Most patients with epithelial ovarian cancer achieve a complete clinical remission (CCR) with normal CA-125 but will still relapse and die from their disease. The present study was designed to determine whether CA-125 levels before, during, and after primary treatment provide prognostic information for both type I and type II ovarian cancer.
In this retrospective study, we identified 410 patients with epithelial ovarian cancer who had achieved a CCR between 1984 and 2011. A Cox proportional hazards model and log-rank test were used to assess associations between the nadir CA-125, histotype, and prognosis.
The baseline serum CA-125 concentration was higher in patients with type II ovarian cancer than in those with type I ovarian cancer (P < 0.001). The nadir CA-125 was an independent predictor of progression-free survival (PFS; P < 0.001) and overall survival (OS; P = 0.035) duration. The PFS and OS durations were 21.7 and 79.4 months in patients with CA-125 of 10 U/mL or less and 13.6 and 64.6 months in those with CA-125 of 11 to 35 U/mL, respectively (P = 0.01 and P = 0.002, respectively). Histotype was an independent predictor of PFS (P = 0.041): the PFS and OS durations of the patients with type I ovarian cancer were longer than those of the patients with type II ovarian cancer (P < 0.001 and P < 0.001, respectively).
The nadir CA-125 and histotype are predictive of PFS and OS durations in patients with ovarian cancers who experienced a CCR. Progression-free survival and OS durations were shorter in the patients with CA-125 levels of 11 to 35 U/mL and type II disease than in those with CA-125 levels of 10 U/mL or less and type I ovarian cancer.
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*Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX; †State Key Laboratory of Bioelectronics, South University, Nanjing, PR China; ‡Department of Gynecologic Oncology, Jiangsu Cancer Hospital, Nanjing, Jiangsu, PR China; §Department of Obstetrics and Gynecology, The First AffiliatedHospital of Nanjing Medical University, Nanjing, PR China; ∥Department of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX; ¶Department of Pathology, Baylor College of Medicine, Houston, TX; #Gynecologic Oncology and Cancer Biology; **Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX; and ††Department of Pathology, State Key Laboratory of Tumor Biology, Xijing Hospital, Fourth Military Medical University, Xi’an, Shaanxi, People’s Republic of China.
Address correspondence and reprint requests to Jinsong Liu, MD, PhD, Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX. E-mail: firstname.lastname@example.org; Robert C. Bast, Jr, MD, PhD, Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX. E-mail: email@example.com.
This work was supported in part by the National Institutes of Health through the shared resources of the M.D. Anderson CCSG NCI P30 CA16672, and donations from the Zarrow Foundation and Stuart and Gaye Lynn Zarrow.
JL was supported by an R01 grant (R01 CA131183-01A2) and an ovarian cancer Specialized Programs of Research Excellence (SPORE) grant (IP50 CA83638) from the National Institutes of Health, the Ovarian Cancer Research Fund, and the National Foundation for Cancer Research. JL and RCB are also supported by multi-investigator award from Cancer Prevention and Research Institute of Texas (CPRIT). Dr. Xiaoxiang Chen is a visiting scientist at MD Anderson, supported by the Jiangsu Health International Exchange Program in 2011 and the Jiangsu Province Institute of Cancer Research Foundation (grant number: ZQ200703). RCB receives royalties from Fujirebio Diagnostics, Inc, for CA-125. The other authors declare no conflicts of interest.
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Received July 18, 2012
Accepted February 27, 2013