This study confirms that, among Ashkenazi OvC patients, BRCA1/2 mutations are associated with improved long-term survival. This may be due to distinct clinical behavior and/or to a better response to chemotherapy.

Ovarian cancer is a component of the autosomal-dominant hereditary breast-ovarian cancer syndrome and may be due to a mutation in either the BRCA1 or BRCA2 genes. Two mutations in BRCA1 (185delAG and 5382insC) and one mutation in BRCA2 (6174delT) are common in the Ashkenazi Jewish population. One of these three mutations is present in approximately 2% of the Jewish population. Each mutation is associated with an increased risk of ovarian cancer, and it is expected that a significant proportion of Jewish women with ovarian cancer will carry one of these mutations. To estimate the proportion of ovarian cancers attributable to founding mutations in BRCA1 and BRCA2 in the Jewish population and the familial cancer risks associated with each, we interviewed 213 Jewish women with ovarian cancer at 11 medical centers in North America and Israel and offered these women genetic testing for the three founder mutations. To establish the presence of nonfounder mutations in this population, we also completed the protein-truncation test on exon 11 of BRCA1 and exons 10 and 11 of BRCA2. We obtained a detailed family history on all women we studied who had cancer and on a control population of 386 Ashkenazi Jewish women without ovarian or breast cancer. A founder mutation was present in 41.3% of the women we studied. The cumulative incidence of ovarian cancer to age 75 years was found to be 6.3% for female first-degree relatives of the patients with ovarian cancer, compared with 2.0% for the female relatives of healthy controls (relative risk 3.2; 95% CI 1.5-6.8; P=.002). The relative risk to age 75 years for breast cancer among the female first-degree relatives was 2.0 (95% CI 1.4-3.0; P=.0001). Only one nonfounder mutation was identified (in this instance, in a woman of mixed ancestry), and the three founding mutations accounted for most of the observed excess risk of ovarian and breast cancer in relatives.

Objective To determine the efficacy of the double balloon device (the Atad Ripener Device) in ripening and dilatation of the unfavourable cervix for induction of labour.Methods Two hundred and fifty women with unfavourable cervices (Bishop score 5 4) underwent induction of labour with the Atad Ripener Device. Indications were pregnancy induced hypertension (n = 11 8), post-dates (n = 69), elective inductions (n = 23), other reasons including nonreassuring nonstress test, intrauterine growth retardation, previous caesarean section and diabetes mellitus (n = 40). The Atad Ripener Device was inserted into the cervix, the uterine balloon inflated in the internal os, and the cervico-vaginal balloon in the external 0 s of the cervix (100 mL of normal saline to each balloon). Pressure produced by the inflated balloons caused gradual dilatation and effacement of the cervix. The Atad Ripener Device was removed 12 h after insertion, the cervix assessed again, and labour managed according to obstetrical criteria. ResultsThe Atad Ripener Device caused an increase in the Bishop score in all subgroups with a mean change of 4.6 (from 2.0 prior to induction to 6.6 upon removal of the Atad Ripener Device; P < 0.05). The mean time interval from insertion of the Atad Ripener Device to delivery was 18.9 h, and from removal to delivery was 6-9 h. Caesarean section was performed in 39/250 patients (1 6%), and the others had a normal vaginal delivery.Conclusions 1. The double balloon device induces significant ripening and dilatation of the unfavourable cervix. 2. Induction of labour was successfully achieved following removal of the Atad Ripener Device. 3. Our caesarean section rate was low compared with rates reported for women with an unfavourable cervix induced by other methods.

We present a possible adverse reaction related to long-term use of Doxil(®) in female patients. We believe that long-term use of Doxil(®) may predispose female patients to oral squamous cell carcinoma. The patients in this report were not exposed to the common risk factors related to oral cancer formation such as smoking or alcohol consumption. Both patients were 59-year-old females. The first patient was diagnosed in 2001 with stage IIIC ovarian cancer. Seven years following treatment with Doxil(®), she was diagnosed with stage III squamous cell carcinoma of the right maxilla. The second patient was diagnosed with Kaposi's sarcoma with evidence of spread to the lungs. Four years following treatment with Doxil(®) she was diagnosed with stage I squamous cell carcinoma of the left maxilla. A literature review did not reveal any report on Doxil(®) and predisposition to oral cancer; however, we found an abstract that was presented at the last annual meeting of the American Society of Clinical Oncology (ASCO) by Cannon et al. When we combine the data from Cannon et al. and the data presented here, a total of six female patients developed an epithelial carcinoma of the oral cavity following long-term treatment with Doxil(®). We believe that a large-scale study should be initiated on patients that were treated with Doxil(®) for more than 3 years, since these patients might be at risk for developing secondary cancer of the oral cavity.