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Mismatch repair deficiency in colorectal cancer patients in a low-incidence area

Vergouwe, F., Boutall, A., Stupart, D., Algar, U., Govender, D., van der Linde, G.D., Mall, A., Ramesar, R. and Goldberg, P.A. 2013, Mismatch repair deficiency in colorectal cancer patients in a low-incidence area, South African journal of surgery, vol. 51, no. 1, pp. 16-21, doi: 10.7196/SAJS.1314.

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Title Mismatch repair deficiency in colorectal cancer patients in a low-incidence area
Author(s) Vergouwe, F.
Boutall, A.
Stupart, D.
Algar, U.
Govender, D.
van der Linde, G.D.
Mall, A.
Ramesar, R.
Goldberg, P.A.
Journal name South African journal of surgery
Volume number 51
Issue number 1
Start page 16
End page 21
Total pages 6
Publisher South African Medical Association
Place of publication Pretoria, South Africa
Publication date 2013-02-14
ISSN 0038-2361
2078-5151
Keyword(s) Adaptor Proteins, Signal Transducing
Adenocarcinoma
Colorectal Neoplasms, Hereditary Nonpolyposis
DNA Repair Enzymes
Female
Gene Expression
Humans
Incidence
Male
Middle Aged
MutL Protein Homolog 1
MutL Proteins
Neoplasm Proteins
Nuclear Proteins
South Africa
Summary BACKGROUND: In a previous study we identified 206 patients with colorectal adenocarcinoma in the Northern Cape province of South Africa, diagnosed between January 2002 and February 2009. The age-standardised incidence was 4.2/100 000 per year world standard population. This is 10% of the rate reported in First-World countries. In high-incidence areas, the rate of abnormal mismatch repair gene expression in colorectal cancers is 2 - 7%.

OBJECTIVES: The aim of this study was to determine the prevalence of hMLH1- and hMSH2-deficient colorectal cancer in the Northern Cape.

METHODS: Formalin-fixed paraffin wax-embedded tissue blocks from 87 colorectal adenocarcinomas identified in the previous study were retrieved. Standard immunohistochemical staining methods were used to detect the expression of hMLH1 and hMSH2 (i.e. products of the hMLH1 and hMSH2 genes) in the tumours using heat-induced antigen retrieval and diaminobenzidene as a chromogen.

RESULTS: In 8 blocks there was insufficient tumour tissue and in 1 case the immunohistochemical staining failed, probably owing to poor fixation, leaving 78 cases for analysis. In 11 cases hMLH1 was deficient and in 6 cases hMSH2 was deficient. Overall, 21.8% of cancers were deficient for hMLH1 or hMSH2.

CONCLUSION: Presuming that 80% of all hMLH1 deficiencies are due to hypermethylation of the gene, we found 10.5% of colorectal cancers in an area with a low incidence of colorectal cancer to be deficient in the product of the mismatch repair gene/s. This is approximately three times the reported rate in high-incidence areas.
Language eng
DOI 10.7196/SAJS.1314
Field of Research 111299 Oncology and Carcinogenesis not elsewhere classified
Socio Economic Objective 0 Not Applicable
HERDC Research category C1.1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2013, The Authors
Free to Read? Yes
Use Rights Creative Commons Attribution non-commercial licence
Persistent URL http://hdl.handle.net/10536/DRO/DU:30100056

Document type: Journal Article
Collections: School of Medicine
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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.