Multiple colorectal adenomas, classic adenomatous polyposis, and germ-line mutations in MYH.

By O. Sieber, L. Lipton, M. Crabtree, K. Heinimann, P. Fidalgo, R. Phillips, M. Bisgaard, T. Orntoft, L. Aaltonen, S. Hodgson and 2 more. New England Journal of Medicine, 2003

926 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/e0836e268b13aabc4cd70d702afc48b3e025c730

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Citations in the corpus

• Guidelines for colorectal cancer screening and surveillance in moderate and high risk groups (update from 2002) (2010, background): “Around 25–30% of polyposis cases with more than 20 polyps and without evidence of a dominant inheritance pattern, in whom genetic analysis has not identified an APC mutation, are due to bi-allelic mutations in the base excision repair (BER) gene, MUTYH (previously MYH).”
• SERIES: Genomic instability in cancer Balancing repair and tolerance of DNA damage caused by alkylating agents (2012, background): “However, the potential for imbalanced BER in human cancer is exemplified by the colorectal cancer predisposition syndrome, MYH-associated polyposis (MAP), which is a consequence of biallelic inherited mutations in the DNA glycosyslase MYH (also known as MUTYH”