Please use this identifier to cite or link to this item: https://doi.org/10.1038/ncomms5988
Title: Complex MSH2 and MSH6 mutations in hypermutated microsatellite unstable advanced prostate cancer
Authors: Pritchard, C.C
Morrissey, C
Kumar, A 
Zhang, X
Smith, C
Coleman, I
Salipante, S.J
Milbank, J
Yu, M
Grady, W.M
Tait, J.F
Corey, E
Vessella, R.L
Walsh, T
Shendure, J
Nelson, P.S
Keywords: protein MSH2
protein MSH6
DNA binding protein
G-T mismatch-binding protein
MSH2 protein, human
protein binding
protein MSH2
cancer
disease incidence
gene expression
genetic differentiation
microstructure
mutation
advanced cancer
Article
autopsy
bioinformatics
cancer growth
controlled study
copy number variation
disease assessment
disease association
DNA repair
frameshift mutation
gene mutation
gene rearrangement
human
human tissue
loss of function mutation
male
microsatellite instability
mismatch repair
prostate cancer
protein expression
enzymology
genetics
metabolism
middle aged
mutation
prostate tumor
DNA Mismatch Repair
DNA-Binding Proteins
Humans
Male
Microsatellite Instability
Middle Aged
Mutation
MutS Homolog 2 Protein
Prostatic Neoplasms
Protein Binding
Issue Date: 2014
Publisher: Nature Publishing Group
Citation: Pritchard, C.C, Morrissey, C, Kumar, A, Zhang, X, Smith, C, Coleman, I, Salipante, S.J, Milbank, J, Yu, M, Grady, W.M, Tait, J.F, Corey, E, Vessella, R.L, Walsh, T, Shendure, J, Nelson, P.S (2014). Complex MSH2 and MSH6 mutations in hypermutated microsatellite unstable advanced prostate cancer. Nature Communications 5 : 4988. ScholarBank@NUS Repository. https://doi.org/10.1038/ncomms5988
Rights: Attribution 4.0 International
Abstract: A hypermutated subtype of advanced prostate cancer was recently described, but prevalence and mechanisms have not been well-characterized. Here we find that 12% (7 of 60) of advanced prostate cancers are hypermutated, and that all hypermutated cancers have mismatch repair gene mutations and microsatellite instability (MSI). Mutations are frequently complex MSH2 or MSH6 structural rearrangements rather than MLH1 epigenetic silencing. Our findings identify parallels and differences in the mechanisms of hypermutation in prostate cancer compared with other MSI-associated cancers. © 2014 Macmillan Publishers Limited. All rights reserved.
Source Title: Nature Communications
URI: https://scholarbank.nus.edu.sg/handle/10635/177773
ISSN: 20411723
DOI: 10.1038/ncomms5988
Rights: Attribution 4.0 International
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