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Objectives: 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.Methods: 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).Results: 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.Conclusions: 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. [ABSTRACT FROM AUTHOR]

STUDY OBJECTIVE: Low birth weight predicts cardiovascular disease in adulthood, and one possible explanation is that children with lower birth weight consume more fat than those born heavier. Therefore, the objective of this study was to investigate associations between birth weight and childhood diet, and in particular, to test the hypothesis that birth weight is inversely related to total and saturated fat intake. DESIGN: Prospective cohort study. SETTING: South west England. PARTICIPANTS: A subgroup of children enrolled in the Avon longitudinal study of parents and children, with data on birth weight and also diet at ages 8, 18, 43 months, and 7 years (1152, 998, 848, and 771 children respectively). MAIN RESULTS: Associations between birth weight and diet increased in strength from age 8 to 43 months, but had diminished by age 7 years. Fat, saturated fat, and protein intakes were inversely, and carbohydrate intake was positively associated with birth weight at 43 months of age, after adjusting for age, sex, and energy intake. After adjustment for other confounders, all associations were weakened, although there was still a suggestion of a relation with saturated fat (-0.48 (95% CI -0.97, 0.02) g/day per 500 g increase in birth weight. Similar patterns were seen in boys and girls separately, and when the sample was restricted to those with complete data at all ages. CONCLUSIONS: A small inverse association was found between birth weight and saturated fat intake in children at 43 months of age but this was not present at 7 years of age. This study therefore provides little evidence that birth weight modifies subsequent childhood diet. [ABSTRACT FROM AUTHOR]

Background: Surgery for hand trauma accounts for a significant proportion of the plastic surgery training curriculum. The aim of this article is to create a standardised simulation training module for hand fracture fixation on open reduction and internal fixation (ORIF) techniques for residents in order to create a standardised hand-training framework that universally hones their skill and prepares them for their first encounter in a clinical setting., Methods: A step-ladder approach training using three-dimensional (3D)-printed ex vivo hand biomimetics was employed on a cohort of 15 plastic surgery residents ( n  = 15). Assessment of skills using a score system (global rating scale) was performed in the beginning and the end of the module by hand experts in our unit., Results: The overall average score of the cohort pre- and post-assessment were 22.08/50 (44.16%) and 41.54/50 (83.08%) respectively. Significant ( p  < 0.01) difference of improvement of skills was noted on all trainees. All trainees confirmed that the simulated models provided in this module were akin to the patient scenario and noted that it helped them improve their skills with regards to ORIF techniques including improvement of their understanding of the 3D bone topography., Conclusion: We demonstrate a standardised simulation training framework that employs 3D-printed ex vivo hand biomimetics proven to improve the skills of residents and which paves the way to more universal, standardised and validated training across hand surgery. This is, to our knowledge, the first standardised method of simulated training on such hand-surgical cases.Level of Evidence: Not ratable., Competing Interests: Conflict of interestTheodora Papavasiliou is a co-founder of Stelth, the company that manufactured the models described in this paper. Gemma Batten, Oliver Bloom, Jeffrey C. Y. Chan, Charles J. Bain, and Lauren Uppal declare no competing interests., (© The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2023, Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.)

Background: Surgery for hand trauma accounts for a significant proportion of the plastic surgery trainee activity. The aim of this article is to create a standardised simulation training module for flexor tendon repair techniques for residents prior to their first encounter in the clinical setting., Methods: A step-ladder approach flexor tendon repair training with four levels of difficulty was conducted using a three-dimensional (3D) printed anatomical simulation model and a silicone tendon rod on a cohort of 28 plastic surgery Senior House Officers (SHOs) of various stages in their training (n=28). Assessment of knowledge (online questionnaire) and practical skills using validated score systems (global rating scale and task specific score) was performed at the beginning and end of the module by hand experts of our unit., Results: The overall average knowledge-based scores of the cohort pre- and post-assessment were 1.48/5 (29.6%) and 3.56/5 (71.5%), respectively. The overall average skills-based scores of the cohort pre- and post-assessments were 3.05/5 (61%) and 4.12/5 (82.5%), respectively. Significant (p<0.01) difference of improvement of knowledge and skills was noted on all trainees. All trainees confirmed that the training module improved their confidence with flexor tendon repair., Conclusion: We demonstrate a standardised simulation training framework that employs a 3D printed flexor tendon simulation model proven to improve the skills of residents especially during their early learning curve and which paves the way to a more universal, standardised and validated training across hand surgery., Competing Interests: Declaration of Competing Interest Dr Papavasiliou is a co-founder of Stelth, the company that manufactured the model described on this paper. The rest of the authors have nothing to declare., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Surgery for hand trauma accounts for a significant proportion of the plastic surgery training curriculum. The aim of this study was to create a standardized simulation training module for hand fracture fixation with Kirschner wire (K-wire) techniques for residents to create a standardized hand training framework that universally hones their skill and prepares them for their first encounter in a clinical setting., Methods: A step-ladder approach training with 6 levels of difficulty on 3-dimensional (3D) printed ex vivo hand biomimetics was employed on a cohort of 20 plastic surgery residents (n = 20). Assessment of skills using a score system (global rating scale) was performed in the beginning and at the end of the module by hand experts of our unit., Results: The overall average scores of the cohort before and after assessment were 23.75/40 (59.4%) and 34.7/40 (86.8%), respectively. Significant ( P < 0.01) difference of improvement of skills was noted on all trainees. All trainees confirmed that the simulated models provided in this module were akin to the patient scenario and noted that it helped them improve their skills with regard to K-wire fixation techniques, including improvement of their understanding of the 3D bone topography., Conclusions: We demonstrate a standardized simulation training framework that employs 3D printed ex vivo hand biomimetics proved to improve the skills of residents and that paves the way to more universal, standardized and validated training across hand surgery. This is, to our knowledge, the first standardized method of simulated training on such hand surgical cases., (Copyright © 2021 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The American Society of Plastic Surgeons.)

Background: Thyroid cancer incidence has increased in many parts of the world since the 1980s, as has the prevalence of obesity. Evidence suggests that people with greater body size have higher thyroid cancer risk. However, it is unclear whether this association is causal or is driven by over-diagnosis of indolent cancers, because overweight/obese people use health services more frequently than those of normal weight, thus conferring greater opportunity for incidental diagnosis. Assessing whether obesity is associated with higher-risk thyroid cancers might help clarify this issue. Methods: We recruited 1013 people diagnosed with thyroid cancer between 2013 and 2016 and 1057 population controls, frequency matched by sex and age group. We used logistic regression to assess the association between body mass index (BMI) and overall thyroid cancer risk as well as by tumor BRAF mutational status as a marker of potentially higher-risk cancer. Results: Overall, obesity was associated with greater risk of thyroid cancer (odds ratio [OR] = 1.72; 95% confidence interval [CI 1.37-2.16] for obese vs. normal BMI). The association with obesity was significantly stronger for BRAF -mutation positive than BRAF -negative papillary thyroid cancers (PTCs; OR = 1.71 [CI 1.17-2.50] for BRAF- positive vs. BRAF -negative cancers). The increased risks associated with overweight/obesity did not vary by histological subtypes or presence/absence of adverse tumor histologic features. Conclusions: Greater risk of BRAF -mutated PTCs among those with high BMI suggests that the association may not merely reflect greater health care service use and indicates an independent relationship between obesity and clinically important thyroid cancer.

Background: The incidence of thyroid cancer has rapidly increased, and ecological evidence suggests this is due in some part to over-diagnosis. Understanding pathways to diagnosis could help determine whether unnecessary diagnosis can be avoided., Methods: A population-based sample (n = 1007) of thyroid cancer patients diagnosed between July 2013 and August 2016 was recruited from Queensland, Australia (response rate 67%). Information from structured telephone interviews was used to describe diagnostic pathways for thyroid cancer, to investigate factors associated with diagnostic pathways, and to assess the most prevalent modes of diagnoses by which the lowest-risk, potentially over-diagnosed thyroid cancers (intrathyroidal microcarcinomas) are detected., Results: Only 38% of participants presented with symptoms potentially related to thyroid cancer. Older age at diagnosis was associated with a lower prevalence of symptomatic diagnosis (prevalence ratio [PR] = 0.46 [confidence interval (CI) 0.31-0.68] for 70-79 vs. <30 years), as was frequent medical contact, while living in rural/regional areas was associated with a higher prevalence of symptomatic diagnosis (PR = 1.17 [CI 1.00-1.37] for rural/regional areas vs. major cities). Symptomatic diagnosis also occurred more for those whose tumors had adverse histopathological features (larger size, lymph node involvement, lymphovascular invasion). The likelihood of diagnosis of intrathyroidal microcarcinomas was greatest for those having surgical resection or monitoring for benign thyroid disease (PR = 3.87 [CI 2.81-5.32] and PR = 2.21 [CI 1.53-3.18], respectively)., Conclusions: A minority of newly detected thyroid cancer cases were diagnosed because of symptoms. Access to medical care and factors related to cancer aggressiveness were associated with how diagnoses occurred. The likelihood of diagnosing the lowest-risk thyroid cancers was higher in situations related to management of other thyroid conditions. Adherence to thyroid management guidelines could reduce some thyroid cancer over-diagnosis, but ultimately better diagnostic tools are needed to differentiate between indolent cancers and those of clinical significance.

Subclinical oral human papillomavirus (HPV) infection that persists for decades is likely to precede an HPV-driven squamous cell carcinoma of the head and neck, but little is known about the natural history of oral HPV. We systematically reviewed and abstracted data from nine manuscripts that examined human immunodeficiency virus-negative and cancer-free subjects for oral HPV DNA to determine the pooled baseline prevalence and incidence of newly acquired oral HPV infections, and specifically for HPV-16. We also documented the clearance rate and the median time to clearance, where data existed. Of 3762 individuals, 7.5 % had an oral infection with any HPV type (1.6 % for HPV-16). Meta-regression analysis estimated the 12-month cumulative incidence to be 4.8 % (95 % confidence interval 3.2-7.3 %). The overall oral HPV clearance was reported to be 0-80 % between studies, and the median time to clearance from 6.5 to 18 months. Oral HPV-16 clearance was 43-83 %, and median time to clearance for HPV-16 was 7-22 months. Oral HPV prevalence, incidence and clearance vary considerably between published studies from different geographical regions. Further research is required to identify predictors of persistent oral HPV infection. Measurable baseline prevalence was observed in all studies, as well as non-trivial incidence of newly acquired oral HPV infections and incomplete clearance.

Background: Thyroid cancer incidence has been increasing worldwide. Some suggest greater ascertainment of indolent tumours is the only driver, but others suggest there has been a true increase. Increases in Australia appear to have been among the largest in the world, so we investigated incidence trends in the Australian state of Queensland to help understand reasons for the rise., Methods: Thyroid cancers diagnoses in Queensland 1982-2008 were ascertained from the Queensland Cancer Registry. We calculated age-standardized incidence rates (ASR) and used Poisson regression to estimate annual percentage change (APC) in thyroid cancer incidence by socio-demographic and tumour-related factors., Results: Thyroid cancer ASR in Queensland increased from 2·2 to 10·6/100 000 between 1982 and 2008 equating to an APC of 5·5% [95% confidence interval (CI) 4·7-6·4] in men and 6·1% (95% CI 5·5-6·6) in women. The rise was evident, and did not significantly differ, across socio-economic and remoteness-of-residence categories. The largest increase seen was in the papillary subtype in women (APC 7·9%, 95% CI 7·3-8·5). Incidence of localized and more advanced-stage cancers rose over time although the increase was greater for early-stage cancers., Conclusion: There has been a marked increase in thyroid cancer incidence in Queensland. The increase is evident in men and women across all adult age groups, socio-economic strata and remoteness-of-residence categories as well as in localized and more advanced-stage cancers. Our results suggest 'overdiagnosis' may not entirely explain rising incidence. Contemporary aetiological data and individual-level information about diagnostic circumstances are required to further understand reasons for rising thyroid cancer incidence., (© 2015 John Wiley & Sons Ltd.)

Objectives: To estimate the proportion and numbers of cancers in Australia in 2010 attributable to infectious agents., Methods: The population attributable fraction (PAF) and number of cancers caused by hepatitis B and C viruses (HBV, HCV), Helicobacter pylori and human immunodeficiency virus (HIV) were calculated using standard formulae incorporating prevalence of infection in the Australian population, the relative risks associated with that infection and cancer incidence. For cancers with very strong associations to the infectious agent (Epstein-Barr virus [EBV], human papillomavirus [HPV] and HIV/Kaposi's sarcoma herpes virus [KSHV]), calculations were based on viral prevalence in the tumour., Results: An estimated 3,421 cancers (2.9% of all cancers) in Australia in 2010 were attributable to infections. Infectious agents causing the largest numbers of cancers were HPV (n=1,706), H. pylori (n=793) and HBV/HCV (n=518). Cancer sites with the greatest number of cancers caused by infections were cervix (n=818), stomach (n=694) and liver (n=483). Cancers with highest proportions attributable to infectious agents were Kaposi's sarcoma (100%), cervix (100%), nasopharynx (87%), anus (84%) and vagina (70%)., Conclusions: Infectious agents cause more than 3,000 cancers annually in Australia., Implications: Opportunities for cancer prevention through infection control are considerable, even in a 'first world' nation like Australia., (© 2015 The Authors.)

Objectives: To estimate the number and proportion of cancers occurring in Australia in 2010 attributable to consumption deficits in fruit, non-starchy vegetables and dietary fibre., Methods: We estimated the population attributable fraction (PAF) for cancers causally associated with inadequate intake of fruit and non-starchy vegetables (oral cavity, pharynx, oesophageal squamous cell carcinoma, stomach, larynx); inadequate intake of fruit (lung); and insufficient intake of fibre (colorectum). We used standard formulae incorporating prevalence of exposure (1995 National Nutrition Survey) and relative risks from independent studies., Results: Overall, 1,555 (1.4% of all) and 311 (0.3% of all) cancers were attributable to inadequate intakes of fruit and non-starchy vegetables, respectively. A further 2,609 colorectal cancers (18% of colorectal) were attributable to insufficient fibre intake. If Australians increased their fibre intake by eating the recommended daily intakes of fruit and vegetables, an estimated 1,293 (8.8%) colorectal cancers could be prevented., Conclusions: One in six colorectal cancer cases was attributable to inadequate intake of dietary fibre and about 1,800 cancers at other sites were attributable to insufficient fruit and non-starchy vegetable consumption., Implications: Increasing the proportion of Australians who consume the recommended intake of fruit, vegetables and fibre could prevent up to 4% of all cancers., (© 2015 The Authors.)

Objectives: To estimate the proportion and number of cancers in Australia in 2010 that may have been prevented from occurring due to daily use of aspirin in the population., Methods: We calculated the Prevented Fraction (PF) of colorectal and oesophageal cancers using standard formulae. The PF is the proportion of the hypothetical total load of cancer in the population that was prevented by exposure to aspirin. The formula incorporates estimates of the prevalence of aspirin use in Australian adult populations, the relative risks associated with aspirin use and cancer incidence., Results: An estimated 335 colorectal cancers, 22 oesophageal adenocarcinomas and 29 oesophageal squamous cell carcinomas (SCC) were potentially prevented due to daily aspirin use. These figures equate to 2.2%, 3.1% and 5.4% of all colorectal cancers, oesophageal adenocarcinomas and oesophageal SCCs, respectively, that would otherwise have occurred but were potentially avoided due to the daily use of aspirin pertaining in the Australian population., Conclusions: At current levels of consumption, a small but measurable reduction in cancer incidence can be attributed to daily aspirin use., Implications: Assuming the benefits outweigh the harms of known gastrointestinal toxicity and other hazards, aspirin use may be considered for some people to prevent the development of particular gastrointestinal cancers., (© 2015 The Authors.)

Objectives: To estimate the proportion and number of cancers occurring in Australia in 2010 attributable to combined oral contraceptive pill (OCP) use., Methods: We estimated the population attributable fraction (PAF) for cancers causally associated with combined OCP use (breast, cervix), and the proportion of endometrial and ovarian cancers prevented (prevented fraction [PF]). We used standard formulae incorporating prevalence of combined OCP use in the Australian population, relative risks of cancer associated with this exposure and cancer incidence., Results: An estimated 105 breast and 52 cervical cancers (0.7% and 6.4% of each cancer, respectively) in Australia in 2010 were attributable to current use of combined OCP. Past combined OCP use was estimated to have prevented 1,032 endometrial and 308 ovarian cancers in 2010, reducing the number of cancers that would otherwise have occurred by 31% and 19%, respectively., Conclusions: A small proportion of breast and cervical cancers is attributable to combined OCP use; OCP use is likely to have prevented larger numbers of endometrial and ovarian cancers., Implications: Women seeking contraceptive advice should be told of potential adverse effects, but should also be told that - along with reproductive health benefits - combined OCP use can reduce long-term risks of ovarian and endometrial cancers., (© 2015 The Authors.)

Objectives: To estimate the proportion and number of cancers occurring in Australia in 2010 attributable to overweight/obesity., Methods: We estimated the population attributable fraction (PAF) and number of cancers causally associated with overweight/obesity. We used standard formulae incorporating Australian prevalence data for body mass index (BMI), relative risks associated with BMI and cancer. We also estimated the proportion change in cancer incidence (potential impact fraction [PIF]) that may have occurred assuming that the prevalence of overweight/obesity had remained at 1990 levels., Results: An estimated 3,917 cancer cases (3.4% of all cancers) diagnosed in 2010 were attributable to overweight/obesity, including 1,101 colon cancers, 971 female post-menopausal breast cancers and 595 endometrial cancers (PAFs of 10%, 8% and 26%, respectively). Highest PAFs were observed for oesophageal adenocarcinoma (31%), endometrial cancer (26%) and kidney cancer (19%). If the prevalence of overweight/obesity in Australia had remained at levels prevailing in 1990, we estimate there would have been 820 fewer cancers diagnosed in 2010 (PIF 2%)., Conclusions: Overweight/obesity causes a substantial number of cancers in Australia., Implications: Public health strategies to reduce the prevalence of overweight and obesity will reduce the incidence of cancer, particularly of the colon, breast and endometrium., (© 2015 The Authors.)

Objectives: To estimate the proportion and number of cancers occurring in Australia in 2010 attributable to menopausal hormone therapy (MHT) use., Methods: We estimated the population attributable fraction for cancers causally associated with MHT (breast, endometrium, ovary), and the proportion of colorectal cancers prevented by MHT. We used standard formulae incorporating Australian prevalence data, relative risks of cancer associated with MHT and cancer incidence. We also estimated potential change in cancer incidence under two hypothetical scenarios whereby 25% fewer Australian women used MHT, or women exclusively used oestrogen-only MHT., Results: An estimated 539 cancers in Australia in 2010 were attributable to MHT: 453 breast, 67 endometrial and 19 ovarian cancers equating to 3.4%, 3.1% and 1.6% of each cancer type, respectively. In contrast, MHT may have prevented 52 colorectal cancers. If 25% fewer women used MHT, then 141 cancers may have been avoided. If women exclusively used oestrogen-only MHT then 240 cancers may have been avoided., Conclusions: MHT use caused more than 500 cancers in Australian women in 2010 and prevented ∼50 colorectal cancers., Implications: MHT use continues to cause an excess of cancers. The risks, benefits, regimen and treatment duration should be carefully considered for each woman before MHT is commenced., (© 2015 The Authors.)

Objectives: To estimate the proportion and numbers of cancers occurring in Australia attributable to solar ultraviolet radiation (UVR) and the proportion and numbers prevented by regular sun protection factor (SPF) 15+ sunscreen use., Methods: We estimated the population attributable fraction (PAF) and numbers of melanomas and keratinocyte cancers (i.e. basal cell carcinomas and squamous cell carcinomas) due to exposure to ambient UVR resulting from residing in Australia versus residing in the UK (for melanoma) or Scandinavia (for keratinocyte cancers). We also estimated the prevented fraction (PF): the proportion of cancers that would have occurred but were likely prevented by regular sunscreen use., Results: An estimated 7,220 melanomas (PAF 63%) and essentially all keratinocyte cancers occurring in Australia were attributable to high ambient UVR levels in Australia. We estimated that regular sunscreen use prevented around 14,190 (PF 9.3%) and 1,730 (PF 14%) people from developing SCC and melanoma, respectively., Conclusions: Although our approach was conservative, a high proportion of skin cancers in Australia are attributable to high ambient levels of UVR. Prevailing levels of sunscreen use probably reduced skin cancer incidence by 10-15%., Implications: Most skin cancers are preventable. Sunscreen should be a component of a comprehensive sun protection strategy., (© 2015 The Authors.)

Objectives: To estimate the population attributable fraction (PAF) and numbers of cancers occurring in Australia in 2010 attributable to tobacco smoking, both personal and by a partner., Methods: We used a modified Peto-Lopez approach to calculate the difference between the number of lung cancer cases observed and the number expected assuming the entire population developed lung cancer at the same rate as never smokers. For cancers other than lung, we applied the standard PAF formula using relative risks from a large cohort and derived notional smoking prevalence. To estimate the PAF for partners' smoking, we used the standard formula incorporating the proportion of non-smoking Australians living with an ever-smoking partner and relative risks associated with partner smoking., Results: An estimated 15,525 (13%) cancers in Australia in 2010 were attributable to tobacco smoke, including 8,324 (81%) lung, 1,973 (59%) oral cavity and pharynx, 855 (60%) oesophagus and 951 (6%) colorectal cancers. Of these, 136 lung cancers in non-smokers were attributable to partner tobacco smoke., Conclusions: More than one in eight cancers in Australia is attributable to tobacco smoking and would be avoided if nobody smoked., Implications: Strategies to reduce the prevalence of smoking remain a high priority for cancer control., (© 2015 The Authors.)

Objective: To describe the approach underpinning a national project to estimate the numbers and proportions of cancers occurring in Australia in 2010 that are attributable to modifiable causal factors., Methods: We estimated the population attributable fraction (PAF) (or prevented fraction) of cancers associated with exposure to causal (or preventive) factors using standard formulae. Where possible, we also estimated the potential impact on cancer incidence resulting from changes in prevalence of exposure. Analyses were restricted to factors declared causal by international agencies: tobacco smoke; alcohol; solar radiation; infectious agents; obesity; insufficient physical activity; insufficient intakes of fruits, vegetables and fibre; red and processed meat; menopausal hormone therapy (MHT); oral contraceptive pill (OCP); and insufficient breast feeding. Separately, we estimated numbers of cancers prevented by: aspirin; sunscreen; MHT; and OCP use. We discuss assumptions pertaining to latent periods between exposure and cancer onset, choices of prevalence data and risk estimates, and approaches to sensitivity analyses., Results: Numbers and population attributable fractions of cancer are presented in accompanying papers., Conclusions: This is the first systematic assessment of population attributable fractions of cancer in Australia., (© 2015 The Authors.)

Objectives: To estimate the proportion and numbers of cancers occurring in Australia in 2010 attributable to insufficient levels of physical activity., Methods: We estimated the population attributable fraction (PAF) of cancers causally associated with insufficient physical activity (colon, post-menopausal breast and endometrium) using standard formulae incorporating prevalence of insufficient physical activity (<60 minutes at least 5 days/week), relative risks associated with physical activity and cancer incidence. We also estimated the proportion change in cancer incidence (potential impact fraction [PIF]) that may have occurred assuming that everyone with insufficient activity levels increased their exercise by 30 minutes/week., Results: An estimated 1,814 cases of colon, post-menopausal breast and endometrial cancer were attributable to insufficient levels of physical activity: 707 (6.5%) colon; 971 (7.8%) post-menopausal breast; and 136 (6.0%) endometrial cancers. If those exercising below the recommended level had increased their activity level by 30 minutes/week, we estimate 314 fewer cancers (17% of those attributable to insufficient physical activity) would have occurred in 2010., Conclusions: More than 1,500 cancers were attributable to insufficient levels of physical activity in the Australian population., Implications: Increasing the proportion of Australians who exercise could reduce the incidence of several common cancers., (© 2015 The Authors.)

Objective: To estimate the proportion and numbers of cancers occurring in Australia in 2010 that are attributable to alcohol consumption., Methods: We estimated the population attributable fraction (PAF) of cancers causally associated with alcohol consumption using standard formulae incorporating prevalence of alcohol consumption and relative risks associated with consumption and cancer. We also estimated the proportion change in cancer incidence (potential impact fraction [PIF]) that might have occurred under the hypothetical scenario that an intervention reduced alcohol consumption, so that no-one drank >2 drinks/day., Results: An estimated 3,208 cancers (2.8% of all cancers) occurring in Australian adults in 2010 could be attributed to alcohol consumption. The greatest numbers were for cancers of the colon (868) and female breast cancer (830). The highest PAFs were for squamous cell carcinomas of the oral cavity/pharynx (31%) and oesophagus (25%). The incidence of alcohol-associated cancer types could have been reduced by 1,442 cases (4.3%)--from 33,537 to 32,083--if no Australian adult consumed >2 drinks/day., Conclusions: More than 3,000 cancers were attributable to alcohol consumption and thus were potentially preventable., Implications: Strategies that limit alcohol consumption to guideline levels could prevent a large number of cancers in Australian adults., (© 2015 The Authors.)

Objectives: To estimate the proportion and number of cancers occurring in Australia in 2010 attributable to parous women having breastfed for total durations of ≤12 months., Methods: We estimated the population attributable fraction (PAF) of breast cancers (the only cancer site with convincing evidence of causal association) associated with women breastfeeding for ≤12 months in total, using standard formulae incorporating breastfeeding prevalence data, relative risks associated with breastfeeding and cancer incidence. We also estimated the proportion change in disease incidence (potential impact fraction [PIF]) that might have occurred under two hypothetical scenarios of women breastfeeding for longer durations., Results: An estimated 235 (1.7%) breast cancer cases that occurred in Australian in 2010 could be attributed to women breastfeeding for total durations of ≤12 months. Assuming a hypothetical increase in breastfeeding, we estimated that the number of breast cancers prevented would range from 36 to 51 (prevented fraction = 0.3% to 0.4%)., Conclusions: More than 200 breast cancers were attributable to women breastfeeding for total durations of ≤12 months., Implications: Policies to increase breastfeeding duration may help prevent breast cancers in the future., (© 2015 The Authors.)

Objectives: To estimate the proportion and numbers of cancers in Australia in 2010 attributable to consuming red/processed meat., Methods: We estimated the population attributable fraction (PAF) for cancers causally associated with red/processed meat consumption (colon, rectum) using standard formulae incorporating prevalence of consumption (1995 National Nutrition Survey), relative risks associated with consumption and cancer incidence. We also estimated the proportion change in cancer incidence (potential impact fraction [PIF]) that might have occurred under two hypothetical interventions whereby Australian adults reduced their consumption of red/processed meat from prevailing levels to ≤100 g or ≤65 g per day, respectively., Results: An estimated 2,614 cases (18%) of colorectal cancer occurring in Australians in 2010 were attributable to red/processed meat consumption (16% of colon cancers; 23% of rectal cancers). We estimated that if all Australian adults had consumed ≤65 g/day or ≤100 g/day of red/processed meat, then the incidence of colorectal cancer would have been 5.4% (798 cancers) or 1.4% (204 cancers) lower, respectively., Conclusions: About one in six colorectal cancers in Australians in 2010 were attributable to red/processed meat consumption., Implications: Reducing red/processed meat intake may reduce colorectal cancer incidence, but must be balanced against nutritional benefits of modest lean meat consumption., (© 2015 The Authors.)

Objective: To estimate the numbers and proportions of cancers occurring in Australia in 2010 attributable to modifiable causal factors., Methods: We estimated the population attributable fraction (PAF) of cancers associated with exposure to 13 causal factors using standard formulae incorporating exposure prevalence and relative risk data. We also calculated the potential impact of changing exposure to some factors., Results: A total of 32% of all cancers diagnosed in Australia in 2010 (excluding keratinocyte cancers) were attributable to the 13 factors assessed (men 33%; women 31%). Leading factors were tobacco smoke (PAF all cancers: 13.4%), solar radiation (6.2%), inadequate diet (6.1%) and overweight/obesity (3.4%). Factors conferring highest PAFs differed by sex: highest PAFs for men were tobacco smoke (15.8%), solar radiation (7.1%) and alcohol (3.0%); while highest PAFs for women were tobacco smoke (10.1%), solar radiation (5.0%) and overweight/obesity (4.5%). Sites with the highest counts of potentially preventable cancers were lung (8,569), colorectal (7,404), melanoma of the skin (7,220) and breast (3,233)., Conclusions: At least one in three cancers in Australia is attributable to exposure to known modifiable factors., Implications: Up to 37,000 cancers could be prevented in Australia each year if the population avoided exposure to 13 common factors known or strongly suspected to cause cancer., (© 2015 The Authors.)

Many burns surgeons avoid excision and direct closure of acute burns owing to concerns over wound dehiscence, scarring and infection. There is no evidence in the literature to support this practice. We present outcomes of a prospective series of 100 patients who underwent excision and direct closure of 138 burns over a 2-year period, along with results from a survey sent to 33 senior burns surgeons to gauge attitudes towards direct closure in burns surgery. 47% of survey respondents never perform direct closure. Dehiscence was cited as the most common concern, followed by hypertrophic scarring (HTS). In our cohort, the superficial dehiscence rate was 12% and the HTS rate was 16%, with no scarring contractures. Patients with healing time greater than 14 days were more likely to develop HTS (p=0.008), as were those with wound dehiscence (p=0.014). Patients undergoing part-grafting in addition to direct closure took significantly longer to heal than those undergoing direct closure alone (p=0.0002), with the donor site or graft delaying healing in the majority. Excision and direct closure of acute burn wounds avoids donor site morbidity and has an acceptable complication rate. It is a safe and effective treatment for full thickness burns in selected cases., (Copyright © 2014 Elsevier Ltd and ISBI. All rights reserved.)

Aim: Obesity is an established risk factor for endometrial cancer. Associations tend to be stronger for the endometrioid subtype. The role of adult weight change and weight cycling is uncertain. Our study aimed to determine whether there is an association between different adult weight trajectories, weight cycling and risk of endometrial cancer overall, and by subtype., Methods: We analysed data from the Australian National Endometrial Cancer study, a population-based case-control study that collected self-reported information on height, weight at three time points (age 20, maximum and 1 year prior to diagnosis [recent]), intentional weight loss/regain (weight cycling) from 1398 women with endometrial cancer and 1538 controls. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using multivariable logistic regression analysis., Results: Relative to women who maintained a stable weight during adulthood, greater weight gain after the age of 20 was associated with increased risk of endometrial cancer (OR for gain 40+kg all subtypes 5.3, 95% CI 3.9-7.3; endometrioid 6.5, 95% CI 4.7-9.0). The strongest associations were observed among women who were continually overweight from the age of 20 (all subtypes OR 3.6, 95% CI 2.6-5.0). Weight cycling was associated with increased risk, particularly among women who had ever been obese (OR 2.9 95% CI 1.8-4.7), with ~3-fold risks seen for both endometrioid and non-endometrioid tumour subtypes. Women who had intentionally lost weight and maintained that weight loss were not at increased risk., Conclusion: These results suggest that higher adult weight gain, and perhaps weight cycling, independently increase the risk of endometrial cancer, however women who lost weight and kept that weight off were not at increased risk., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

While dietary antioxidants are emerging as potentially modifiable risk factors for esophageal adenocarcinoma (EAC), studies on dietary antioxidants and its precursor Barrett's esophagus (BE) are limited. The present study extends previous work on BE by investigating risks of nondysplastic BE, dysplastic BE and EAC associated with intake of antioxidants such as vitamin C, vitamin E, β-carotene, and selenium. Age and sex matched control subjects (n=577 for BE; n=1,507 for EAC) were sampled from an Australian population register. Information on demography, and well established EAC risk factors were obtained using self-administered questionnaires. Intake of antioxidants for patients newly diagnosed with nondysplastic BE (n=266), dysplastic BE (n=101), or EAC (n=299), aged 18-79 years, were obtained using a food frequency questionnaire. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using multivariable adjusted logistic regression models. High intake of β-carotene from food and supplement sources combined was inversely associated with risk of dysplastic BE (OR Q4 vs. Q1=0.45; 95%CI: 0.20-1.00). High intake of vitamin E from food sources (OR Q4 vs. Q1=0.43; 95%CI: 0.28-0.67), from food and supplements combined (OR Q4 vs. Q1=0.64; 95%CI: 0.43-0.96), and a high antioxidant index score were inversely associated with risk of EAC. We found no significant trends between intake of β-carotene, vitamin C, vitamin E, and selenium and risk of nondysplastic or dysplastic BE. However, our data suggest that a high intake of β-carotene may be associated with decreased risk of dysplastic BE., (Copyright © 2013 UICC.)

We present a case of infection of an alloplastic chin implant occurring 45 years after placement. The patient was referred to the clinic with an ulcerated submental lesion, which was thought to be a squamoproliferative lesion until surgery. The authors discuss the management of the case with reference to the literature on genioplasty and late infection of alloplastic implants., (Copyright © 2012 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved.)

Background/objective: Folates are essential for DNA synthesis and methylation, and thus may have a role in carcinogenesis. Limited evidence suggests folate-containing foods might protect against some cancers and may partially mitigate the increased risk of breast cancer associated with alcohol intake, but there is little information regarding ovarian cancer. Our aim was to evaluate the role of folate and related micronutrients, polymorphisms in key folate-metabolising genes and environmental factors in ovarian carcinogenesis., Subjects/methods: Participants in the Australian Ovarian Cancer Study (1363 cases, 1414 controls) self-completed risk factor and food-frequency questionnaires. DNA samples (1638 cases, 1278 controls) were genotyped for 49 tag single-nucleotide polymorphisms (SNPs) in the methylene tetrahydrofolate reductase (MTHFR), methionine synthase (MTR) and MTR reductase (MTRR) genes. Logistic regression models were used to generate adjusted odds ratios and 95% confidence intervals., Results: We saw no overall association between the intake of folate, B vitamins or other methyl donors and ovarian cancer risk, although increasing folate from foods was associated with reduced risk among current smokers (P(trend)=0.03) and folic acid intake was associated with borderline significant increased risks among women who consumed ≥1 standard alcoholic drinks/day (odds ratio (OR)=1.64; 95% confidence interval (CI) 1.05-2.54, P(trend)=0.05). Two SNPs (rs7365052, rs7526063) showed borderline significant inverse associations with ovarian cancer risk; both had very low minor allele frequencies. There was little evidence for interaction between genotype and micronutrient intake or for variation between different histological subtypes of ovarian cancer., Conclusions: Our data provide little evidence to support a protective role for folate in ovarian carcinogenesis but suggest further evaluation of the joint effects of folic acid and alcohol is warranted.

Background: Nursing and midwifery are demanding professions. Efforts to understand the health consequences and workforce needs of these professions are urgently needed. Using a novel electronic approach, the Nurses and Midwives e-cohort Study (NMeS) aims to investigate longitudinally Australian and New Zealand nurses' and midwives' work/life balance and health. This paper describes NMeS participation; provides key baseline demographic, workforce and health indicators; compares these baseline descriptions with external norms; and assesses the feasibility of the electronic approach., Methods: From 1 April 2006 to 31 March 2008, nurses in Australia and New Zealand, and midwives in Australia were invited to participate. Potential participants were directed to a purpose-built NMeS Internet site, where study information was provided and consent sought. Once obtained, a range of standardized tools combined into one comprehensive electronic questionnaire was elicited., Results: Overall, 7633 (2.3%) eligible nurses and midwives participated (6308 from Australia and 1325 from New Zealand) from a total pool of 334,400. Age, gender, occupational and health profiles were similar between countries and to national figures. However, some differences were noted; for instance, Queensland participants were over-represented, while Victorian and South Australian participants were under-represented, and 28.2% of Australians were in high strain positions compared with 18.8% of New Zealanders., Conclusions: Using an internationally novel web-based approach, a large cohort, which appears generally similar to population norms, has been established. Provided participant retention is adequate, the NMeS will provide insight into understanding the drivers of nurses' and midwives' workforce retention and work-related factors associated with their health., (© 2011 The Authors. International Nursing Review © 2011 International Council of Nurses.)

Objective: 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., Methods: 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., Results: 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 for >or=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., Conclusion: Overall, our findings provide some support for the hypothesis that tea consumption reduces the risk of ovarian cancer.

Background: Variation in meat and fish intakes has been associated with a risk of some cancers, but evidence for ovarian cancer is limited and inconsistent., Objective: We examined the association between intakes of total meat, red meat, processed meat, poultry, and fish and ovarian cancer risk., Design: Data came from 2 Australian population-based case-control studies conducted 10 y apart. Analyses included a total of 2049 cases and 2191 control subjects. We obtained dietary information via a food-frequency questionnaire. We estimated multivariable-adjusted odds ratios (ORs) for each study by using logistic regression and combined results of the 2 studies by using random-effects models. We also assembled the published evidence in a systematic review and meta-analysis., Results: Although there was no association between total or red meat intake and ovarian cancer risk, women with the highest intake of processed meat had a significantly increased risk of ovarian cancer in the 2 case-control studies (combined OR: 1.18; 95% CI: 1.15, 1.21) and the meta-analysis [7 studies; pooled relative risk (RR): 1.20; 95% CI: 1.07, 1.34]. In contrast, a frequent intake of poultry was associated with borderline significant reductions in risk in the 2 case-control studies (combined OR: 0.83; 95% CI: 0.67, 1.03) and the meta-analysis including 7 additional studies (pooled RR: 0.90; 95% CI: 0.79, 1.01). High fish intake was associated with a significantly reduced risk in the 2 case-control studies (combined OR: 0.76; 95% CI: 0.62, 0.94) and a smaller borderline significant reduction in the meta-analysis (6 additional studies; pooled RR: 0.84; 95% CI: 0.68, 1.03)., Conclusion: Our results suggest that low consumption of processed meat and higher consumption of poultry and fish may reduce the risk of ovarian cancer.

In 1998, Risch proposed a hypothesis for the pathogenesis of ovarian cancer relating to the role of androgens in stimulating epithelial cell proliferation. Although this hypothesis has been widely discussed, direct evidence to support it is scant. To address this issue, we have conducted a detailed analysis of factors possibly associated with high circulating levels of androgens, including polycystic ovary syndrome (PCOS), hirsutism and acne (all clinically associated with hyperandrogenism) using the data collected in an Australia-wide, population-based case-control study. Cases aged 18-79 years with a new diagnosis of invasive epithelial ovarian cancer (n=1276) or borderline malignant tumour (n=315) were identified through a network of clinics and cancer registries throughout Australia. Controls (n=1508) were selected from the National Electoral Roll. Women self-reported a history of PCOS, acne, hirsutism and also use of testosterone supplements or the androgenic medication Danazol. We found no evidence that a history of PCOS, acne or hirsutism was associated with ovarian cancer overall, or with specific subtypes, with the exception of serous borderline tumours that were positively associated with a history of PCOS (OR 2.6; 95% CI 1.0-6.1). Women who had ever used testosterone supplements had an increased risk of ovarian cancer (OR 3.7; 95% CI 1.1-12.0); however, use of the androgenic medication Danazol did not increase risk (OR 1.0; 95% CI 0.4-2.9). Overall, our results do not support the hypothesis that androgen-related disorders increase the risk of ovarian cancer.

Leukoplakia is an asymptomatic, potentially malignant change in the oral mucosa. Previous studies have reported that smoking and betel quid chewing are associated with increased risk of leukoplakia; few studies have reported on these associations in populations where betel quid does not contain tobacco. We conducted a case-control study nested in a cross-sectional study in Papua New Guinea and a systematic review of studies that included chewers of betel quid without tobacco. Our study recruited 1,670 adults. We recorded betel quid chewing and smoking. The prevalence of leukoplakia was 11.7%. In the nested case-control study of 197 cases and 1,282 controls, current betel chewing was associated with increased risk of leukoplakia with an adjusted odds ratio for current chewers of 3.8 (95% CI 1.7, 8.4) and in the heaviest chewers of 4.1 (95% CI 1.8, 9.1) compared to non-chewers. Current smoking was associated with an increased risk of leukoplakia with an adjusted odds ratio for current smokers of 6.4 (95% CI 4.1, 9.9) and amongst heaviest smokers of 9.8 (95% CI 5.9, 16.4) compared to non-smokers. The systematic review identified 5 studies examining risk of leukoplakia associated with betel quid chewing in populations where betel quid did not contain tobacco and that controlled for smoking. In studies that adjusted for smoking, the combined random effect odds ratio was 7.9 (95% CI 4.3, 14.6) in betel quid chewers. The results of this study and systematic review of similar studies provide evidence of the role of betel quid not containing tobacco and leukoplakia.

Reproductive and hormonal exposures are known to influence ovarian carcinogenesis, but little is known about the effect of these factors on survival. We have studied survival according to hormonal and reproductive history in a population-based cohort of 676 Australian women aged 18-79, newly diagnosed with invasive epithelial ovarian cancer in the early 1990s. In order to place our findings in context, we have also undertaken a systematic review of the pertinent literature. Detailed information about each woman's reproductive and contraceptive history was obtained from pregnancy and contraceptive calendars at the time of diagnosis. Cox regression was used to obtain multivariate adjusted hazard ratios (HR) and 95% confidence intervals (CI). A total of 419 (62%) of the 676 women died during the follow-up (giving a 5-year survival proportion of 44%). Apart from better survival for women who had ever breastfed (multivariate HR 0.74, 95% CI 0.55-0.98), we found no association between survival from invasive ovarian cancer and a range of hormonal and gynecological factors including parity, use of oral contraceptives, and histories of tubal sterilization or hysterectomy. Systematic review of the literature generally supported the lack of influence of these factors on survival from ovarian cancer. We conclude that, except for a possible survival advantage among women with a history of breastfeeding, reproductive and hormonal exposures prior to diagnosis do not influence survival from invasive ovarian cancer, in contrast to their substantial effects on etiology of this disease.

Background: Frequent consumption of aspirin and nonsteroidal anti-inflammatory drugs (NSAID) has been associated with reduced occurrence of cancers of the esophagus, although potential modifying effects of other causal factors remain relatively unexplored., Methods: We compared nationwide samples of Australian patients with adenocarcinomas of the esophagus (EAC; n = 367) or esophagogastric junction (EGJAC; n = 426) or esophageal squamous cell carcinoma (ESCC; n = 309) with control participants sampled from a population register (n = 1,580). Intakes of aspirin, other NSAIDs, and acetaminophen (paracetamol) were assessed from self-reports. We calculated odds ratios (OR) and 95% confidence intervals (95% CI) using multivariable logistic regression., Results: Compared with never-users of aspirin, those who used aspirin at least weekly had significantly lower risks of EAC (OR, 0.48; 95% CI, 0.32-0.72), EGJAC (OR, 0.71; 95% CI, 0.49-1.01), and ESCC (OR, 0.63; 95% CI, 0.40-0.98). At least weekly use of other NSAIDs was also associated with reduced risks of EAC (OR, 0.74; 95% CI, 0.51-1.08), EGJAC (OR, 0.53; 95% CI, 0.37-0.77), and ESCC (OR, 0.46; 95% CI, 0.30-0.73). No association was observed between frequent use of acetaminophen and esophageal cancer. Risk reductions for EAC among users of aspirin and NSAIDs were greater among those who experienced at least weekly symptoms of reflux (OR, 0.26; 95% CI, 0.12-0.55 and OR, 0.41; 95% CI, 0.21-0.77, respectively) than those who did not experience reflux (OR, 0.96; 95% CI, 0.46-2.00 and OR, 0.78; 95% CI, 0.35-1.72, respectively). Recent use of NSAIDs in the past 5 years was associated with greater risk reductions., Conclusions: Frequent use of aspirin and NSAIDs is associated with reduced occurrence of esophageal cancers, particularly among those with frequent symptoms of gastroesophageal reflux.

Invasive serous cancers are diagnosed in the ovary, fallopian tube and peritoneum. It is widely believed that these are variants of the same malignancy but little is known about fallopian tube and primary peritoneal cancers. A comparison of risk factors for these tumor types may shed light on common or distinct aetiological pathways involved in these types of cancer. We investigated risk factors for the three cancers using data from a large Australian population-based case-control study. We included women with incident invasive serous ovarian (n = 627), primary peritoneal (n = 129) and fallopian tube (n = 45) cancer and 1,508 control women. Participants completed a comprehensive reproductive and lifestyle questionnaire. Logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). Hormonal contraceptive use was inversely related to risk of all three cancers. Parity and breast-feeding were also inversely related to risk of serous ovarian and fallopian tube cancer. In contrast, parous women had an increased risk of peritoneal cancer (OR = 1.8, 95%CI 0.8-3.9), and increasing parity did not lower risk. There was also no association between breast-feeding and peritoneal cancer. However, obesity was associated with a doubling of risk for peritoneal cancer alone (OR = 2.1, 95%CI = 1.3-3.4). The strikingly similar patterns of risk for serous ovarian and fallopian tube cancers and the somewhat different results for primary peritoneal cancer suggest that peritoneal cancers may develop along a different pathway. These results also call into question the role of the physical effects of ovulation in the development of serous ovarian cancer., ((c) 2007 Wiley-Liss, Inc.)

Objective: To measure the relative risks of adenocarcinomas of the oesophagus and gastro-oesophageal junction associated with measures of obesity, and their interactions with age, sex, gastro-oesophageal reflux symptoms and smoking., Design and Setting: Population-based case-control study in Australia., Patients: Patients with adenocarcinomas of the oesophagus (n = 367) or gastro-oesophageal junction (n = 426) were compared with control participants (n = 1580) sampled from a population register., Main Outcome Measure: Relative risk of adenocarcinoma of the oesophagus or gastro-oesophageal junction., Results: Risks of oesophageal adenocarcinoma increased monotonically with body mass index (BMI) (p(trend) <0.001). Highest risks were seen for BMI >or=40 kg/m2 (odds ratio (OR) = 6.1, 95% CI 2.7 to 13.6) compared with "healthy" BMI (18.5-24.9 kg/m2). Adjustment for gastro-oesophageal reflux and other factors modestly attenuated risks. Risks associated with obesity were substantially higher among men (OR = 2.6, 95% CI 1.8 to 3.9) than women (OR = 1.4, 95% CI 0.5 to 3.5), and among those aged <50 years (OR = 7.5, 95% CI 1.7 to 33.0) than those aged >or=50 years (OR = 2.2, 95% CI 1.5 to 3.1). Obese people with frequent symptoms of gastro-oesophageal reflux had significantly higher risks (OR = 16.5, 95% CI 8.9 to 30.6) than people with obesity but no reflux (OR = 2.2, 95% CI 1.1 to 4.3) or reflux but no obesity (OR = 5.6, 95% 2.8 to 11.3), consistent with a synergistic interaction between these factors. Similar associations, but of smaller magnitude, were seen for gastro-oesophageal junction adenocarcinomas., Conclusions: Obesity increases the risk of oesophageal adenocarcinoma independently of other factors, particularly among men. From a clinical perspective, these data suggest that patients with obesity and frequent symptoms of gastro-oesophageal reflux are at especially increased risk of adenocarcinoma.

It remains unclear whether physical activity is associated with epithelial ovarian cancer risk. We therefore examined the association between recreational physical activity and risk of ovarian cancer in a national population-based case-control study in Australia. We also systematically reviewed all the available evidence linking physical activity with ovarian cancer to provide the best summary estimate of the association. The case-control study included women ages 18 to 79 years with a new diagnosis of invasive (n=1,269) or borderline (n=311) epithelial ovarian cancer identified through a network of clinics, physicians, and state cancer registries throughout Australia. Controls (n=1,509) were randomly selected from the national electoral roll and were frequency matched to cases by age and state. For the systematic review, we identified eligible studies using Medline, the ISI Science Citation Index, and manual review of retrieved references, and included all case-control or cohort studies that permitted assessment of an association between physical activity (recreational/occupational/sedentary behavior) and histologically confirmed ovarian cancer. Meta-analysis was restricted to the subset of these studies that reported on recreational physical activity. In our case-control study, we observed weakly inverse or null associations between recreational physical activity and risk of epithelial ovarian cancer overall. There was no evidence that the effects varied by tumor behavior or histologic subtype. Twelve studies were included in the meta-analysis, which gave summary estimates of 0.79 (95% confidence interval, 0.70-0.85) for case-control studies and 0.81 (95% confidence interval, 0.57-1.17) for cohort studies for the risk of ovarian cancer associated with highest versus lowest levels of recreational physical activity. Thus, pooled results from observational studies suggest that a modest inverse association exists between level of recreational physical activity and the risk of ovarian cancer.

Torsion or rupture of an ovarian cyst may present as an acute abdomen. A case is presented where the diagnosis was made at laparoscopy and laparoscopic resection was done. Controlled aspiration of the cyst contents allowed the cyst to be easily removed from the abdomen.

Smoking and betel quid chewing are associated with increased risk of oral cancer but few studies have reported on associations in populations where betel quid does not contain tobacco. We conducted a case-control study in Papua New Guinea and a systematic review. Our case-control study recruited 143 cases with oral cancer and 477 controls. We collected information on smoking and betel quid chewing. Current smoking was associated with an increased risk of oral cancer with an adjusted odds ratio (OR) for daily smokers of 2.63 (95% confidence intervals (95% CI) 1.32, 5.22) and amongst heaviest smokers of 4.63 (95% CI 2.07, 10.36) compared to never-smokers. Betel chewing was associated with increased risk of oral cancer with an adjusted OR for current chewers of 2.03 (95% CI 1.01, 4.09) and in the heaviest chewers of 2.47 (95% CI 1.13, 5.40) compared to nonchewers. The OR in those who both smoked tobacco and chewed betel quid was 4.85 (95% 1.10, 22.25), relative to those who neither smoked nor chewed. The systematic review identified 10 previous studies that examined risk of oral cancer associated with betel quid chewing that controlled for smoking in populations where betel quid did not contain tobacco. In studies that reported results for non-smokers the combined OR was 2.14 (95% CI 1.06, 4.32) in betel quid chewers and in studies that adjusted for smoking the combined OR was 3.50 (95% CI 2.16, 5.65) in betel quid chewers. Preventive efforts should discourage betel quid chewing as well as smoking., ((c) 2006 Wiley-Liss, Inc.)

We have examined the association between cigarette smoking and ovarian cancer survival in 676 women with invasive epithelial ovarian cancer, recruited into a case-control study in the early 1990s. Information about cigarette smoking and other personal and reproductive factors was obtained from a personal interview at the time of diagnosis. Cox proportional hazards models were used to evaluate the association between cigarette smoking and time to ovarian cancer death. Current smokers at diagnosis were more likely to die early than women who had never smoked [adjusted hazard ratio (HR), 1.36; 95% confidence interval (95% CI), 1.01-1.84]. Increased risks of dying were greater among those who had accumulated more pack-years of smoking (HR for 30+ pack-years compared with never smokers, 1.94; 95% CI, 1.41-2.66) and smoked more cigarettes per day (HR, 1.93; 95% CI, 1.37-2.73). All these associations were stronger among women with late-stage disease (HR for current versus never smokers, 1.58; 95% CI, 1.15-2.18). Time since quitting had little effect on survival after adjusting for lifetime smoking exposure. These results validate and extend recent findings and suggest that premorbid cigarette smoking is related to worse outcome in ovarian cancer patients.

Objective: To compare the accuracy, costs and utility of using the National Death Index (NDI) and state-based cancer registries in determining the mortality status of a cohort of women diagnosed with ovarian cancer in the early 1990s., Methods: As part of a large prognostic study, identifying information on 822 women diagnosed with ovarian cancer between 1990 and 1993, was simultaneously submitted to the NDI and three state-based cancer registries to identify deceased women as of June 30, 1999. This was compared to the gold standard of "definite deaths". A comparative evaluation was also made of the time and costs associated with the two methods., Results: Of the 450 definite deaths in our cohort the NDI correctly identified 417 and all of the 372 women known to be alive (sensitivity 93%, specificity 100%). Inconsistencies in identifiers recorded in our cohort files, particularly names, were responsible for the majority of known deaths not matching with the NDI, and if eliminated would increase the sensitivity to 98%. The cancer registries correctly identified 431 of the 450 definite deaths (sensitivity 96%). The costs associated with the NDI search were the same as the cancer registry searches, but the cancer registries took two months longer to conduct the searches., Conclusions and Implications: This study indicates that the cancer registries are valuable, cost effective agencies for follow-up of mortality outcome in cancer cohorts, particularly where cohort members were residents of those states. For following large national cohorts the NDI provides additional information and flexibility when searching for deaths in Australia. This study also shows that women can be followed up for mortality with a high degree of accuracy using either service. Because each service makes a valuable contribution to the identification of deceased cancer subjects, both should be considered for optimal mortality follow-up in studies of cancer patients.