title: Low proliferation activity may be associated with chemoresistance in clear cell carcinoma of the ovary.
abstract: OBJECTIVE
  To estimate whether and how the biologic behavior of clear cell carcinoma contributes to the chemoresistance mechanism.
  
  
  METHODS
  Forty-one patients with clear cell carcinoma and 90 patients with serous adenocarcinoma, who had measurable disease after initial surgery, were examined. All patients underwent cytoreductive surgery followed by platinum-based chemotherapy. P-glycoprotein, multidrug resistance-associated protein, and Ki-67 expression were determined by immunohistochemical staining.
  
  
  RESULTS
  The 5-year survival rate for patients with clear cell carcinoma was significantly poorer, compared with serous adenocarcinoma (20.0% versus 31.9%). Response rate to chemotherapy was 14.6% for clear cell carcinoma and 72.2% for serous adenocarcinoma. The expression of P-glycoprotein and multidrug resistance-associated protein did not differ between responders and nonresponders in both tumor types. The Ki-67 labeling index (LI) in clear cell carcinoma was significantly lower than serous adenocarcinoma (18.4% versus 38.8%). The LI for responders was significantly higher than that for nonresponders in both tumor types. In clear cell carcinoma, the mean value of LI was 15.3% for nonresponders, but that for responders was 30.2%, which was similar to that for serous adenocarcinoma. When the cutoff value of LI was set at 18.4% (mean value), the 5-year survival rate for high LI (over 18.4%) patients was significantly greater than that for low LI patients (46.3% versus 9.2%). Multivariable analysis revealed that LI and residual tumor size were the independent prognostic factors.
  
  
  CONCLUSIONS
  Lower proliferation of tumor may be a behavior of clear cell carcinoma of the ovary that contributes to its resistance to chemotherapy.
authors.affiliation: Department of Obstetrics and Gynecology, Tottori University, Yonago, Japan.
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Itamochi
authors.forename: Junzo
authors.initials: J
authors.lastname: Kigawa
authors.forename: Toru
authors.initials: T
authors.lastname: Sugiyama
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Kikuchi
authors.forename: Mitsuaki
authors.initials: M
authors.lastname: Suzuki
authors.forename: Naoki
authors.initials: N
authors.lastname: Terakawa
mesh_terms: D018262:Adenocarcinoma, Clear Cell / Q000188:drug therapy* / Q000401:mortality / Q000473:pathology* / Q000601:surgery; D002288:Adenocarcinoma, Mucinous / Q000188:drug therapy* / Q000401:mortality / Q000473:pathology* / Q000601:surgery; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000008:administration & dosage*; D002455:Cell Division / Q000187:drug effects / Q000502:physiology; D017024:Chemotherapy, Adjuvant; D015331:Cohort Studies; D016001:Confidence Intervals; D018432:Drug Resistance, Multiple; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000032:analysis; D008875:Middle Aged; D015999:Multivariate Analysis; D009367:Neoplasm Staging; D010051:Ovarian Neoplasms / Q000188:drug therapy* / Q000401:mortality / Q000473:pathology* / Q000601:surgery; D010052:Ovariectomy / Q000379:methods; D011379:Prognosis; D016016:Proportional Hazards Models; D012189:Retrospective Studies; D016019:Survival Analysis
chemical_list: D019394:Ki-67 Antigen