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Predominance of CIN versus MSI in the development of rectal cancer at young age.

Fernebro, Eva LU ; Halvarsson, Britta LU ; Baldetorp, Bo LU and Nilbert, Mef LU (2002) In BMC Cancer 2(1). p.25-25
Abstract
BACKGROUND: Development of proximal and distal colorectal cancers involve partly different mechanisms associated with the microsatellite instability (MSI) and the chromosomal instability (CIN) pathways. Colorectal cancers in patients under 50 years of age represent about 5% of the total number of tumors and have been associated with an increased frequency of MSI tumors. However, MSI and CIN may play different roles in the development of colon cancer and rectal cancer, and we have specifically investigated their contribution to the development of rectal cancer at young age. METHODS: Thirty rectal cancers diagnosed before the age of 50 were characterized for DNA-ploidy, MSI, mutations of KRAS and CTNNB1 and immunohistochemical expression of... (More)
BACKGROUND: Development of proximal and distal colorectal cancers involve partly different mechanisms associated with the microsatellite instability (MSI) and the chromosomal instability (CIN) pathways. Colorectal cancers in patients under 50 years of age represent about 5% of the total number of tumors and have been associated with an increased frequency of MSI tumors. However, MSI and CIN may play different roles in the development of colon cancer and rectal cancer, and we have specifically investigated their contribution to the development of rectal cancer at young age. METHODS: Thirty rectal cancers diagnosed before the age of 50 were characterized for DNA-ploidy, MSI, mutations of KRAS and CTNNB1 and immunohistochemical expression of p53, beta-catenin and of the mismatch repair (MMR) proteins MLH1 and MSH2. RESULTS: DNA aneuploidy was detected in 21/30 tumors, KRAS mutations in 6 tumors, no mutations of CTNNB1 were detected but immunohistochemical staining for beta-catenin showed nuclear staining in 6 tumors, and immunohistochemical expression of p53 was detected in 18 tumors. MSI was detected in 3/30 tumors, all of which showed and immunohistochemical loss of staining for the MMR protein MSH2, which strongly indicates a phenotype associated with hereditary nonpolyposis colorectal cancer (HNPCC). CONCLUSIONS: MSI occurs only in a small fraction of the tumors from young patients with rectal cancer, but when present it strongly indicates an underlying HNPCC-causing mutation, and other mechanisms than HNPCC thus cause rectal cancer in the majority of young patients. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
BMC Cancer
volume
2
issue
1
pages
25 - 25
publisher
BioMed Central
external identifiers
  • pmid:12379157
  • wos:000180227800001
  • scopus:3042798448
ISSN
1471-2407
DOI
10.1186/1471-2407-2-25
language
English
LU publication?
yes
id
b7bb6770-c435-4a80-b100-f584581ba657 (old id 110646)
alternative location
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=12379157&dopt=Abstract
date added to LUP
2007-07-18 16:06:12
date last changed
2017-01-01 07:02:31
@article{b7bb6770-c435-4a80-b100-f584581ba657,
  abstract     = {BACKGROUND: Development of proximal and distal colorectal cancers involve partly different mechanisms associated with the microsatellite instability (MSI) and the chromosomal instability (CIN) pathways. Colorectal cancers in patients under 50 years of age represent about 5% of the total number of tumors and have been associated with an increased frequency of MSI tumors. However, MSI and CIN may play different roles in the development of colon cancer and rectal cancer, and we have specifically investigated their contribution to the development of rectal cancer at young age. METHODS: Thirty rectal cancers diagnosed before the age of 50 were characterized for DNA-ploidy, MSI, mutations of KRAS and CTNNB1 and immunohistochemical expression of p53, beta-catenin and of the mismatch repair (MMR) proteins MLH1 and MSH2. RESULTS: DNA aneuploidy was detected in 21/30 tumors, KRAS mutations in 6 tumors, no mutations of CTNNB1 were detected but immunohistochemical staining for beta-catenin showed nuclear staining in 6 tumors, and immunohistochemical expression of p53 was detected in 18 tumors. MSI was detected in 3/30 tumors, all of which showed and immunohistochemical loss of staining for the MMR protein MSH2, which strongly indicates a phenotype associated with hereditary nonpolyposis colorectal cancer (HNPCC). CONCLUSIONS: MSI occurs only in a small fraction of the tumors from young patients with rectal cancer, but when present it strongly indicates an underlying HNPCC-causing mutation, and other mechanisms than HNPCC thus cause rectal cancer in the majority of young patients.},
  author       = {Fernebro, Eva and Halvarsson, Britta and Baldetorp, Bo and Nilbert, Mef},
  issn         = {1471-2407},
  language     = {eng},
  number       = {1},
  pages        = {25--25},
  publisher    = {BioMed Central},
  series       = {BMC Cancer},
  title        = {Predominance of CIN versus MSI in the development of rectal cancer at young age.},
  url          = {http://dx.doi.org/10.1186/1471-2407-2-25},
  volume       = {2},
  year         = {2002},
}