title: The pathological phenotype of colon cancer with microsatellite instability.
abstract: BACKGROUND
  Colorectal cancer is a common malignant disease, caused by different aetiologies and molecular pathways. Heterogeneous results have been published regarding the association of microsatellite instability and clinicopathological features. The aim of this study was to compare clinicopathological features of microsatellite unstable tumours with stable ones.
  
  
  METHODS
  Data were collected retrospectively, but the pathological analyses were all made prospectively. The study included a total of 833 patients undergoing resection of their colon tumour at Nordsjællands Hospital - Hillerød, with mismatch repair analysis from 1 January 2007 to 30 November 2012. The study was performed in a setting with complete mesocolic excision surgery and post-operative expert pathological examination of the tumours. Mismatch repair analysis was done by immuno-histochemical staining for the mismatch repair proteins: pMLH1, pMSH2, pMSH6 and pPMS2 for the determination of microsatellite instability. Microsatellite instability was defined as deficient expression of one or more of these proteins.
  
  
  RESULTS
  Of the 833 patients, 177 had microsatellite instable tumours (21%). Using multivariable logistic regression analysis, we demonstrated that microsatellite unstable cancers were significantly associated with a lower degree of lymph node metastases (odds ratio (OR) = 0.92), distant metastases (OR = 0.33) and tumour budding (OR = 0.41).
  
  
  CONCLUSIONS
  We found that microsatellite unstable tumours show a pathological profile that appears less aggressive than the pathological profile of stable tumours.
  
  
  BACKGROUND
  none.
  
  
  BACKGROUND
  not relevant.
authors.affiliation: helene@ksandersen.dk.
authors.forename: Helene Schou
authors.initials: HS
authors.lastname: Andersen
authors.forename: Claus Anders
authors.initials: CA
authors.lastname: Bertelsen
authors.forename: Rikke
authors.initials: R
authors.lastname: Henriksen
authors.forename: Andre Heiner
authors.initials: AH
authors.lastname: Campos
authors.forename: Bent
authors.initials: B
authors.lastname: Kristensen
authors.forename: Peter
authors.initials: P
authors.lastname: Ingeholm
authors.forename: Ismail
authors.initials: I
authors.lastname: Gögenur
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000032:analysis / Q000235:genetics; D000251:Adenosine Triphosphatases / Q000032:analysis / Q000235:genetics; D000368:Aged; D000369:Aged, 80 and over; D002277:Carcinoma / Q000737:chemistry / Q000235:genetics* / Q000556:secondary; D003110:Colonic Neoplasms / Q000737:chemistry / Q000235:genetics* / Q000473:pathology*; D053843:DNA Mismatch Repair / Q000235:genetics; D045643:DNA Repair Enzymes / Q000032:analysis / Q000235:genetics; D004268:DNA-Binding Proteins / Q000032:analysis / Q000235:genetics; D005260:Female; D006801:Humans; D008207:Lymphatic Metastasis; D008297:Male; D053842:Microsatellite Instability; D008875:Middle Aged; D000070976:Mismatch Repair Endonuclease PMS2; D000070957:MutL Protein Homolog 1; D051718:MutS Homolog 2 Protein / Q000032:analysis / Q000235:genetics; D009367:Neoplasm Staging; D009687:Nuclear Proteins / Q000032:analysis / Q000235:genetics; D010641:Phenotype; D012189:Retrospective Studies
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D004268:DNA-Binding Proteins; C094443:G-T mismatch-binding protein; C501486:MLH1 protein, human; D009687:Nuclear Proteins; D000251:Adenosine Triphosphatases; C094934:PMS2 protein, human; C497172:MSH2 protein, human; D000070976:Mismatch Repair Endonuclease PMS2; D000070957:MutL Protein Homolog 1; D051718:MutS Homolog 2 Protein; D045643:DNA Repair Enzymes