The DOI matches its Crossref record; 96 of the 96 references it cites were found in a registry or an index.
Poised epigenetic states and acquired drug resistance in cancer
Abstract
Epigenetic events, which are somatically inherited through cell division, are potential drivers of acquired drug resistance in cancer. The high rate of epigenetic change in tumours generates diversity in gene expression patterns that can rapidly evolve through drug selection during treatment, leading to the development of acquired resistance. This will potentially confound stratified chemotherapy decisions that are solely based on mutation biomarkers. Poised epigenetic states in tumour cells may drive multistep epigenetic fixation of gene expression during the acquisition of drug resistance, which has implications for clinical strategies to prevent the emergence of drug resistance.
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“This is not surprising, since decades of research on targeted cancer therapy have shown that the majority of patients who respond well to initial treatment develop resistance.57, 58, 59, 60”
From Overcoming Resistance to Drugs Targeting KRAS Mutation (2020) · cites this paper as [59]
Citations
Cites
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The polycomb group protein EZH2 is involved in progression of prostate cancer
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Tumour heterogeneity and cancer cell plasticity
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The Different Mechanisms of Cancer Drug Resistance: A Brief Review
Mansoori, B., Mohammadi, A., Davudian, S., Shirjang, S., & Baradaran, B. (2017) · Advanced Pharmaceutical Bulletin · doi:10.15171/apb.2017.041 · Cited by 1,957
The rediscovery of platinum-based cancer therapy
Rottenberg, S., Disler, C., & Perego, P. (2020) · Nature reviews. Cancer · doi:10.1038/s41568-020-00308-y · Cited by 993
Targeting MAPK Signaling in Cancer: Mechanisms of Drug Resistance and Sensitivity
Lee, S., Rauch, J., & Kölch, W. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21031102 · Cited by 823
Tumorigenesis: it takes a village
Tabassum, D. P., & Polyák, K. (2015) · Nature reviews. Cancer · doi:10.1038/nrc3971 · Cited by 558
Apoptosis Deregulation and the Development of Cancer Multi-Drug Resistance
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Metadata
- Authors
- Brown, R., Curry, E., Magnani, L., Wilhelm-Benartzi, C. S., & Borley, J.
- Affiliations
- Hammersmith Hospital (GB)
- Corresponding author
- Brown, Robert
- Venue
- Nature Reviews Cancer
- Published
- 2014-09-25
- Volume
- 14
- Issue
- 11
- Pages
- 747-753
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W2095124748
- Cited by
- 301
- References
- 96
- Citations by year
- 2026: 4 · 2025: 16 · 2024: 23 · 2023: 21 · 2022: 26 · 2021: 41 · 2020: 37 · 2019: 34 · 2018: 27 · 2017: 23 · 2016: 30 · 2015: 18 · 2014: 1
- FWCI
- 2.29
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- ORCA Online Research @Cardiff (Cardiff University) (submittedVersion)
- Funders
- Cancer Research UK (13086, A13086, 15954)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- epigenetic heterogeneity, acquired drug resistance, cancer, epigenetic targeting, chemoresistance, gene expression evolution
- MeSH terms
- Animals, Humans, Neoplasms, Gene Expression Regulation, Neoplastic, Drug Resistance, Neoplasm, Epigenesis, Genetic
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