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BMC Cancer
Published in: BMC Cancer 1/2001

Open Access 01-12-2001 | Research article

COL11A1 in FAP polyps and in sporadic colorectal tumors

Authors: Heléne Fischer, Sima Salahshor, Roger Stenling, Jan Björk, Gudrun Lindmark, Lennart Iselius, Carlos Rubio, Annika Lindblom

Published in: BMC Cancer | Issue 1/2001

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Abstract

Background

We previously reported that the α-1 chain of type 11 collagen (COL11A1), not normally expressed in the colon, was up-regulated in stromal fibroblasts in most sporadic colorectal carcinomas. Patients with germline mutations in the APC gene show, besides colonic polyposis, symptoms of stromal fibroblast involvement, which could be related to COL11A1 expression. Most colorectal carcinomas are suggested to be a result of an activated Wnt- pathway, most often involving an inactivation of the APC gene or activation of β-catenin.

Methods

We used normal and polyp tissue samples from one FAP patient and a set of 37 sporadic colorectal carcinomas to find out if the up-regulation of COL11A1 was associated with an active APC/β-catenin pathway.

Results

In this study we found a statistically significant difference in COL11A1 expression between normal tissue and adenomas from one FAP patient, and all adenomas gave evidence for an active APC/β-catenin pathway. An active Wnt pathway has been suggested to involve stromal expression of WISP-1. We found a strong correlation between WISP-1 and COL11A1 expression in sporadic carcinomas.

Conclusions

Our results suggest that expression of COL11A1 in colorectal tumors could be associated with the APC/β-catenin pathway in FAP and sporadic colorectal cancer.
Appendix
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Metadata
Title
COL11A1 in FAP polyps and in sporadic colorectal tumors
Authors
Heléne Fischer
Sima Salahshor
Roger Stenling
Jan Björk
Gudrun Lindmark
Lennart Iselius
Carlos Rubio
Annika Lindblom
Publication date
01-12-2001
Publisher
BioMed Central
Published in
BMC Cancer / Issue 1/2001
Electronic ISSN: 1471-2407
DOI
https://doi.org/10.1186/1471-2407-1-17

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