Lifetime caffeine intake and the risk of epithelial ovarian cancer.

BACKGROUND: Caffeine intake has been inconsistently associated with the risk of ovarian cancer in previous studies. The measure of caffeine in these studies has not always distinguished between caffeinated and decaffeinated sources, and the time for which intake was assessed was often for late adulthood and thus may have excluded the etiologic window. We investigated lifetime caffeine intake from caffeinated coffee, black tea, green tea and cola sodas in relation to ovarian cancer risk. METHODS: Among 497 cases and 904 controls in a population-based case-control study in Montreal, Canada, lifetime intake of caffeinated coffee, black tea, green tea and cola sodas was assessed and used to calculate lifetime total intake of caffeine. Unconditional multivariable logistic regression was used to estimate odds ratios (ORs) with 95% confidence intervals (CIs) for the association between caffeine intake and ovarian cancer risk overall, as well as by menopausal status. Multivariable polytomous logistic regression was used to estimate the associations for invasive and borderline ovarian cancers separately. RESULTS: Almost all participants (98.4% of cases and 97.5% of controls) had consumed caffeine in their lifetime. The mean (standard deviation) daily consumption of caffeine over the lifetime was of 117 (89) mg/day among cases and 120 (118) mg/day among controls. The OR (95% CI) of ovarian cancer for the highest versus lowest quartile of lifetime caffeine intake was 1.17 (0.83-1.64). According to menopausal status, the OR (95% CI) was 1.56 (0.85-2.86) for premenopausal women and 0.94 (0.66-1.34) for postmenopausal women, comparing the highest to lowest tertiles of intake. Associations for invasive and borderline ovarian cancers separately were similar to that observed for ovarian cancer overall. CONCLUSION: Lifetime caffeine intake was not strongly associated with ovarian cancer risk. A difference in relationship by menopausal status is possible.

The effect of folate intake on ovarian cancer risk: A meta-analysis of observational studies.

BACKGROUND: Previous publications studied the correction about folate intake and ovarian cancer risk, with inconsistent results. This meta-analysis aimed to explore the association between folate intake and ovarian cancer risk using the existing published articles. METHOD: We searched for relevant studies in electronic databases of PubMed, Web of Science, Embase, Cochrane, and Wanfang databases from inception to May 31, 2020. The overall relative risk (RR) and its 95% confidence intervals (95% CI) were pooled using a random-effect model. RESULTS: A total of 12 articles with 6304 ovarian cancer cases were suitable for the inclusion criteria. The evaluated of the ovarian cancer risk with total folate intake and dietary folate intake were reported in 6 articles and 10 articles, respectively. Overall, highest category of dietary folate intake compared with lowest category had nonsignificant association on the risk of ovarian cancer (RR = 0.90, 95% CI = 0.77-1.06). The association was not significant between total folate intake and ovarian cancer risk (RR = 1.06, 95% CI = 0.89-1.27). The results in subgroup analyses by study design and geographic location were not changed either in dietary folate intake analysis or in total folate intake analysis. CONCLUSION: Our meta-analysis demonstrates that folate intake had no significant association on the risk of ovarian cancer. Study design and geographic location were not associated with ovarian cancer while some other related factors were not investigated due to the limited information provided in each included study. Therefore, further studies are needed to verify our results.

Low rate of intraperitoneal port placement in ovarian cancer patients, a population-based assessment.

INTRODUCTION: The National Comprehensive Cancer Network (NCCN) guidelines recommend intraperitoneal chemotherapy in optimally debulked stage III ovarian cancer patients. The objective of this investigation was to determine the rate of intraperitoneal port placement in patients undergoing surgery for ovarian cancer in a national database maintained by the American College of Surgeons. METHOD: We identified ovarian cancer patients in the National Surgical Quality Improvement Program database from 2006 to 2012. Demographics, comorbidities, operative outcomes, and postoperative complications were abstracted. Descriptive analyses were conducted using Wilcoxon rank-sum and Chi square tests, and multivariate regression models were used to analyze pre-operative and post-operative variables associated with intraperitoneal port placement. RESULTS: We identified 2659 ovarian cancer patients who underwent primary surgical management. Of these patients, only 128 (4.8%) had an intraperitoneal port placed at the time of surgery. In multivariable analyses, intraperitoneal ports were associated with body mass index ≤25, disseminated cancer, later portion of the study period (2009-2012), and operative time >200 min. Intraperitoneal port placement was not associated with any difference in surgical site infection, wound disruption, major postoperative complication, readmission within 30 days, or death within 30 days. DISCUSSION: Recent investigation of practice at NCCN institutions between 2003 and 2012 found only 35% of eligible ovarian cancer patients received intraperitoneal chemotherapy. Using intraperitoneal port placement as a surrogate for intraperitoneal chemotherapy administration, our investigation suggests an even lower rate (4.8%) nationally.

Coffee and caffeine intake and risk of ovarian cancer: a systematic review and meta-analysis.

BACKGROUND: Results from earlier publications on the association of coffee and caffeine and risk of ovarian cancer are inconsistent. OBJECTIVE: To evaluate the link between coffee, caffeine, caffeinated coffee, and decaffeinated coffee consumption and risk of ovarian cancer. METHODS: We searched PubMed/Medline, ISI Web of Science, Scopus, and Google Scholar to identify relevant publications up to April 2018. All case-control studies that considered coffee, caffeine, caffeinated coffee, or decaffeinated coffee as the exposure variables and ovarian cancer as the main outcome variable or as one of the outcomes were included in the systematic review. Publications in which odds ratios (ORs) or rate or risk ratios (RRs) and 95% confidence intervals (CIs) were reported, were included in the meta-analysis. RESULTS: A total of 22 case-control studies were included in the systematic review, and 20 studies in the meta-analysis. Overall, 40 140 participants, including 8568 patients with ovarian cancer, aged ≥ 17 years were included. Combining 21 effect sizes from 18 studies, no significant association was observed between total coffee intake and risk of ovarian cancer (OR=1.09; 95% CI 0.94 to 1.26). There was no significant association between total caffeine intake and ovarian cancer risk (OR=0.89; 95% CI 0.55 to 1.45). In addition, caffeinated coffee intake was not significantly associated with ovarian cancer (OR=1.05; 95% CI 0.87 to 1.28). However, combining effect sizes from five studies, we found an inverse significant association between decaffeinated coffee intake and risk of ovarian cancer (OR=0.72; 95% CI 0.58 to 0.90). CONCLUSIONS: Our findings indicated an inverse association between decaffeinated coffee consumption and risk of ovarian cancer. No significant association was found between coffee, caffeine or caffeinated coffee intake and risk of ovarian cancer.

Epithelial ovarian cancer.

Epithelial ovarian cancer generally presents at an advanced stage and is the most common cause of gynaecological cancer death. Treatment requires expert multidisciplinary care. Population-based screening has been ineffective, but new approaches for early diagnosis and prevention that leverage molecular genomics are in development. Initial therapy includes surgery and adjuvant therapy. Epithelial ovarian cancer is composed of distinct histological subtypes with unique genomic characteristics, which are improving the precision and effectiveness of therapy, allowing discovery of predictors of response such as mutations in breast cancer susceptibility genes BRCA1 and BRCA2, and homologous recombination deficiency for DNA damage response pathway inhibitors or resistance (cyclin E1). Rapidly evolving techniques to measure genomic changes in tumour and blood allow for assessment of sensitivity and emergence of resistance to therapy, and might be accurate indicators of residual disease. Recurrence is usually incurable, and patient symptom control and quality of life are key considerations at this stage. Treatments for recurrence have to be designed from a patient's perspective and incorporate meaningful measures of benefit. Urgent progress is needed to develop evidence and consensus-based treatment guidelines for each subgroup, and requires close international cooperation in conducting clinical trials through academic research groups such as the Gynecologic Cancer Intergroup.

Ovarian cancer in Switzerland: incidence and treatment according to hospital registry data.

OBJECTIVE: The methods used to diagnose and classify ovarian cancer have changed over the past decade. We used hospital registry data to assess the incidence, treatment durations and hospital costs of ovarian cancer in Switzerland. METHODS: We carried out a retrospective analysis of a hospital registry covering all inpatient care episodes in Switzerland between 1998 and 2012. Ovarian cancer incidence was assessed by identifying patients with a first ovarian cancer diagnosis as the main reason for hospital stay after an event-free period. We assessed the duration and cost of ovarian cancer treatment sequences as well as the evolution of hospital patient volume over time. RESULTS: The average age-adjusted incidence rate was 14.6 per 100,000 women per year between 2004 and 2012. This rate is substantially higher (+35.5%) than the corresponding rate published by the National Institute for Cancer Epidemiology and Registration (NICER). Hospital patient volume was low in most cases, with more than 40% of patients treated in hospitals with fewer than 20 cases per year. However, the share of patients treated in hospitals with more than 30 cases per year has increased substantially since 2009. CONCLUSIONS: We found a substantial difference between the ovarian cancer incidence estimate based on hospital registry data and the corresponding estimate by NICER. The reasons for this substantial difference should be carefully explored. A case-wise comparison could determine whether the difference is due to over- or under-reporting in one of the two registries. The low ovarian cancer patient volume in many hospitals is in conflict with the numbers required for certified specialised cancer centres. The recent increase in patient volume in specialised cancer centres, however, might reflect a growing understanding of the needs and requirements of comprehensive cancer care.

Assessment of moderate coffee consumption and risk of epithelial ovarian cancer: a Mendelian randomization study.

Background: Coffee consumption has been shown to be associated with various health outcomes in observational studies. However, evidence for its association with epithelial ovarian cancer (EOC) is inconsistent and it is unclear whether these associations are causal. Methods: We used single nucleotide polymorphisms associated with (i) coffee and (ii) caffeine consumption to perform Mendelian randomization (MR) on EOC risk. We conducted a two-sample MR using genetic data on 44 062 individuals of European ancestry from the Ovarian Cancer Association Consortium (OCAC), and combined instrumental variable estimates using a Wald-type ratio estimator. Results: For all EOC cases, the causal odds ratio (COR) for genetically predicted consumption of one additional cup of coffee per day was 0.92 [95% confidence interval (CI): 0.79, 1.06]. The COR was 0.90 (95% CI: 0.73, 1.10) for high-grade serous EOC. The COR for genetically predicted consumption of an additional 80 mg caffeine was 1.01 (95% CI: 0.92, 1.11) for all EOC cases and 0.90 (95% CI: 0.73, 1.10) for high-grade serous cases. Conclusions: We found no evidence indicative of a strong association between EOC risk and genetically predicted coffee or caffeine levels. However, our estimates were not statistically inconsistent with earlier observational studies and we were unable to rule out small protective associations.