Biochimie. 2003 Nov;85(11):1149-60.

Human mismatch repair, drug-induced DNA damage, and secondary cancer.

Source

Cancer Research UK, London Research Institute, Clare Hall Laboratories, Blanche Lane, South Mimms, Herts EN6 3LD, UK. peter.karran@cancer.org.uk

Abstract

DNA mismatch repair (MMR) is an important replication error avoidance mechanism that prevents mutation. The association of defective MMR with familial and sporadic gastrointestinal and endometrial cancer has been acknowledged for some years. More recently, it has become apparent that MMR defects are common in acute myeloid leukaemia/myelodysplastic syndrome (AML/MDS) that follows successful chemotherapy for a primary malignancy. Therapy-related haematological malignancies are often associated with treatment with alkylating agents. Their frequency is increasing and they now account for at least 10% of all AML cases. There is also evidence for an association between MMR deficient AML/MDS and immunosuppressive treatment with thiopurine drugs. Here we review how MMR interacts with alkylating agent and thiopurine-induced DNA damage and suggest possible ways in which MMR defects may arise in therapy-related AML/MDS.

PMID:: 14726020; [PubMed - indexed for MEDLINE]

Publication Types, MeSH Terms, Substances

Publication Types

Review

MeSH Terms

Substances

Antineoplastic Agents

LinkOut - more resources

Full Text Sources

Other Literature Sources

Labome Researcher Resource - ExactAntigen/Labome

Medical

Supplemental Content

Related citations

Defective DNA mismatch repair in acute myeloid leukemia/myelodysplastic syndrome after organ transplantation. [Blood. 2004]
Defective DNA mismatch repair in acute myeloid leukemia/myelodysplastic syndrome after organ transplantation.
Offman J, Opelz G, Doehler B, Cummins D, Halil O, Banner NR, Burke MM, Sullivan D, Macpherson P, Karran P. Blood. 2004 Aug 1; 104(3):822-8. Epub 2004 Apr 15.
Drug treatment in the development of mismatch repair defective acute leukemia and myelodysplastic syndrome. [DNA Repair (Amst). 2003]
Drug treatment in the development of mismatch repair defective acute leukemia and myelodysplastic syndrome.
Casorelli I, Offman J, Mele L, Pagano L, Sica S, D'Errico M, Giannini G, Leone G, Bignami M, Karran P. DNA Repair (Amst). 2003 May 13; 2(5):547-59.
Review Targeting DNA mismatch repair for radiosensitization. [Semin Radiat Oncol. 2001]
Review Targeting DNA mismatch repair for radiosensitization.
Berry SE, Kinsella TJ. Semin Radiat Oncol. 2001 Oct; 11(4):300-15.
Defective DNA-mismatch repair: a potential mediator of leukemogenic susceptibility in therapy-related myelodysplasia and leukemia. [Genes Chromosomes Cancer. 2002]
Defective DNA-mismatch repair: a potential mediator of leukemogenic susceptibility in therapy-related myelodysplasia and leukemia.
Olipitz W, Hopfinger G, Aguiar RC, Gunsilius E, Girschikofsky M, Bodner C, Hiden K, Linkesch W, Hoefler G, Sill H. Genes Chromosomes Cancer. 2002 Jun; 34(2):243-8.
Review Therapy-related myelodysplastic syndrome with monosomy 5 after successful treatment of acute myeloid leukemia (M2). [Am J Hematol. 2005]
Review Therapy-related myelodysplastic syndrome with monosomy 5 after successful treatment of acute myeloid leukemia (M2).
Ogasawara T, Yasuyama M, Kawauchi K. Am J Hematol. 2005 Jun; 79(2):136-41.

See reviews... See all...

Cited by 10 PubMed Central articles

Review Chemoresistance of glioblastoma cancer stem cells--much more complex than expected. [Mol Cancer. 2011]
Review Chemoresistance of glioblastoma cancer stem cells--much more complex than expected.
Beier D, Schulz JB, Beier CP. Mol Cancer. 2011 Oct 11; 10:128. Epub 2011 Oct 11.
The homologous recombination protein RAD51D mediates the processing of 6-thioguanine lesions downstream of mismatch repair. [Mol Cancer Res. 2011]
The homologous recombination protein RAD51D mediates the processing of 6-thioguanine lesions downstream of mismatch repair.
Rajesh P, Litvinchuk AV, Pittman DL, Wyatt MD. Mol Cancer Res. 2011 Feb; 9(2):206-14. Epub 2011 Jan 4.
Prolonged cell cycle response of HeLa cells to low-level alkylation exposure. [Cancer Res. 2009]
Prolonged cell cycle response of HeLa cells to low-level alkylation exposure.
Schroering AG, Kothandapani A, Patrick SM, Kaliyaperumal S, Sharma VP, Williams KJ. Cancer Res. 2009 Aug 1; 69(15):6307-14. Epub 2009 Jul 28.

See all...

Related information

Related Citations
Calculated set of PubMed citations closely related to the selected article(s) retrieved using a word weight algorithm. Related articles are displayed in ranked order from most to least relevant, with the “linked from” citation displayed first.
Cited in PMC
Full-text articles in the PubMed Central Database that cite the current articles.

Recent activity

Clear Turn Off Turn On

Human mismatch repair, drug-induced DNA damage, and secondary cancer.
Human mismatch repair, drug-induced DNA damage, and secondary cancer.
Biochimie. 2003 Nov ;85(11):1149-60.

PubMed
Structure-function relationships in methionine adenosyltransferases.
Structure-function relationships in methionine adenosyltransferases.
Cell Mol Life Sci. 2009 Feb ;66(4):636-48.

PubMed
Association of nasomaxillary asymmetry in children with unilateral cleft lip and...
Association of nasomaxillary asymmetry in children with unilateral cleft lip and palate and their parents.
Cleft Palate Craniofac J. 2003 Sep ;40(5):493-7.

PubMed
Quantal and nonquantal transmission in calyx-bearing fibers of the turtle poster...
Quantal and nonquantal transmission in calyx-bearing fibers of the turtle posterior crista.
J Neurophysiol. 2007 Sep ;98(3):1083-101. Epub 2007 Jun 27 .

PubMed
HIV-specific cytotoxic cell frequencies measured directly ex vivo by the Lysispo...
HIV-specific cytotoxic cell frequencies measured directly ex vivo by the Lysispot assay can be higher or lower than the frequencies of IFN-gamma-secreting cells: anti-HIV cytotoxicity is not generally impaired relative to other chronic virus responses.
J Immunol. 2006 Feb 15 ;176(4):2662-8.

PubMed

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

PubMed

Display Settings:

Send to: