Epigenetic mechanisms in tumorigenesis, tumor cell heterogeneity and drug resistance

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 d...

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Podrobná bibliografia
Vydané v:Drug resistance updates Ročník 15; číslo 1-2; s. 21 - 38
Hlavní autori: Wilting, Roel H., Dannenberg, Jan-Hermen
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Scotland Elsevier Ltd 01.02.2012
Predmet:
Acetylation
Acquired drug resistance
Animals
Antineoplastic Agents - therapeutic use
Cell Transformation, Neoplastic - genetics
DNA Methylation
Drug Resistance, Neoplasm - drug effects
Drug Resistance, Neoplasm - genetics
Epigenesis, Genetic
Epigenetic therapy
Epigenetics
Gene Expression Regulation, Neoplastic - drug effects
Genetic Heterogeneity
Hematology, Oncology and Palliative Medicine
Histones - genetics
Histones - metabolism
Humans
Infectious Disease
Mice
Neoplasm Proteins - genetics
Neoplasm Proteins - metabolism
Neoplasms - drug therapy
Neoplasms - genetics
Neoplasms - metabolism
Oncogenic histone modifications
Signal Transduction - drug effects
Signal Transduction - genetics
Tumor heterogeneity
Tumor heterogeneity
Epigenetics
Epigenetic therapy
Acquired drug resistance
Oncogenic histone modifications
ISSN:1368-7646, 1532-2084, 1532-2084
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Abstract 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.
AbstractList 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.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.
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.
Abstract 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.
Author Dannenberg, Jan-Hermen
Wilting, Roel H.
Author_xml – sequence: 1
  givenname: Roel H.
  surname: Wilting
  fullname: Wilting, Roel H.
– sequence: 2
  givenname: Jan-Hermen
  surname: Dannenberg
  fullname: Dannenberg, Jan-Hermen
  email: j.dannenberg@nki.nl
BackLink https://www.ncbi.nlm.nih.gov/pubmed/22356866$$D View this record in MEDLINE/PubMed
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Issue 1-2
Keywords Tumor heterogeneity
Epigenetics
Epigenetic therapy
Acquired drug resistance
Oncogenic histone modifications
Language English
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Snippet Resistance of cancer cells to chemotherapeutics and emerging targeted drugs is a devastating problem in the treatment of cancer patients. Multiple mechanisms...
Abstract Resistance of cancer cells to chemotherapeutics and emerging targeted drugs is a devastating problem in the treatment of cancer patients. Multiple...
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SubjectTerms Acetylation
Acquired drug resistance
Animals
Antineoplastic Agents - therapeutic use
Cell Transformation, Neoplastic - genetics
DNA Methylation
Drug Resistance, Neoplasm - drug effects
Drug Resistance, Neoplasm - genetics
Epigenesis, Genetic
Epigenetic therapy
Epigenetics
Gene Expression Regulation, Neoplastic - drug effects
Genetic Heterogeneity
Hematology, Oncology and Palliative Medicine
Histones - genetics
Histones - metabolism
Humans
Infectious Disease
Mice
Neoplasm Proteins - genetics
Neoplasm Proteins - metabolism
Neoplasms - drug therapy
Neoplasms - genetics
Neoplasms - metabolism
Oncogenic histone modifications
Signal Transduction - drug effects
Signal Transduction - genetics
Tumor heterogeneity
Title Epigenetic mechanisms in tumorigenesis, tumor cell heterogeneity and drug resistance
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https://dx.doi.org/10.1016/j.drup.2012.01.008
https://www.ncbi.nlm.nih.gov/pubmed/22356866
https://www.proquest.com/docview/1011851445
Volume 15
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