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Multiple Colorectal Adenomas, Classic Adenomatous Polyposis, and Germ-Line Mutations in MYH
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Multiple Colorectal Adenomas, Classic Adenomatous Polyposis, and Germ-Line Mutations in MYH
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Journal Article
Multiple Colorectal Adenomas, Classic Adenomatous Polyposis, and Germ-Line Mutations in MYH
2003
Overview
This study explores the link between germ-line mutations in the DNA-repair gene
MYH
and recessive inheritance of multiple colorectal adenomas and classic adenomatous polyposis coli. Patients with biallelic mutations and multiple colorectal adenomas had more polyps and were more likely to have colon cancer than those without
MYH
mutations.
Most Mendelian predispositions to colorectal tumors are dominant and involve tumor-suppressor genes. Recently, Al-Tassan et al.
1
reported on a single Welsh family with three affected members and recessive inheritance of multiple colorectal adenomas and carcinoma. The patients' tumors had an excess of somatic mutations consisting of the substitution of a thymine–adenine pair for a guanine–cytosine pair (G:C→T:A) in the adenomatous polyposis coli (
APC
) gene, which is typical of changes caused by oxidative damage to DNA.
2
–
7
This damage produces the stable guanine adduct 8-oxo-7,8-dihydroxy-2'-deoxyguanosine, which tends to mispair with adenine, leading to the observed mutation. Levels of 8-oxo-7,8-dihydroxy-2'-deoxyguanosine . . .
Publisher
Massachusetts Medical Society
Subject
/ Adenomatous Polyposis Coli - genetics
/ Adult
/ Aged
/ Biological and medical sciences
/ Child
/ Colorectal Neoplasms - genetics
/ DNA-Formamidopyrimidine Glycosylase
/ Female
/ Gastroenterology. Liver. Pancreas. Abdomen
/ Genes
/ Humans
/ Male
/ Mutation
/ N-Glycosyl Hydrolases - genetics
/ Phosphoric Monoester Hydrolases - genetics
/ Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
/ Tumors
