title: Evaluation of colorectal adenocarcinomas at single-institution with respect to microsatellite instability.
abstract: OBJECTIVE
  Hereditary non-poliposis colorectal cancers exhibit a high rate of microsatellite instability. Comparative studies involving stage and other prognostic parameters demonstrate a better prognosis in the presence of microsatellite instability versus colon cancers without microsatellite instability.
  
  
  METHODS
  Our study included 608 cases diagnosed with colorectal adenocarcinoma by our laboratory between 2004-2010. The cases were re-evaluated with respect to criteria defined for MSI, taking into consideration age, anatomic localization, and histopathological criteria. Immunohistochemical study was performed in appropriate blocks for using MLH-1, MSH-2, MSH-6, and PMS-2.
  
  
  RESULTS
  The specimens were re-evaluated according to the histological criteria defined for microsatellite instability. Anti-MLH-1, anti-MSH-2, anti-MSH-6, and anti-PMS-2 antibodies were applied to the paraffin blocks of 27 cases which presented morphological criteria suggestive of DNA repair mutation and had a high Mspath score. Immunohistochemical study with MLH-1, MSH-2, MSH-6, and PMS-2 for the analysis of mismatch repair was refined using the cases with higher Mspath scores.
  
  
  CONCLUSIONS
  In this study, we reviewed the clinical and histopathological features of 608 cases with colorectal adenocarcinoma diagnosed in our laboratory between 2004-2010 and assessed pathological features in terms of microsatellite instability. The results were discussed in view of the literature.
authors: Department of Pathology, Haydarpasa Numune Education and Research Hospital, Istanbul, Turkey. selvinazo@gmail.com
authors: S
authors: S
authors: Ozkara
authors: B
authors: B
authors: Sari
authors: A
authors: A
authors: Yesil
authors: A
authors: A
authors: Aktekin
authors: M
authors: M
authors: Sezikli
authors: Z
authors: Z
authors: Cetinkaya
authors: F
authors: F
authors: Aker
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics; D000230:Adenocarcinoma / Q000175:diagnosis / Q000235:genetics*; D002288:Adenocarcinoma, Mucinous / Q000235:genetics; D000251:Adenosine Triphosphatases / Q000235:genetics; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D014408:Biomarkers, Tumor / Q000378:metabolism; D018279:Carcinoma, Signet Ring Cell / Q000235:genetics; D015179:Colorectal Neoplasms / Q000175:diagnosis / Q000235:genetics*; D053843:DNA Mismatch Repair; D045643:DNA Repair Enzymes / Q000235:genetics; D004268:DNA-Binding Proteins / Q000235:genetics; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D053842:Microsatellite Instability; D008875:Middle Aged; D000070976:Mismatch Repair Endonuclease PMS2; D000070957:MutL Protein Homolog 1; D051718:MutS Homolog 2 Protein / Q000235:genetics; D009687:Nuclear Proteins / Q000235:genetics; D011237:Predictive Value of Tests; D011379:Prognosis; D011971:Receptors, Immunologic / Q000235:genetics; D012680:Sensitivity and Specificity
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D014408:Biomarkers, Tumor; D004268:DNA-Binding Proteins; C094443:G-T mismatch-binding protein; C501486:MLH1 protein, human; D009687:Nuclear Proteins; D011971:Receptors, Immunologic; C573592:macrophage MHC receptor 1, human; 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