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Low frequency of defective mismatch repair in a population-based series of upper urothelial carcinoma

Journal Article:

Abstract

Upper urothelial cancer (UUC), i.e. transitional cell carcinomas of the renal pelvis and the ureter, occur at an increased frequency in patients with hereditary nonpolyposis colorectal cancer (HNPCC). Defective mismatch repair (MMR) specifically characterizes HNPCC-associated tumors, but also occurs in subsets of some sporadic tumors, e.g. in gastrointestinal cancer and endometrial cancer. We assessed the contribution of defective MMR to the development of UUC in a population-based series from the southern Swedish Cancer Registry, through microsatellite instability (MSI) analysis and immunohistochemical evaluation of expression of the MMR proteins MLH1, PMS2, MSH2, and MSH6. A MSI-high phenotype was identified in 9/216 (4%) successfully analyzed patients and a MSI-low phenotype in 5/216 (2%). Loss of MMR protein immunostaining was found in 11/216 (5%) tumors, and affected most commonly MSH2 and MSH6. This population-based series indicates that somatic MMR inactivation is a minor pathway in the development of UUC, but tumors that display defective MMR are, based on the immunohistochemical expression pattern, likely to be associated with HNPCC.
Authors:
Ericson, Kajsa M; Isinger, Anna P; [1]  Isfoss, Björn L; [2]  Nilbert, Mef C [1] 
  1. Departments of Oncology, University Hospital, Lund (Sweden)
  2. Departments of Pathology, University Hospital, Lund (Sweden)
Publication Date:
Jan 01, 2005
Product Type:
Journal Article
Resource Relation:
Journal Name: BMC cancer (Online); Journal Volume: 5; Other Information: PMCID: PMC555534; PUBLISHER-ID: 1471-2407-5-23; PMID: 15740628; OAI: oai:pubmedcentral.nih.gov:555534; Copyright (c) 2005 Ericson et al; licensee BioMed Central Ltd.; This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.; Country of input: International Atomic Energy Agency (IAEA)
Subject:
62 RADIOLOGY AND NUCLEAR MEDICINE; CARCINOMAS; EVALUATION; INACTIVATION; NEOPLASMS; PATIENTS; PELVIS; PHENOTYPE; PROTEINS; REPAIR; URETERS
OSTI ID:
22376825
Country of Origin:
United Kingdom
Language:
English
Other Identifying Numbers:
Journal ID: ISSN 1471-2407; TRN: GB15$2097082287
Availability:
Available from http://dx.doi.org/10.1186/1471-2407-5-23; Available from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC555534
Submitting Site:
INIS
Size:
page(s) 23
Announcement Date:
Aug 13, 2015

Journal Article:

Citation Formats

Ericson, Kajsa M, Isinger, Anna P, Isfoss, Björn L, and Nilbert, Mef C. Low frequency of defective mismatch repair in a population-based series of upper urothelial carcinoma. United Kingdom: N. p., 2005. Web. doi:10.1186/1471-2407-5-23.
Ericson, Kajsa M, Isinger, Anna P, Isfoss, Björn L, & Nilbert, Mef C. Low frequency of defective mismatch repair in a population-based series of upper urothelial carcinoma. United Kingdom. doi:10.1186/1471-2407-5-23.
Ericson, Kajsa M, Isinger, Anna P, Isfoss, Björn L, and Nilbert, Mef C. 2005. "Low frequency of defective mismatch repair in a population-based series of upper urothelial carcinoma." United Kingdom. doi:10.1186/1471-2407-5-23. https://www.osti.gov/servlets/purl/10.1186/1471-2407-5-23.
@misc{etde_22376825,
title = {Low frequency of defective mismatch repair in a population-based series of upper urothelial carcinoma}
author = {Ericson, Kajsa M, Isinger, Anna P, Isfoss, Björn L, and Nilbert, Mef C}
abstractNote = {Upper urothelial cancer (UUC), i.e. transitional cell carcinomas of the renal pelvis and the ureter, occur at an increased frequency in patients with hereditary nonpolyposis colorectal cancer (HNPCC). Defective mismatch repair (MMR) specifically characterizes HNPCC-associated tumors, but also occurs in subsets of some sporadic tumors, e.g. in gastrointestinal cancer and endometrial cancer. We assessed the contribution of defective MMR to the development of UUC in a population-based series from the southern Swedish Cancer Registry, through microsatellite instability (MSI) analysis and immunohistochemical evaluation of expression of the MMR proteins MLH1, PMS2, MSH2, and MSH6. A MSI-high phenotype was identified in 9/216 (4%) successfully analyzed patients and a MSI-low phenotype in 5/216 (2%). Loss of MMR protein immunostaining was found in 11/216 (5%) tumors, and affected most commonly MSH2 and MSH6. This population-based series indicates that somatic MMR inactivation is a minor pathway in the development of UUC, but tumors that display defective MMR are, based on the immunohistochemical expression pattern, likely to be associated with HNPCC.}
doi = {10.1186/1471-2407-5-23}
journal = {BMC cancer (Online)}
volume = {5}
journal type = {AC}
place = {United Kingdom}
year = {2005}
month = {Jan}
}