Oral MPA is active against endometrial carcinoma. Response to progestin therapy is more frequent among patients with a well-differentiated histology and positive progesterone receptor status. This study provides no evidence to support the use of MPA 1,000 mg/d orally instead of MPA 200 mg/d orally. In fact, the trends suggest the opposite. The use of oral MPA 200 mg/d is a reasonable initial approach to the treatment of advanced or recurrent endometrial carcinoma, particularly those lesions that are well-differentiated and/or progesterone receptor-positive (> 50 fmol/mg cytosol protein). Patients with poorly differentiated and/or progesterone receptor levels less than 50 fmol/mg cytosol protein had only an 8% to 9% response rate.

These data add to the literature documenting the possible therapeutic benefit of selective lymphadenectomy in management of patients with apparent early-stage endometrial cancer.

This review summarizes the primary management of molar pregnancies, surveillance after evacuation, and the evaluation and management of malignant gestational trophoblastic neoplasia (GTN). Most women with gestational trophoblastic disease can be successfully managed with preservation of their normal reproductive function. It is important to manage molar pregnancies properly to minimize acute complications and identify malignant sequelae promptly. Current International Federation of Gynecology and Obstetrics (FIGO) guidelines for making the diagnosis and staging of GTN allow uniformity for reporting results of treatment. It is important to individualize treatment for women with malignant GTN based upon risk factors, using less toxic therapy for patients with low-risk disease and aggressive multiagent therapy for those with high-risk disease. Patients with malignant GTN should be managed in consultation with an individual experienced in the complex, multimodality treatment of these patients.

No abstract

We hypothesized that mutations in homologous recombination repair (HRR) genes beyond and improve outcomes for ovarian carcinoma patients treated with platinum therapy and would impact the relative benefit of adding prolonged bevacizumab. We sequenced DNA from blood and/or neoplasm from 1,195 women enrolled in GOG-0218, a randomized phase III trial in advanced ovarian carcinoma of bevacizumab added to carboplatin and paclitaxel. Defects in HRR were defined as damaging mutations in 16 genes. Proportional hazards models were used to estimate relative hazards for progression-free survival (PFS) and overall survival (OS). Of 1,195 women with ovarian carcinoma, HRR mutations were identified in 307 (25.7%). Adjusted hazards for progression and death compared with those without mutations were lower for women with non- HRR mutations [HR = 0.73; 95% confidence interval (CI), 0.57-0.94; = 0.01 for PFS; HR = 0.67; 95% CI, 0.50-0.90; = 0.007 for OS] and mutations (HR = 0.80; 95% CI, 0.66-0.97; = 0.02 for PFS; HR = 0.74; 95% CI, 0.59-0.94; = 0.01 for OS) and were lowest for mutations (HR = 0.52; 95% CI, 0.40-0.67; < 0.0001 for PFS; HR = 0.36; 95% CI, 0.25-0.53; < 0.0001 for OS). A test of interaction showed no difference in the effect of bevacizumab on PFS between cases with and without mutations. HRR mutations, including non- genes, significantly prolong PFS and OS in ovarian carcinoma and should be stratified for in clinical trials. The benefit of adding bevacizumab was not significantly modified by mutation status. .