).”
- DNA Methylation in Cancer and Aging. (2016, background): “Alternatively, a subpopulation of normal cells that have already undergone changes in methylation, perhaps as a result of aging, may represent preferred targets for oncogenic transformation (11, 19).”