Human Cancers Express a Mutator Phenotype: Hypothesis, Origin, and Consequences
- PMID: 27197248
- PMCID: PMC5004728
- DOI: 10.1158/0008-5472.CAN-16-0794
Human Cancers Express a Mutator Phenotype: Hypothesis, Origin, and Consequences
Abstract
The mutator phenotype hypothesis was postulated more than 40 years ago. It was based on the multiple enzymatic steps required to precisely replicate the 6 billion bases in the human genome each time a normal cell divides. A reduction in this accuracy during tumor progression could be responsible for the striking heterogeneity of malignant cells within a tumor and for the rapidity by which cancers become resistant to therapy. Cancer Res; 76(8); 2057-9. ©2016 AACRSee related article by Loeb et al. Cancer Res. 1974;34:2311-21.
©2016 American Association for Cancer Research.
Conflict of interest statement
of Potential Conflicts of Interest No potential conflicts of interest were disclosed.
References
-
- Loeb LA, Springgate CF, Battula N. Errors in DNA replication as a basis of malignant changes. Cancer Res. 1974;34:2311–21. - PubMed
-
- Kunkel TA, Loeb LA. Fidelity of mammalian DNA polymerases. Science. 1981;213:765–7. - PubMed
-
- Cleaver JE. Defective repair replication of DNA in xeroderma pigmentosum. Nature. 1968;218:652–6. - PubMed
Publication types
MeSH terms
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
