Advanced

Loss of mismatch repair protein immunostaining in colorectal adenomas from patients with hereditary nonpolyposis colorectal cancer.

Halvarsson, Britta LU ; Lindblom, Annika ; Johansson, Leif LU ; Lagerstedt, Kristina and Nilbert, Mef LU (2005) In Modern Pathology 18(8). p.1095-1101
Abstract
Colorectal adenomas occur at younger age, at increased frequency and have a greater tendency for malignant transformation in patients with hereditary nonpolyposis colorectal cancer (HNPCC). We performed immunostaining for the mismatch repair proteins MLH1, PMS2, MSH2 and MSH6 in 35 colorectal adenomas from 26 patients with HNPCC and identified loss of immunostaining in 23/35 (0.66) adenomas. Loss of mismatch repair protein immunostaining was particularly frequent in large (>5 mm) (14/16) and proximally located (13/15) adenomas, whereas the gene mutated - MLH1 or MSH2 - and the type of mutation did not seem to affect the results. We conclude that loss of mismatch repair protein immunostaining is detected at a lower rate in adenomas than... (More)
Colorectal adenomas occur at younger age, at increased frequency and have a greater tendency for malignant transformation in patients with hereditary nonpolyposis colorectal cancer (HNPCC). We performed immunostaining for the mismatch repair proteins MLH1, PMS2, MSH2 and MSH6 in 35 colorectal adenomas from 26 patients with HNPCC and identified loss of immunostaining in 23/35 (0.66) adenomas. Loss of mismatch repair protein immunostaining was particularly frequent in large (>5 mm) (14/16) and proximally located (13/15) adenomas, whereas the gene mutated - MLH1 or MSH2 - and the type of mutation did not seem to affect the results. We conclude that loss of mismatch repair protein immunostaining is detected at a lower rate in adenomas than in carcinomas associated with HNPCC. Adenomatous tissue can thus be used for immunostaining of mismatch repair proteins in clinical investigations of HNPCC, but whereas loss of immunostaining may pinpoint the gene affected and thereby guide mutation analysis, retained staining cannot exclude that the adenoma developed as part of the syndrome due to reduced sensitivity. However, the analysis has a greater chance of being informative if large and proximally located adenomas are selected. (Less)
Please use this url to cite or link to this publication:
author
; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
immunohistochemistry, repair, hereditary nonpolyposis colorectal cancer (HNPCC), adenoma, mismatch
in
Modern Pathology
volume
18
issue
8
pages
1095 - 1101
publisher
Nature Publishing Group
external identifiers
  • pmid:15731775
  • wos:000230646000011
  • scopus:24044540727
ISSN
1530-0285
DOI
10.1038/modpathol.3800392
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Pathology, (Lund) (013030000), Oncology, MV (013035000)
id
150ad538-46c1-4b63-8eb4-ab02a823a56e (old id 133548)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15731775&dopt=Abstract
date added to LUP
2016-04-01 16:42:04
date last changed
2021-01-06 05:11:31
@article{150ad538-46c1-4b63-8eb4-ab02a823a56e,
  abstract     = {Colorectal adenomas occur at younger age, at increased frequency and have a greater tendency for malignant transformation in patients with hereditary nonpolyposis colorectal cancer (HNPCC). We performed immunostaining for the mismatch repair proteins MLH1, PMS2, MSH2 and MSH6 in 35 colorectal adenomas from 26 patients with HNPCC and identified loss of immunostaining in 23/35 (0.66) adenomas. Loss of mismatch repair protein immunostaining was particularly frequent in large (>5 mm) (14/16) and proximally located (13/15) adenomas, whereas the gene mutated - MLH1 or MSH2 - and the type of mutation did not seem to affect the results. We conclude that loss of mismatch repair protein immunostaining is detected at a lower rate in adenomas than in carcinomas associated with HNPCC. Adenomatous tissue can thus be used for immunostaining of mismatch repair proteins in clinical investigations of HNPCC, but whereas loss of immunostaining may pinpoint the gene affected and thereby guide mutation analysis, retained staining cannot exclude that the adenoma developed as part of the syndrome due to reduced sensitivity. However, the analysis has a greater chance of being informative if large and proximally located adenomas are selected.},
  author       = {Halvarsson, Britta and Lindblom, Annika and Johansson, Leif and Lagerstedt, Kristina and Nilbert, Mef},
  issn         = {1530-0285},
  language     = {eng},
  number       = {8},
  pages        = {1095--1101},
  publisher    = {Nature Publishing Group},
  series       = {Modern Pathology},
  title        = {Loss of mismatch repair protein immunostaining in colorectal adenomas from patients with hereditary nonpolyposis colorectal cancer.},
  url          = {http://dx.doi.org/10.1038/modpathol.3800392},
  doi          = {10.1038/modpathol.3800392},
  volume       = {18},
  year         = {2005},
}