Impact of viral oncogenesis on responses to anti-cancer drugs and irradiation

Publication type:
Journal article
Metadata:
Autoren
Autoren-URL
https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=fis-test-1&SrcAuth=WosAPI&KeyUT=WOS:000089384300004&DestLinkType=FullRecord&DestApp=WOS_CPL
eISSN
2162-6448
Externe Identifier
  • Clarivate Analytics Document Solution ID: 355KF
  • PubMed Identifier: 11005511
ISSN
0893-9675
Ausgabe der Veröffentlichung
2
Zeitschrift
CRITICAL REVIEWS IN ONCOGENESIS
Schlüsselwörter
  • apoptosis
  • DNA repair
  • drug resistance
  • growth arrest
  • radioresistance
  • viral oncogenes
Paginierung
165 - 187
Datum der Veröffentlichung
2000
Status
Published
Titel
Impact of viral oncogenesis on responses to anti-cancer drugs and irradiation
Sub types
  • Review
Ausgabe der Zeitschrift
11

Data source: Web of Science (Lite)

Other metadata sources:
Abstract
The view that chemical or physical oncogenesis and tumor therapy resistance represent different parts of common cellular alterations gained considerable attractiveness, because it explains the inherent unreponsiveness of many tumors. Viruses are potent oncogenes and are causally linked to approximately one-fifth of all human malignancies. Whether viral oncogenesis exerts comparable effects was less clear. Recent progress in experimental research provided ample evidence that viruses affect response of tumor cells toward anti-cancer drugs and irradiation. Resistance to cytostatic drugs and radiation develops by alterations at the drug-target sites (i.e., DNA or specific target proteins), upstream (i.e., detoxification mechanisms), or downstream of them (i.e., programmed cell death). Viruses interfere with specific cellular genes at these three levels. Viral proteins induce the expression and expression of drug resistance genes, that is, MDR1, DHFR, or CAD. Viral interactions with the tumor suppressor genes (p53, pRB) abrogate cell cycle arrests and disturb DNA repair of drug- and radiation-induced DNA lesions. The readiness to commit cellular suicide (apoptosis) is also affected by viral genes. The connection between viral oncogenesis and the response of tumor cells to treatment adds a new dimension to tumor biology and may have important consequences for oncological treatment modalities in the future.
Addresses
  • Institute for Clinical and Molecular Virology, University of Erlangen-Nürnberg, Erlangen, Germany.
Autoren
Externe Identifier
  • PubMed Identifier: 11005511
Open access
false
ISSN
0893-9675
Ausgabe der Veröffentlichung
2
Zeitschrift
Critical reviews in oncogenesis
Schlüsselwörter
  • Animals
  • Humans
  • Hepadnaviridae
  • Herpesviridae
  • Papillomaviridae
  • Polyomaviridae
  • Tumor Virus Infections
  • Neoplasms
  • Lymphoma
  • Carcinoma
  • Antineoplastic Agents
  • Signal Transduction
  • Gene Expression
  • Drug Resistance, Neoplasm
  • Genes, p53
  • ATP Binding Cassette Transporter, Subfamily B, Member 1
Sprache
eng
Medium
Print
Paginierung
165 - 187
Datum der Veröffentlichung
2000
Status
Published
Datum der Datenerfassung
2000
Titel
Impact of viral oncogenesis on responses to anti-cancer drugs and irradiation.
Sub types
  • Review
  • Journal Article
Ausgabe der Zeitschrift
11

Data source: Europe PubMed Central

Abstract
The view that chemical or physical oncogenesis and tumor therapy resistance represent different parts of common cellular alterations gained considerable attractiveness, because it explains the inherent unreponsiveness of many tumors. Viruses are potent oncogenes and are causally linked to approximately one-fifth of all human malignancies. Whether viral oncogenesis exerts comparable effects was less clear. Recent progress in experimental research provided ample evidence that viruses affect response of tumor cells toward anti-cancer drugs and irradiation. Resistance to cytostatic drugs and radiation develops by alterations at the drug-target sites (i.e., DNA or specific target proteins), upstream (i.e., detoxification mechanisms), or downstream of them (i.e., programmed cell death). Viruses interfere with specific cellular genes at these three levels. Viral proteins induce the expression and expression of drug resistance genes, that is, MDR1, DHFR, or CAD. Viral interactions with the tumor suppressor genes (p53, pRB) abrogate cell cycle arrests and disturb DNA repair of drug- and radiation-induced DNA lesions. The readiness to commit cellular suicide (apoptosis) is also affected by viral genes. The connection between viral oncogenesis and the response of tumor cells to treatment adds a new dimension to tumor biology and may have important consequences for oncological treatment modalities in the future.
Autoren
Autoren-URL
https://www.ncbi.nlm.nih.gov/pubmed/11005511
ISSN
0893-9675
Ausgabe der Veröffentlichung
2
Zeitschrift
Crit Rev Oncog
Schlüsselwörter
  • ATP Binding Cassette Transporter, Subfamily B, Member 1
  • Animals
  • Antineoplastic Agents
  • Carcinoma
  • Drug Resistance, Neoplasm
  • Gene Expression
  • Genes, p53
  • Hepadnaviridae
  • Herpesviridae
  • Humans
  • Lymphoma
  • Neoplasms
  • Papillomaviridae
  • Polyomaviridae
  • Signal Transduction
  • Tumor Virus Infections
Sprache
eng
Country
United States
Paginierung
165 - 187
Datum der Veröffentlichung
2000
Status
Published
Datum, an dem der Datensatz öffentlich gemacht wurde
2001
Titel
Impact of viral oncogenesis on responses to anti-cancer drugs and irradiation.
Sub types
  • Journal Article
  • Review
Ausgabe der Zeitschrift
11

Data source: PubMed

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