The DOI matches its Crossref record; 18 of the 18 references it cites were found in a registry or an index.
Throwing the cancer switch: reciprocal roles of polycomb and trithorax proteins
Open accessAbstract
The discovery that cancer can be governed above and beyond the level of our DNA presents a new era for designing therapies that reverse the epigenetic state of a tumour cell. Understanding how altered chromatin dynamics leads to malignancy is essential for controlling tumour cells while sparing normal cells. Polycomb and trithorax group proteins are evolutionarily conserved and maintain chromatin in the 'off' or 'on' states, thereby preventing or promoting gene expression, respectively. Recent work highlights the dynamic interplay between these opposing classes of proteins, providing new avenues for understanding how these epigenetic regulators function in tumorigenesis.
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Cited by
The epigenetics of epithelial-mesenchymal plasticity in cancer
Tam, W. L., & Weinberg, R. A. (2013) · Nature Medicine · doi:10.1038/nm.3336 · Cited by 1,163
Epigenetic balance of gene expression by Polycomb and COMPASS families
Piunti, A., & Shilatifard, A. (2016) · Science · doi:10.1126/science.aad9780 · Cited by 524
Maintaining cell identity: PRC2-mediated regulation of transcription and cancer
Comet, I., Riising, E. M., Leblanc, B., & Helin, K. (2016) · Nature Reviews Cancer · doi:10.1038/nrc.2016.83 · Cited by 432
Roles of the Polycomb group proteins in stem cells and cancer
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Interplay between Epigenetics and Genetics in Cancer
Choi, J. D., & Lee, J.-S. (2013) · Genomics & Informatics · doi:10.5808/gi.2013.11.4.164 · Cited by 131
Metadata
- Authors
- Mills, A. A.
- Venue
- Nature Reviews Cancer
- Published
- 2010-09-24
- Volume
- 10
- Issue
- 10
- Pages
- 669-682
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W2075853235
- Cited by
- 249
- References
- 18
- FWCI
- 1.62
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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