The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
Epigenetic mechanisms in tumorigenesis, tumor cell heterogeneity and drug resistance
Open accessAbstract
Resistance of cancer cells to chemotherapeutics and emerging targeted drugs is a devastating problem in the treatment of cancer patients. Multiple mechanisms contribute to drug resistance such as increased drug efflux, altered drug metabolism, secondary mutations in drug targets, and activation of downstream or parallel signal transduction pathways. The rapid kinetics, the reversibility of acquired drug resistance and the absence of genetic mutations suggest an epigenetic basis for drug insensitivity. Similar to the cellular variance seen in the human body, epigenetic mechanisms, through reversible histone modifications and DNA methylation patterns, generate a variety of transcriptional states resulting in a dynamic heterogeneous tumor cell population. Consequently, epigenomes favoring survival in the presence of a drug by aberrant transcription of drug transporters, DNA-repair enzymes and pro-apoptotic factors render cytotoxic and targeted drugs ineffective and allow selection of rare drug-resistant tumor cells. Recent advances in charting cancer genomes indeed strongly indicate a role for epigenetic regulators in driving cancer, which may result in the acquisition of additional (epi)genetic modifications leading to drug resistance. These observations have important clinical consequences as they provide an opportunity for "epigenetic drugs" to change reversible drug-resistance-associated epigenomes to prevent or reverse non-responsiveness to anti-cancer drugs.
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Cites
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Cited by
Targeting epigenetic regulators for cancer therapy: mechanisms and advances in clinical trials
Cheng, Y., He, C., Wang, M., Ma, X., Mo, F., Yang, S., Han, J., & Wei, X. (2019) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-019-0095-0 · Cited by 1,097
“Recently, DNA methylation in cancer has generally been associated with drug resistance and predicting response to treatment.(36) For example, MGMT (O-6-methylguanine DNA methyltransferase) hypermethylation is still the best independent predictor of response to BCNU (carmustine) and temozolomide in gliomas because hype…”
BackgroundDrug resistance and combating drug resistance in cancer
Wang, X., Zhang, H., & Chen, X. (2019) · Cancer Drug Resistance · doi:10.20517/cdr.2019.10 · Cited by 1,085
The multi-factorial nature of clinical multidrug resistance in cancer
Assaraf, Y. G., Brozovic, A., Gonçalves, A. C., Jurkovicova, D., Linē, A., Machuqueiro, M., Saponara, S., Sarmento-Ribeiro, A. B., Xavier, C. P. R., & Vasconcelos, M. H. (2019) · Drug Resistance Updates · doi:10.1016/j.drup.2019.100645 · Cited by 528
Next-Generation Metal Anticancer Complexes: Multitargeting via Redox Modulation
Romero-Canelón, I., & Sadler, P. J. (2013) · Inorganic Chemistry · doi:10.1021/ic400835n · Cited by 396
Taylor, S., Spugnini, E. P., Assaraf, Y. G., Azzarito, T., Rauch, C., & Fais, S. (2015) · Drug Resistance Updates · doi:10.1016/j.drup.2015.08.004 · Cited by 259
Metadata
- Authors
- Wilting, R. H., & Dannenberg, J.-H.
- Venue
- Drug Resistance Updates
- Publisher
- Elsevier BV
- Published
- 2012-02
- Volume
- 15
- Issue
- 1-2
- Pages
- 21-38
- ISSN
- 1368-7646 (ISSN-L)
- OpenAlex
- W2047941151
- Cited by
- 303
- References
- 33
- FWCI
- 7.20
- Type
- journal article
- Language
- en
- Open access
- hybrid
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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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