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Chronic inflammation has been implicated in endometrial carcinogenesis yet the impact of potentially modifiable exposures that might affect inflammation, like diet, has been understudied. This study examined the association between the dietary inflammatory index (DII®), a literature-derived tool to assess the inflammatory potential of diet, and risk of developing, and survival after a diagnosis of endometrial cancer (EC). This study included data from 1,287 women with EC and 1,435 population controls who participated in the Australian National Endometrial Cancer Study. Energy-adjusted DII (E-DII) scores were calculated from pre-diagnostic dietary intake obtained using a semi-quantitative food frequency questionnaire. Logistic regression was used to assess the association between E-DII scores and risk of EC and proportional-hazards models were used for survival analyses. Higher E-DII scores, reflecting a more pro-inflammatory diet, were not associated with risk of EC [adjusted odds ratio (OR) 0.98, 95% CI 0.77–1.24, p-trend = 0.7]. However, in stratified analyses, higher E-DII scores were associated with increased risk of EC among very obese (BMI 35 + kg/m2) women (OR 1.60, 95% CI 0.80–3.21, p-trend = 0.049, p-interaction = 0.045). After a median follow-up of 7.2 years there were 160 deaths, of which 110 (69%) were from EC. We found no association between E-DII score and survival. Greater inflammatory potential of pre-diagnostic diet was not associated with EC risk or survival. Secondary stratified analysis suggested greater inflammatory potential may be associated with EC risk in very obese women.

PURPOSE: Previous epidemiologic studies have shown that smoking, obesity, and physical inactivity are associated with poor survival following a diagnosis of ovarian cancer. Yet, the combined relationship of these unfavorable lifestyle factors on ovarian cancer survival has not been sufficiently investigated. METHODS: Using data pooled from 13 studies, we examined the associations between combined exposures to smoking, overweight/obesity weight, and physical inactivity and overall survival (OS) as well as progression-free survival (PFS) among women diagnosed with invasive epithelial ovarian carcinoma (N=7,022). Using age-, stage, and site-adjusted Cox proportional hazards regression models, we estimated hazard ratios (HRs) and 95% confidence intervals (CIs) associated with joint exposure to these factors. RESULTS: Combined exposure to current smoking, overweight/obesity, and physical inactivity prior to diagnosis was associated with a significantly increased risk of mortality compared to women who never smoked, had normal body mass index (BMI), and were physically active (HR=1.37; 95% CI=1.10–1.70). The association for a joint exposure to these factors exceeded that of each exposure individually. In fact, exposure to both current smoking and overweight/obesity, and current smoking and physical inactivity was also associated with increased risk of death (HR=1.28; 95 % CI=1.08–1.52, and HR=1.26; 95% CI=1.04–1.54, respectively). The associations were of a similar magnitude when former smoking was assessed in combination with the other exposures and when excessive weight was limited to obesity only. No significant associations were observed between joint exposure to any of these factors and PFS. CONCLUSIONS: Joint exposure to smoking, excessive weight, and physical inactivity may negatively impact survival of ovarian cancer patients. These results suggest the importance of examining the combined effect of lifestyle factors on ovarian cancer patients’ survival.

To compare trends in ovarian cancer incidence in the USA and Australia in relation to changes in oral contraceptive pill (OCP) and menopausal hormone therapy (MHT) use. US cancer incidence data (1973–2013) were accessed via SEER*Stat; Australian data (1982–2012) were accessed from the Australian Institute of Health and Welfare Cancer Incidence and Mortality books. Age-period-cohort models were constructed to assess trends in ovarian cancer incidence by birth cohort and year of diagnosis. Ovarian cancer rates were increasing until the cohorts born around 1918 in the USA and 1923 in Australia who were the first to use the OCP. They then declined dramatically across subsequent cohorts such that rates for the 1968 cohort were about half those of women born 45 years earlier; however, there are early suggestions that this decline may not continue in more recent cohorts. In contrast, despite the large reduction in MHT use, there was no convincing evidence that ovarian cancer incidence rates in either country were lower after 2002 than would have been expected based on the declining trend from 1985. The major driver of ovarian cancer incidence rates appears to be the OCP. This means that when those women born since the late 1960s (who have used the OCP at high rates from an early age) reach their 60s and 70s, incidence rates are likely to stop falling and may even increase with changes in the prevalence of other factors such as tubal ligation and obesity. Forward predictions based on past trends may thus underestimate future rates and numbers of women likely to be affected.

Gastric colonization with Helicobacter pylori (H. pylori) has been implicated in the pathogenesis of pancreatic cancer, but results of epidemiological studies have been inconclusive. We analyzed data from the Queensland Pancreatic Cancer Study, an Australian population-based case–control study, and incorporated our findings into an updated meta-analysis. Blood samples were obtained from 580 patients and 626 controls, and enzyme-linked immunosorbent assay kits were used to determine seropositivity to H. pylori and its virulence protein, cytotoxin-associated gene A (CagA). Odds ratios (ORs) and 95 % confidence intervals (CIs) were calculated using logistic regression. Results were incorporated into a meta-analysis along with results of studies identified through systematic literature review. Adjusted ORs and 95 % CIs were calculated using the DerSimonian and Laird random-effects model. No overall association was observed between H. pylori seropositivity and risk of pancreatic cancer (OR 1.00; 95 % CI 0.74–1.35). Nonsignificantly decreased pancreatic cancer risk was observed with CagA seropositivity (OR 0.74; 95 % CI 0.48–1.15) and increased risk with CagA-negative H. pylori seropositivity (OR 1.23; 95 % CI 0.83–1.82). Ten studies were included in the meta-analysis. There was no significant overall association between H. pylori seropositivity and pancreatic cancer risk (OR 1.13; 95 % CI 0.86–1.50), but evidence of CagA strain-specific associations (OR 0.78; 95 % CI 0.67–0.91 and OR 1.30; 95 % CI 1.02–1.65 for CagA-positive and CagA-negative strains, respectively). Our results provide further evidence for the existence of strain-specific associations between H. pylori and pancreatic cancer.

Contains fulltext : 118139.pdf (Publisher’s version ) (Closed access) PURPOSE: The majority of previous studies have observed an increased risk of mucinous ovarian tumors associated with cigarette smoking, but the association with other histological types is unclear. In a large pooled analysis, we examined the risk of epithelial ovarian cancer associated with multiple measures of cigarette smoking with a focus on characterizing risks according to tumor behavior and histology. METHODS: We used data from 21 case-control studies of ovarian cancer (19,066 controls, 11,972 invasive and 2,752 borderline cases). Study-specific odds ratios (OR) and 95 % confidence intervals (CI) were obtained from logistic regression models and combined into a pooled odds ratio using a random effects model. RESULTS: Current cigarette smoking increased the risk of invasive mucinous (OR = 1.31; 95 % CI: 1.03-1.65) and borderline mucinous ovarian tumors (OR = 1.83; 95 % CI: 1.39-2.41), while former smoking increased the risk of borderline serous ovarian tumors (OR = 1.30; 95 % CI: 1.12-1.50). For these histological types, consistent dose-response associations were observed. No convincing associations between smoking and risk of invasive serous and endometrioid ovarian cancer were observed, while our results provided some evidence of a decreased risk of invasive clear cell ovarian cancer. CONCLUSIONS: Our results revealed marked differences in the risk profiles of histological types of ovarian cancer with regard to cigarette smoking, although the magnitude of the observed associations was modest. Our findings, which may reflect different etiologies of the histological types, add to the fact that ovarian cancer is a heterogeneous disease.

Limited experimental evidence suggests that omega-3 polyunsaturated (n-3) fatty acids inhibit the proliferation of ovarian cancer cells in vitro, whereas omega-6 polyunsaturated (n-6) fatty acids have been shown to promote carcinogenesis, but epidemiological studies to date have been inconclusive. Our aim was to evaluate the role of polyunsaturated fatty acids in ovarian carcinogenesis.Participants in the Australian Ovarian Cancer Study (1,366 cases and 1,414 population controls) self-completed risk factor and food frequency questionnaires. Logistic regression models were used to calculate adjusted odds ratio (OR) and 95 % confidence intervals (CI).We found no association between intake of total n-3 fatty acids from foods, or the individual n-3 fatty acids-alpha-linolenic, eicosapentaenoic, docosapentaenoic, docosahexaenoic acids-and ovarian cancer risk. High intake of total n-6 fatty acids was inversely associated with risk (OR for highest vs. lowest category 0.78, 95 % CI 0.60-1.00, p-trend 0.04); however, the association was restricted to n-6 fatty acids from avocado, vegetables, and nuts. Neither higher intake of the individual n-6 fatty acids nor the ratio of n-3 to n-6 fatty acids was associated with ovarian cancer risk. We found no evidence that risk varied by supplement use.Our data provide no evidence of a protective role for n-3 fatty acids in ovarian carcinogenesis. The benefit, if any, of higher intake of n-6 fatty acids is due to general properties of the food sources, rather than due to the n-6 fatty acids per se.

Although polycystic ovary syndrome (PCOS) is commonly cited as a risk factor for endometrial cancer, supporting epidemiological evidence is currently very limited. Our aim was to assess the associations between PCOS, PCOS symptoms, and risk of endometrial cancer in women aged less than 50 years. Data came from a national population-based case–control study in Australia. Cases with newly diagnosed histologically confirmed endometrial cancer were identified through treatment clinics and cancer registries Australia wide. Controls were randomly selected from the national electoral roll. Women were interviewed about their reproductive and medical history, including self-reported PCOS, and lifestyle. Current analyses were restricted to women aged under 50 (156 cases, 398 controls). We estimated odds ratios (OR) using logistic regression to adjust for confounding factors. Women with PCOS had a fourfold increased risk of endometrial cancer compared to women without PCOS (OR 4.0, 95% CI 1.7–9.3). This association was attenuated when additionally adjusted for body mass index (OR 2.2, 95% CI 0.9–5.7). Risk was slightly greater when restricted to Type I cancers. PCOS symptoms including hirsutism and very irregular periods were significantly associated with endometrial cancer risk. These data extend existing findings, including adjustment for confounders, suggesting PCOS is a risk factor for endometrial cancer.

Although the growth inhibitory effects of tea, particularly green tea, and tea polyphenols have been demonstrated in animal models of ovarian cancer, the results of epidemiological studies have been inconclusive.We investigated this issue using data from an Australian population-based, case-control study (1,368 cases; 1,416 controls). We also systemically reviewed all the available evidence regarding the potential association between green tea and risk of ovarian cancer, given the abundance of bioavailable polyphenols and higher antioxidant capacity of green tea than black tea, to provide the best summary estimate of the association.In our case-control study, while we found uniformly inverse odds ratios (OR) for tea drinkers compared to non-tea drinkers [4 + cups/day any tea OR 0.71 (95% CI 0.52-0.97); green tea OR 0.82 (95% CI 0.38-1.79); herbal tea OR 0.77 (95% CI 0.28-2.14): black tea OR 0.88 (95% CI 0.66-1.18)], we saw no dose-response trends. Our meta-analysis provided some evidence that women who drink green tea have a lower risk of ovarian cancer, although the summary estimate did not reach statistical significance (0.58, 95% CI 0.33-1.01 foror=1 cup/green tea day). This result is consistent with two recent meta-analyses that evaluated the association of tea (all types combined) and ovarian cancer risk.Overall, our findings provide some support for the hypothesis that tea consumption reduces the risk of ovarian cancer.

Several studies have found inverse associations between breastfeeding and ovarian cancer occurrence but there are inconsistencies. The relationship with breastfeeding duration is unclear, and it is uncertain whether the association varies according to histological subtype of ovarian cancer. We sought to clarify these issues. Parous women who participated in an Australia-wide population-based case–control study of epithelial ovarian cancer between 2001 and 2005 (1,092 cases and 1,288 controls) completed a reproductive/lifestyle questionnaire. Logistic regression was used to calculate odds ratios and 95% confidence intervals to investigate relations between breastfeeding and ovarian cancer. We found a strong inverse association between total duration of breastfeeding (all episodes combined) and ovarian cancer occurrence (OR = 0.986, 95% CI 0.978–0.994 per month of breastfeeding) that appeared to be independent of parity. However, individual episodes of lactation beyond 12 months conferred no appreciable additional benefit. The relation with breastfeeding appeared to vary by histological subtype such that we saw no association between duration of breastfeeding and borderline serous cancers or mucinous cancers, but inverse associations for the other subtypes, although these were not always statistically significant. A long total duration of breastfeeding appears to be associated with a substantial reduction in the overall risk of ovarian cancer, independent of the decrease in risk due to childbirth, but this may vary according to histological subtype.

Objective: Studies evaluating the relationships between coffee, tea and caffeine and ovarian cancer risk have given inconsistent results. We have examined these associations using data from an Australian population-based case–control study. Methods: Women with epithelial ovarian cancer (EOC)(n = 696) and control women selected from the Electoral Roll (n = 786) provided comprehensive reproductive and lifestyle data and completed a food frequency questionnaire. Results: Increasing coffee consumption was associated with a decreased risk of invasive EOC (p trend = 0.009) with an odds ratio (OR) of 0.51 (95% confidence interval (CI) 0.32–0.80) for consumption of ≥4 cups of coffee per day compared to non-drinkers. The association was significant only for serous and endometrioid/clear cell histological subtypes. There was no association with borderline tumours (OR: 1.20, 95% CI: 0.58–2.47). An inverse relationship was also seen between caffeine intake and EOC but tea consumption was not related to EOC (OR: 1.10 95% CI: 0.76–1.61 for ≥4 cups/day versus none). Conclusions: As tea contributed significantly to caffeine intake in this population we conclude that the association we observed with coffee is not due to caffeine, but to other components within coffee. We suggest future studies consider the type as well as the amount of each beverage consumed.