Camille C Gunderson1, Sonia Dutta2, Amanda Nickles Fader3, Kruti P Maniar4, Niloo Nasseri-Nik5, Robert E Bristow6, Teresa P Diaz-Montes7, Robert Palermo8, Robert J Kurman9. 1. University of Oklahoma Health Sciences Center, Department of Obstetrics and Gynecology, Division of Gynecologic Oncology; Oklahoma City, OK, USA. Electronic address: ccgunder@gmail.com. 2. Johns Hopkins Hospital, Department of Gynecology and Obstetrics, Division of Gynecologic Oncology; Baltimore, MD, USA. Electronic address: sonia.dutta@gmail.com. 3. Johns Hopkins Medical Institutions/Greater Baltimore Medical Center, Department of Gynecology and Obstetrics, Division of Gynecologic Oncology; Baltimore, MD, USA. Electronic address: amandanfader@gmail.com. 4. Johns Hopkins Hospital, Departments of Gynecology and Obstetrics, Pathology, Division of Gynecologic Pathology and Oncology; Baltimore, MD, USA. Electronic address: kpmaniar@gmail.com. 5. Johns Hopkins Hospital, Departments of Gynecology and Obstetrics, Pathology, Division of Gynecologic Pathology and Oncology; Baltimore, MD, USA. Electronic address: niloofar_nik@yahoo.com. 6. University of California Irvine, Department of Obstetrics and Gynecology, Division of Gynecologic Oncology; Orange, CA, USA. Electronic address: rbristow@uci.edu. 7. Johns Hopkins Hospital, Department of Gynecology and Obstetrics, Division of Gynecologic Oncology; Baltimore, MD, USA. Electronic address: tdiazmo12@gmail.com. 8. Greater Baltimore Medical Center, Department of Pathology; Baltimore, MD, USA. Electronic address: rpalermo@gbmc.org. 9. Johns Hopkins Hospital, Departments of Gynecology and Obstetrics, Pathology, Division of Gynecologic Pathology and Oncology; Baltimore, MD, USA. Electronic address: rkurman@jhmi.edu.
Abstract
OBJECTIVE: To determine the response of complex atypical hyperplasia (CAH) and well differentiated endometrioid adenocarcinoma of the uterus (WDC) to progestin therapy and whether pre-treatment estrogen and progesterone receptor status predicts outcome. METHODS: We performed a retrospective review encompassing women treated with progestin therapy for CAH or WDC at two institutions. Clinicopathologic, treatment, and recurrence data were recorded. Pre/post-treatment pathologic evaluation was performed. SAS 9.2 was used for statistical analyses. RESULTS: Forty-six patients were included. The median age was 35, and median BMI was 36.9. Thirty-seven percent were diagnosed with CAH and 63% had WDC. Megestrol acetate was the most commonly used agent (89%); 24% received multiple progestin therapies. Median treatment length was 6 months (range, 1-84); 36% of the patients underwent eventual hysterectomy, and 17.4% had carcinoma in their uterine specimens (8 primary endometrial, 1 primary ovarian). After a median follow-up of 35 months (range, 2-162), 65% experienced a complete response (CR), 28% had persistent or progressive disease, and 23% had a CR followed by recurrence. On univariate analysis, decreased post-treatment glandular cellularity (p = 0.0006), absence of post-treatment mitotic figures (p = 0.0008), and use of multiple progestin agents (p = 0.025) were associated with CR; however, only decreased glandular cellularity was significant on multivariate analysis (p = 0.007). Estrogen and progesterone receptor expression was not associated with treatment response. CONCLUSION: In women with CAH or WDC, the overall response rate to progestin therapy was 65%; pre-treatment estrogen/progesterone receptor status did not predict response to treatment.
OBJECTIVE: To determine the response of complex atypical hyperplasia (CAH) and well differentiated endometrioid adenocarcinoma of the uterus (WDC) to progestin therapy and whether pre-treatment estrogen and progesterone receptor status predicts outcome. METHODS: We performed a retrospective review encompassing women treated with progestin therapy for CAH or WDC at two institutions. Clinicopathologic, treatment, and recurrence data were recorded. Pre/post-treatment pathologic evaluation was performed. SAS 9.2 was used for statistical analyses. RESULTS: Forty-six patients were included. The median age was 35, and median BMI was 36.9. Thirty-seven percent were diagnosed with CAH and 63% had WDC. Megestrol acetate was the most commonly used agent (89%); 24% received multiple progestin therapies. Median treatment length was 6 months (range, 1-84); 36% of the patients underwent eventual hysterectomy, and 17.4% had carcinoma in their uterine specimens (8 primary endometrial, 1 primary ovarian). After a median follow-up of 35 months (range, 2-162), 65% experienced a complete response (CR), 28% had persistent or progressive disease, and 23% had a CR followed by recurrence. On univariate analysis, decreased post-treatment glandular cellularity (p = 0.0006), absence of post-treatment mitotic figures (p = 0.0008), and use of multiple progestin agents (p = 0.025) were associated with CR; however, only decreased glandular cellularity was significant on multivariate analysis (p = 0.007). Estrogen and progesterone receptor expression was not associated with treatment response. CONCLUSION: In women with CAH or WDC, the overall response rate to progestin therapy was 65%; pre-treatment estrogen/progesterone receptor status did not predict response to treatment.
Authors: Henry D Reyes; Matthew J Carlson; Eric J Devor; Yuping Zhang; Kristina W Thiel; Megan I Samuelson; Megan McDonald; Shujie Yang; Jean-Marie Stephan; Erica C Savage; Donghai Dai; Michael J Goodheart; Kimberly K Leslie Journal: Gynecol Oncol Date: 2015-10-30 Impact factor: 5.482
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