title: [The expression of DNA mismatch repair genes and detection of DNA ploidy in young patients with colorectal carcinoma].
abstract: OBJECTIVE
  To investigate the clinicopathologic characters and carcinogentic pathways of young (age < 36) colorectal carcinomas (CRCs) in Guangzhou, China.
  
  
  METHODS
  Immunohistochemistry and flow cytometry methods were used to detect the expression of hMSH(2) and hMLH(1), status of DNA ploidy in 63 cases of young CRCs from Guangzhou, China, and analyze their correlations with patient's clinicopathological characters.
  
  
  RESULTS
  Of the 63 young CRCs studied, forty-four (69.8%) tumors were non-mucinous carcinomas, thirty-nine (61.9%) patients were in Dukes' C or D stage. Of the 59 CRCs which were successfully detected by immunohistochemistry and flow cytometry, ten (16.9%) CRCs lost either hMSH(2) or hMLH(1) and showed DNA diploid or near-diploid, while twenty-six (44.1%) had aneuploid DNA content and all with the normal expression of hMSH(2) and hMLH(1). In addition, there existed a significant percentage (23/59, 39%) of young CRCs showing no loss of either of these two mismatch repair proteins and having a diploid or near diploid DNA content.
  
  
  CONCLUSIONS
  The overall percentage of young CRCs in Guangzhou is significantly higher than those in Caucasian predominant countries and about seventy percent of young CRCs in Guangzhou are conventional carcinomas. 39% of young CRCs in Guangzhou showed no evidence of either chromosomal instability or microsatellite instability carcinogentic pathway, indicating that there must be at least a third pathway which triggers the CRCs in these special subgroups of young patients in Guangzhou, China.
authors.affiliation: Department of Pathology, Sun Yat-Sen University of Medical Sciences, Guangzhou 510089, China.
authors.forename: D
authors.initials: D
authors.lastname: Xie
authors.forename: S
authors.initials: S
authors.lastname: Leung
authors.forename: W
authors.initials: W
authors.lastname: Zeng
authors.forename: M
authors.initials: M
authors.lastname: Zhang
authors.forename: A
authors.initials: A
authors.lastname: Chan
authors.forename: S
authors.initials: S
authors.lastname: Yuen
authors.forename: J
authors.initials: J
authors.lastname: Wen
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D000230:Adenocarcinoma / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D002288:Adenocarcinoma, Mucinous / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D000293:Adolescent; D000328:Adult; D000782:Aneuploidy; D044466:Asian People; D020137:Base Pair Mismatch; D002352:Carrier Proteins; D002681:China; D003110:Colonic Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D004260:DNA Repair; D004273:DNA, Neoplasm / Q000235:genetics; D004268:DNA-Binding Proteins / Q000378:metabolism*; D004171:Diploidy; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008297:Male; D000070957:MutL Protein Homolog 1; D051718:MutS Homolog 2 Protein; D009363:Neoplasm Proteins / Q000378:metabolism*; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D012004:Rectal Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D013045:Species Specificity
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D002352:Carrier Proteins; D004273:DNA, Neoplasm; D004268:DNA-Binding Proteins; C501486:MLH1 protein, human; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; C497172:MSH2 protein, human; D000070957:MutL Protein Homolog 1; D051718:MutS Homolog 2 Protein