title: COL11A1 in FAP polyps and in sporadic colorectal tumors.
abstract: BACKGROUND
  We previously reported that the alpha-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 beta-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/beta-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/beta-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/beta-catenin pathway in FAP and sporadic colorectal cancer.
authors.affiliation: Department Molecular Medicine, Karolinska Institute, S 171 76 Stockholm, Sweden. helene.fischer@cmm.ki.se
authors.forename: H
authors.initials: H
authors.lastname: Fischer
authors.forename: S
authors.initials: S
authors.lastname: Salahshor
authors.forename: R
authors.initials: R
authors.lastname: Stenling
authors.forename: J
authors.initials: J
authors.lastname: Björk
authors.forename: G
authors.initials: G
authors.lastname: Lindmark
authors.forename: L
authors.initials: L
authors.lastname: Iselius
authors.forename: C
authors.initials: C
authors.lastname: Rubio
authors.forename: A
authors.initials: A
authors.lastname: Lindblom
mesh_terms: D011125:Adenomatous Polyposis Coli / Q000235:genetics*; D025601:Adenomatous Polyposis Coli Protein / Q000235:genetics / Q000378:metabolism; D055511:CCN Intercellular Signaling Proteins; D002277:Carcinoma / Q000235:genetics*; D024161:Collagen Type XI / Q000096:biosynthesis / Q000235:genetics*; D015179:Colorectal Neoplasms / Q000235:genetics*; D003598:Cytoskeletal Proteins / Q000235:genetics / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics; D017491:Genes, APC; D006133:Growth Substances / Q000096:biosynthesis / Q000235:genetics; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins; D015513:Oncogene Proteins / Q000096:biosynthesis / Q000235:genetics; D011518:Proto-Oncogene Proteins; D015534:Trans-Activators / Q000235:genetics / Q000378:metabolism; D015854:Up-Regulation / Q000235:genetics; D051176:beta Catenin
chemical_list: D025601:Adenomatous Polyposis Coli Protein; D055511:CCN Intercellular Signaling Proteins; C116396:CCN4 protein, human; C495270:CTNNB1 protein, human; D024161:Collagen Type XI; D003598:Cytoskeletal Proteins; D006133:Growth Substances; D047908:Intracellular Signaling Peptides and Proteins; D015513:Oncogene Proteins; D011518:Proto-Oncogene Proteins; D015534:Trans-Activators; D051176:beta Catenin