title: [Expression of DNA mismatch repair protein in endometrial carcinomas and its correlation with clinicopathologic features].
abstract: OBJECTIVE
  To study the expression of mismatch repair protein in a series of endometrial carcinomas and its correlation with clinicopathologic features.
  
  
  METHODS
  The clinical data of 150 consecutive cases of endometrial carcinoma were collected during the period from December, 2014 to August, 2015 in Fudan University Cancer Center. Morphologic features including tumor infiltrating lymphocytes (TIL), peritumoral lymphocytes and tumor heterogeneity were reviewed. Immunohistochemistry for expression of mismatch repair proteins was performed. The correlation with clinicopathologic features was analyzed.
  
  
  RESULTS
  Loss of mismatch repair protein expression was observed in 43 cases (28.7%), including loss of MLH1/PMS2 in 27 cases (18%), loss of MSH2/MSH6 in 7 cases (4.7%), loss of MSH6 in 6 cases (4%) and loss of PMS2 in 3 cases (2%). There were 23.3% and 27.1% of mismatch repair protein-deficient endometrial carcinomas in women under and above 50 years of age, respectively, which was not statistically significant. Amongst the 12 cases with family history of tumors, 4 of the 6 mismatch repair protein-deficient cases were under 50 years of age, which was higher than that in the 6 cases with mismatch repair protein expression (P=0.014). The mismatch repair protein-deficient group showed significantly more prominent TIL and peritumoral lymphocytes than protein-expression group (P=0.033 and <0.001). Moreover, there were also significant differences in depth of myometrial invasion and occurrence of synchronous malignancy (2 cases of ovarian clear cell carcinoma and 1 case of colonic carcinoma) between the two groups (P=0.039 and 0.022). However, there were no significant differences in lymph node metastasis, tumor heterogeneity, lower uterine segment involvement and tumor stage between the two groups.
  
  
  CONCLUSIONS
  Prominent TIL and peritumoral lymphocytes characteristically occur in mismatch repair protein-deficient endometrial carcinomas. Patient age does not significantly correlate with the loss of mismatch repair protein expression, but individuals under 50 years of age are more likely to have no expression if there is family history of tumors.
authors.affiliation: Department of Pathology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
authors.forename: R
authors.initials: R
authors.lastname: Bi
authors.forename: X Y
authors.initials: XY
authors.lastname: Tu
authors.forename: Y X
authors.initials: YX
authors.lastname: Xiao
authors.forename: B E
authors.initials: BE
authors.lastname: Shan
authors.forename: H Y
authors.initials: HY
authors.lastname: Wang
authors.forename: X
authors.initials: X
authors.lastname: Cai
authors.forename: X Y
authors.initials: XY
authors.lastname: Zhou
authors.forename: W T
authors.initials: WT
authors.lastname: Yang
mesh_terms: D018262:Adenocarcinoma, Clear Cell / Q000378:metabolism / Q000473:pathology; D000367:Age Factors; D053843:DNA Mismatch Repair; D045643:DNA Repair Enzymes / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism*; D016889:Endometrial Neoplasms / Q000378:metabolism* / Q000473:pathology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D016246:Lymphocytes, Tumor-Infiltrating; D008875:Middle Aged; D000070976:Mismatch Repair Endonuclease PMS2 / Q000378:metabolism; D000070957:MutL Protein Homolog 1 / Q000378:metabolism; D051718:MutS Homolog 2 Protein / Q000378:metabolism
chemical_list: D004268:DNA-Binding Proteins; C094443:G-T mismatch-binding protein; 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