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Aim. To assess the effect of various lifestyle risk factors on the risk of salivary gland cancer in Canada using data from a population-based case-control study.Methods. Data from a population-based case-control study of 132 incident cases of salivary gland cancer and 3076 population controls were collected through self-administered questionnaire and analysed using unconditional logistic regression.Results. Four or more servings/week of processed meat product was associated with an adjusted odds ratio (OR) and corresponding 95% confidence interval (CI) of 1.62 (1.02–2.58). Nonsignificantly increased ORs were also related to obesity, >7 drinks/week of alcohol consumption, and occupational exposure to radiation. Furthermore, nonsignificantly decreased ORs were found to be associated with high education level (>12 years) (OR=0.65), high consumption of spinach/squash (OR=0.62) and all vegetables/vegetable juices (OR=0.75), and >30 sessions/month of recreational physical activity (OR=0.78).Conclusions. This study suggests positive associations with consumption of processed meat, smoking, obesity, alcohol drinking, and occupational exposure to radiation as well as negative associations with higher education, consumption of spinach/squash, and physical activity, which suggest a role of lifestyle factors in the etiology of salivary gland cancer. However, these findings were based on small number of cases and were nonsignificant. Further larger studies are warranted to confirm our findings.

Background: Cosmetic breast implants may impair the ability to detect breast cancers. The aims of this study were to examine whether implants and implant characteristics are associated with more advanced breast tumors at diagnosis and poorer survival. Methods: Study population includes all invasive breast cancer cases diagnosed during follow-up of the large Canadian Breast Implant Cohort. A total of 409 women with cosmetic breast implants and 444 women with other cosmetic surgery were diagnosed with breast cancer. These women were compared for stage at diagnosis using multinomial logistic regression models. Cox proportional hazards regression models were used for breast cancer-specific mortality analyses. Comparisons were also conducted according to implant characteristics. Results: Compared with women with other cosmetic surgery, those with cosmetic breast implants had at later stage breast cancer diagnosis (OR of having stage III/IV vs. stage I at diagnosis: 3.04, 95% confidence interval (CI): 1.81–5.10; P < 0.001). A nonstatistically significant increase in breast cancer-specific mortality rate for women with breast implants relative to surgical controls was observed (HR = 1.32, 95% CI: 0.94–1.83, P = 0.11). No statistically significant differences in stage and breast cancer mortality were observed according to implant characteristics. Conclusions: At diagnosis, breast cancers tended to be at more advanced stages among women with cosmetic breast implants. Breast cancer-specific survival was lower in these women although the reduction did not reach statistical significance. Impact: Further investigations of the effect of breast implants on breast cancer prognosis are warranted. Cancer Epidemiol Biomarkers Prev; 21(10); 1868–76. ©2012 AACR.

Cosmetic breast implants are not associated with increased breast cancer incidence, but variations of risk according to implant characteristics are still poorly understood. As well, the assessment of cancer risk for sites other than breast needs to be clarified. The purpose of this study was to fill these research gaps. This study presents an extended analysis of 10 more years of follow-up of a large Canadian cohort of women who received either cosmetic breast implants (n = 24,558) or other cosmetic surgery (15,893). Over 70% of the implant cohort was followed for over 20 years. Cancer incidence among implant women was compared to those of controls using multivariate Poisson models and the general female population using the standardized incidence ratios (SIRs). Women with breast implants had reduced rates of breast and endometrial cancers compared to other surgery women. Subglandular implants were associated to a reduced rate of breast cancer compared to submuscular implants [incidence rate ratio (IRR) = 0.78, 95% confidence interval (CI) = 0.63-0.96] and this reduction persisted over time. We observed a sevenfold increased rate (IRR = 7.36, 95% CI = 1.86-29.12) of breast cancer in the first 5 years after the date of surgery for polyurethane-coated subglandular implant women but this IRR decreased progressively over time (p value for trend = 0.02). We also observed no increased risk of rarer forms of cancer among augmented women. A reduction in breast cancer incidence was observed for women with subglandular implants relative to women with submuscular implants. Possible increase of breast cancer incidence shortly after breast augmentation with polyurethane implants needs to be verified.

Objective: The relationship between breast cancer risk and residential proximity to paper mills, pulp mills, petroleum refineries, steel mills, thermal power plants, alum smelters, nickel smelters, lead smelters, copper smelters, and zinc smelters was assessed. Methods: We conducted a population-based case-control study of 2343 cases with breast cancer and 2467 controls using residential proximity at some time between 1960 and 5 years before the completion of questionnaire in Canada. Results: Adjusted odds ratios were statistically significantly increased for residing near steel mills (0.8 to 3.2 km) and thermal power plants (

Background Insulin resistance is a pathogenic factor for type II diabetes and has been associated with metabolic abnormalities and adverse clinical outcomes. The purpose of this study was to examine the relationship between insulin resistance and socio-demographics, adiposity and behavioral factors in the general, non-diabetic adult Canadian population. Methods Data for 3515 non-diabetic adults aged 18 to 79 years from the Canadian Health Measures Survey (cycles 1 and 2, 2007–2011) were analyzed. Insulin resistance index was measured by the homeostasis model assessment of insulin resistance (HOMA-IR), and insulin resistance (IR) was defined as individuals in the highest quartile of the HOMA-IR index. Logistic regression models were used to examine the effect of demographics, lifestyle factors and adiposity measurements on HOMA-IR. Results The risk of IR increased with age, particularly in men. Individuals had adjusted odds ratio (OR) (with corresponding 95 % confidence interval) of 5.97 (2.90–8.52) and 25.12 (15.20–41.51) associated with a body-mass-index (BMI) between 25.0 and 0.57), and of 6.30 (4.33–9.16) with a high waist-to-hip ratio (>0.90 for men and >0.85 for women). Physically inactive people and non-alcohol consumer also had a significantly higher odd of IR. Conclusions This study found that men and older, obese and physically inactive people were at increased risk for IR. Adiposity indices including BMI, waist circumstance, waist-to-height ratio and waist-to-hip ratio were highly associated with IR with similar magnitude of association.

Objective: To examine national trends in mortality rates for injuries among Canadian children younger than 15 years in 1979–2002. Methods: Data on injury deaths were obtained from the Canadian Vital Statistics system at Statistics Canada. Injuries were classified using the codes for external cause of injury and poisoning (E-codes) by intent and by mechanism. Mortality rates were age adjusted to the 1990 world standard population. Negative binomial regression was used to estimate the secular trends. Results: Annual mortality rates for total and unintentional injuries declined substantially (from 23.8 and 21.7 in 1979 to 7.2 and 5.8 in 2002, respectively), whereas suicide deaths among children aged 10–14 showed an increasing trend. All Canadian provinces and territories showed a decreasing trend in mortality rates of total injuries. Motor vehicle related injuries were the most common cause of injury deaths (accounted for an average of 36.4% of total injury deaths), followed by suffocation (14.3%), drowning (13.5%), and burning (11.1%); however, suffocation was the leading cause for infants. The number of potential years of life lost due to injury before age 75 decreased from 89 343 in 1979 to 27 948 in 2002 for children aged 0–14 years. Conclusions: During the period 1979–2002, there were dramatic decreases in childhood mortality for total injuries and unintentional injuries as well as various degrees of reduction for all causes of injury except suffocation in children aged 10–14 years and drowning in infants. The reason for the reduction in injury mortality might be multifactoral.

The authors conducted a population-based case-control study of 1,030 cases with histologically confirmed, incident non-Hodgkin’s lymphoma (NHL) and 3,106 controls to assess the impact of recreational physical activity, obesity, and energy intake on NHL risk in Canada from 1994 to 1997. Compared with those for subjects in the lowest quartiles of total recreational physical activity, multivariable-adjusted odds ratios for subjects in the highest quartile were 0.79 (95% confidence interval (CI): 0.59, 1.05) for men and 0.59 (95% CI: 0.42, 0.81) for women. Obesity (body mass index � 30 kg/m 2 ) was associated with odds ratios of 1.59 (95% CI: 1.18, 2.12) for men and 1.36 (95% CI: 1.00, 1.84) for women. For men and women with a lifetime maximum body mass index of � 30 kg/m 2 , respective odds ratios were 1.55 (95% CI: 1.16, 2.06) and 1.10 (95% CI: 0.83, 1.46). For men and women in the highest quartiles of calorie intake, respective odds ratios were 1.95 (95% CI: 1.45, 2.62) and 1.13 (95% CI: 0.84, 1.52). Some differences were found between histologic subtypes of NHL for these associations. This study suggests that recreational physical activity decreases NHL risk, while obesity and excess calorie intake increase it. More studies are needed to confirm these results, especially the differences between histologic subtypes. case-control studies; energy intake; exercise; lymphoma, non-Hodgkin; obesity; recreation

We sought to examine the impact of occupational exposure on brain cancer risk.Mailed questionnaires were used to collect information on lifetime employment history, occupational exposure to 18 chemicals, and other risk factors for 1009 incident cases of brain cancer and 5039 control subjects in Canada in 1994 to 1997.People exposed to asphalt and welding had respective odds ratio (and 95% confidence interval) of 1.29 (1.02-1.62) and 1.26 (0.98-1.45). An increased risk of brain cancer might be associated with exposure to asbestos, benzene, mineral or lubricating oil, isopropyl oil, and wood dust and with following occupations: teaching; protective service; metal processing and related jobs, and metal shaping and forming; knitting in textile processing; construction trades; and transport equipment operating.Our study suggests a possible role for occupational exposure in the etiology of brain cancer.

We evaluated the impact of recreational and occupational physical activity on ovarian cancer risk using data from a population-based case-control study of 442 cases with histologically confirmed incident ovarian cancer and 2,135 controls aged 20-76 years, conducted in 1994-1997 in Canada. Frequency and intensity of physical activity were collected through self-administered questionnaires. Compared to women in the lowest tertiles of moderate, vigorous and total recreational activity, those in the highest tertiles had multivariable-adjusted odds ratios (and 95% confidence intervals) of 0.67 (0.50-0.88), 0.93 (0.70-1.24) and 0.73 (0.58-0.98), respectively. There were statistically significant trends of decreasing risk with increasing levels of moderate and total recreational activity, with similar patterns for premenopausal and postmenopausal women. A significant reduction in risk associated with higher level of moderate recreational activity was observed for serous, endometrioid and other but not mucinous types of tumors. The analyses in one province with the largest number of cases and controls indicated that occupational activity was associated with reduced ovarian cancer risk by lifetime activity and by various life periods (early 20s, early 30s, early 50s and 2 years before interview). Our study suggests that occupational and regular moderate recreational physical activity reduce ovarian cancer risk.

The authors conducted a population-based, case-control study of 21,022 incident cases of 19 types of cancer and 5,039 controls aged 20-76 years during 1994-1997 to examine the association between obesity and the risks of various cancers. Compared with people with a body mass index of less than 25 kg/m(2), obese (body mass index of > or = 30 kg/m(2)) men and women had an increased risk of overall cancer (multivariable adjusted odds ratio = 1.34, 95% confidence interval (CI): 1.22, 1.48), non-Hodgkin's lymphoma (odds ratio = 1.46, 95% CI: 1.24, 1.72), leukemia (odds ratio = 1.61, 95% CI: 1.32, 1.96), multiple myeloma (odds ratio = 2.06, 95% CI: 1.46, 2.89), and cancers of the kidney (odds ratio = 2.74, 95% CI: 2.30, 3.25), colon (odds ratio = 1.93, 95% CI: 1.61, 2.31), rectum (odds ratio = 1.65, 95% CI: 1.36, 2.00), pancreas (odds ratio = 1.51, 95% CI: 1.19, 1.92), breast (in postmenopausal women) (odds ratio = 1.66, 95% CI: 1.33, 2.06), ovary (odds ratio = 1.95, 95% CI: 1.44, 2.64), and prostate (odds ratio = 1.27, 95% CI: 1.09, 1.47). Overall, excess body mass accounted for 7.7% of all cancers in Canada-9.7% in men and 5.9% in women. This study provides further evidence that obesity increases the risk of overall cancer, non-Hodgkin's lymphoma, leukemia, multiple myeloma, and cancers of the kidney, colon, rectum, breast (in postmenopausal women), pancreas, ovary, and prostate.

Cigarette smoking may be associated with ovarian cancer risk. This association may differ by histological type. The authors conducted a population-based case-control study in Canada of 442 incident cases of ovarian cancer and 2,135 controls 20-76 years of age during 1994-1997 to examine this association, overall and by histological type. Compared to women who never smoked, those who smoked had higher odds (odds ratio [OR] = 1.22; 95% confidence interval [CI] = 0.98-1.53) of having ovarian cancer, and the OR was larger for ex-smokers (1.30; 95% CI = 1.01-1.67) than for current smokers (1.10; 95% CI = 0.81-1.49). The association with cigarette smoking was stronger for mucinous tumors (OR = 1.77; 95% CI = 1.06-2.96) than for nonmucinous tumors (OR = 1.13; 95% CI = 0.89-1.44). In addition, the odds of smokers having mucinous tumors increased with years of smoking (OR = 1.36, 1.88, 1.19, 4.89 for20, 21-30, 31-40 and40 years, respectively; p for trend = 0.002), number of cigarettes smoked per day (OR = 1.55, 1.89, 2.28 for10, 11-20 and20 cigarettes/day, respectively; p for trend = 0.014) and smoking pack-years (OR = 1.13, 2.65, 1.77 and 2.39 for10, 11-20, 21-30 and30 pack-years, respectively; p for trend = 0.004). Our data suggest that cigarette smoking is associated with an increased risk of ovarian cancer, especially for mucinous types.

Background The effect of antioxidants on breast cancer is still controversial. Our objective was to assess the association between antioxidants and breast cancer risk in a large population-based case-control study. Methods The study population included 2,362 cases with pathologically confirmed incident breast cancer (866 premenopausal and 1,496 postmenopausal) and 2,462 controls in Canada. Intakes of antioxidants from diet and from supplementation as well as other potential risk factors for breast cancer were collected by a self-reported questionnaire. Results Compared with subjects with no supplementation, 10 years or longer supplementation of zinc had multivariable-adjusted odds ratios (OR) and 95% confidence intervals (CI) of 0.46 (0.25-0.85) for premenopausal women, while supplementation of 10 years or longer of multiple vitamin, beta-carotene, vitamin C, vitamin E and zinc had multivariable-adjusted ORs (95% CIs) of 0.74 (0.59, 0.92), 0.58 (0.36, 0.95), 0.79 (0.63-0.99), 0.75 (0.58, 0.97), and 0.47 (0.28-0.78), respectively, for postmenopausal women. No significant effect of antioxidants from dietary sources (including beta-carotene, alpha-carotene, lycopene, lutein and zeaxanthin, vitamin C, vitamin E, selenium and zinc) or from supplementation less than 10 years was observed. Conclusions This study suggests that supplementation of zinc in premenopausal women, and supplementation of multiple vitamin, beta-carotene, vitamin C, vitamin E and zinc in postmenopausal women for 10 or more years may protect women from developing breast cancer. However, we were unable to determine the overall effect of total dose or intake from both diet and supplement.

Our study aimed to assess 1) the temporal trends in incidence and mortality of liver cancer and 2) age-period-cohort effects on the incidence in Canada.We analyzed data obtained from the Canadian Cancer Registry Database and Canadian Vital Statistics Death Database. We first examined temporal trends by sex, age group, and birth cohort between 1972 and 2006. Three-year period rates and annual percentage change (APC) were calculated to compare the changes over the study period. We used age-period-cohort modelling to estimate underlying effects on the observed trends in incidence.The overall age-adjusted incidence rates increased from 2.6 and 1.5 per 100 000 in 1972-74 to 6.5 (APC: 2.9) and 2.2 (APC: 1.2) per 100 000 in 2004-06 among males and females, respectively. The age-adjusted mortality rates increased from 3.3 and 2.0 per 100 000 in 1972-74 to 6.0 (APC: 2.3) and 2.6 (APC: 1.2) per 100 000 in 2004-06 among males and females, respectively. The incidence increased most rapidly in men aged 45-54 years (APC: 4.1) and women aged 65-74 years (APC: 1.7) over the period of study.The age-period-cohort analysis suggests that birth-cohort effect is underlying the increase in incidence. While the exact reason for the increased incidence of liver cancer remains unknown, reported increase in HBV and HCV infections, and immigration from high-risk regions of the world may be important factors.

This chapter presents the epidemiologic evidence on the association between physical activity and hematologic cancers and related hypothesized biologic mechanisms. Some preliminary indications of a protective role for physical activity for non-Hodgkin's lymphoma, leukemia, multiple myeloma, and Hodgkin's lymphoma exist, but the level of epidemiologic evidence is still insufficient to make any definitive conclusions regarding the nature of these associations. Several plausible biologic mechanisms underlying the possible associations between physical activity and hematologic cancers have been proposed, including enhancement of immune function, reduction in obesity, improvement of antioxidant defense systems, impact on metabolic hormones, and anti-inflammatory effects. Future studies should improve the estimation of physical activity by using more reliable, valid, and comprehensive measurement tools, assessing all components of physical activity (type, intensity, and time period), and conducting intervention studies to evaluate the effect of physical activity on various biomarkers of cancer in order to provide further insight into plausible biologic mechanisms underlying the possible association between physical activity and hematologic cancers.

This chapter presents the epidemiologic evidence on the association between physical activity and hematologic cancers and related hypothesized biologic mechanisms. Some preliminary indications of a protective role for physical activity for non-Hodgkin’s lymphoma, leukemia, multiple myeloma, and Hodgkin’s lymphoma exist, but the level of epidemiologic evidence is still insufficient to make any definitive conclusions regarding the nature of these associations. Several plausible biologic mechanisms underlying the possible associations between physical activity and hematologic cancers have been proposed, including enhancement of immune function, reduction in obesity, improvement of antioxidant defense systems, impact on metabolic hormones, and anti-inflammatory effects. Future studies should improve the estimation of physical activity by using more reliable, valid, and comprehensive measurement tools, assessing all components of physical activity (type, intensity, and time period), and conducting intervention studies to evaluate the effect of physical activity on various biomarkers of cancer in order to provide further insight into plausible biologic mechanisms underlying the possible association between physical activity and hematologic cancers.

Background The identification of various individual, social and physical environmental factors affecting physical activity (PA) behavior in Canada can help in the development of more tailored intervention strategies for promoting higher PA levels in Canada. This study examined the influences of various individual, social and physical environmental factors on PA participation by gender, age and socioeconomic status, using data from the 2002 nationwide survey of the Physical Activity Monitor. Methods In 2002, 5,167 Canadians aged 15–79 years, selected by random-digit dialling from household-based telephone exchanges, completed a telephone survey. The short version of the International Physical Activity Questionnaire was used to collect information on total physical activity. The effects of socio-economical status, self-rated health, self-efficacy, intention, perceived barriers to PA, health benefits of PA, social support, and facility availability on PA level were examined by multiple logistic regression analyses. Results Self-efficacy and intention were the strongest correlates and had the greatest effect on PA. Family income, self-rated health and perceived barriers were also consistently associated with PA. The effects of the perceived health benefits, education and family income were more salient to older people, whereas the influence of education was more important to women and the influence of perceived barriers was more salient to women and younger people. Facility availability was more strongly associated with PA among people with a university degree than among people with a lower education level. However, social support was not significantly related to PA in any subgroup. Conclusion This study suggests that PA promotion strategies should be tailored to enhance people's confidence to engage in PA, motivate people to be more active, educate people on PA's health benefits and reduce barriers, as well as target different factors for men and women and for differing socio-economic and demographic groups.

Energy intake, physical activity, and obesity are modifiable lifestyle factors. This chapter reviews and summarizes the epidemiologic evidence on the relation of energy intake, physical activity, and obesity to cancer. High energy intake may increase the risk of cancers of colon-rectum, prostate (especially advanced prostate cancer), and breast. However, because physical activity, body size, and metabolic efficiency are highly related to total energy intake and expenditure, it is difficult to assess the independent effect of energy intake on cancer risk. There are sufficient evidences to support a role of physical activity in preventing cancers of the colon and breast, whereas the association is stronger in men than in women for colon cancer and in postmenopausal than in premenopausal women for breast cancer. The evidence also suggests that physical activity likely reduces the risk of cancers of endometrium, lung, and prostate (to a lesser extent). On the other hand, there is little or no evidence that the risk of rectal cancer is related to physical activity, whereas the results have been inconsistent regarding the association between physical activity and the risks of cancers of pancreas, ovary and kidney. Epidemiologic studies provide sufficient evidence that obesity is a risk factor for both cancer incidence and mortality. The evidence supports strong links of obesity with the risk of cancers of the colon, rectum, breast (in postmenopausal women), endometrium, kidney (renal cell), and adenocarcinoma of the esophagus. Epidemiologic evidence also indicates that obesity is probably related to cancers of the pancreas, liver, and gallbladder, and aggressive prostate cancer, while it seems that obesity is not associated with lung cancer. The role of obesity in other cancer risks is unclear.

Energy intake, physical activity, and obesity are modifiable lifestyle factors. This chapter reviews and summarizes the epidemiologic evidence on the relation of energy intake, physical activity, and obesity to cancer. High energy intake may increase the risk of cancers of colon-rectum, prostate (especially advanced prostate cancer), and breast. However, because physical activity, body size, and metabolic efficiency are highly related to total energy intake and expenditure, it is difficult to assess the independent effect of energy intake on cancer risk. There are sufficient evidences to support a role of physical activity in preventing cancers of the colon and breast, whereas the association is stronger in men than in women for colon cancer and in postmenopausal than in premenopausal women for breast cancer. The evidence also suggests that physical activity likely reduces the risk of cancers of endometrium, lung, and prostate (to a lesser extent). On the other hand, there is little or no evidence that the risk of rectal cancer is related to physical activity, whereas the results have been inconsistent regarding the association between physical activity and the risks of cancers of pancreas, ovary and kidney. Epidemiologic studies provide sufficient evidence that obesity is a risk factor for both cancer incidence and mortality. The evidence supports strong links of obesity with the risk of cancers of the colon, rectum, breast (in postmenopausal women), endometrium, kidney (renal cell), and adenocarcinoma of the esophagus. Epidemiologic evidence also indicates that obesity is probably related to cancers of the pancreas, liver, and gallbladder, and aggressive prostate cancer, while it seems that obesity is not associated with lung cancer. The role of obesity in other cancer risks is unclear.

The authors conducted a population-based case-control study of 810 cases with histologically confirmed incident kidney cancer and 3,106 controls to assess the effect of obesity, energy intake, and recreational physical activity on renal cell and non–renal cell cancer risk in Canada from 1994 to 1997. Compared with normal body mass index (BMI; 18.5 to

Purpose To understand the magnitude and the national trends of mortality and hospitalization due to injuries among Canadian adolescents aged 15–19 years in 1979–2003. Methods Data on injury deaths and hospitalizations were obtained from the national Vital Statistical System and the Hospital Morbidity Database. Injuries were classified by intent and by mechanism. Results In 15–19-year-olds, 75.6% of all deaths and 16.6% of all hospitalizations were attributed to injuries. Unintentional and self-inflicted injuries accounted for 70.2% and 24.1%, respectively, of total injury deaths as well as 72.6% and 17.4%, respectively, of total injury hospitalizations. The main causes for injury were motor vehicle traffic-related injury (MVT), suffocation, firearm, poisoning, and drowning for injury deaths; and MVT, poisoning, fall, struck by/against, and cut/pierce for injury hospitalizations. Mortality and hospitalization rates of total and unintentional injuries decreased substantially, whereas those of self-inflicted injuries decreased only slightly, with a small increase in females. Rates also decreased for all causes except suffocation, which showed an increasing trend. Males had higher rates for all intents and causes than females, except for self-inflicted injury hospitalization (higher in females). The territories and Prairie Provinces also had higher ones of total injuries and self-inflicted injuries than in other provinces. Conclusions Injury is the leading cause of deaths and a major source of hospitalizations in Canadian adolescents. However, prevention programs in Canada have made significant progress in reducing injury mortality and hospitalization. The graduated driver licensing, enforcement of seat-belt use, speed limit and alcohol control, and Canadian tough gun control may have contributed to the decline.

Epidemiologic studies have suggested that some dietary factors may play a role in the etiology of ovarian cancer, but the findings have been inconsistent. We assessed the association of ovarian cancer with dietary factors in a population-based case-control study in Canada. Diet information was collected on 442 incident cases of ovarian cancer diagnosed in 1994 to 1997 and 2,135 population controls via a self-administered questionnaire. Compared with women in the lowest quartile of cholesterol intake, those in the second, third, and fourth quartiles had a multivariate adjusted odds ratio [OR; 95% confidence interval (95% CI)] of 1.12 (0.81-1.56), 1.20 (0.85-1.68), and 1.42 (1.03-1.97), respectively (P for trend = 0.031). Higher egg consumption was also associated with a nonsignificant increase in ovarian cancer risk. The ORs (95% CIs) for ovarian cancer were 0.77 (0.60-1.04) and 0.76 (0.56-0.99) among women in the highest quartile of total vegetable and cruciferous vegetable intake as compared with women in the lowest quartile. Women who took supplements of vitamin E, beta-carotene, and B-complex vitamins foror =10 years had ORs (95% CIs) of 0.49 (0.30-0.81), 0.31 (0.11-0.91), and 0.61 (0.36-1.05), respectively. However, we did not observe an association of ovarian cancer risk with dietary fat intake, including saturated, monounsaturated, and polyunsaturated fatty acids, protein, carbohydrate, dietary fiber, fruit, dairy products, meat products, fish, chicken, grain products, nut products, baked desserts, margarine, butter, mayonnaise, and supplement of multiple vitamins, vitamin A, vitamin C, calcium, iron, zinc, and selenium. Our findings suggested that ovarian cancer risk was positively associated with higher consumption of dietary cholesterol and eggs and inversely associated with higher intake of total vegetables and cruciferous vegetables and supplementation of vitamin E, beta-carotene, and B-complex vitamins.

Objectives To evaluate whether the stage distribution among women diagnosed as having breast cancer differs between those who have received breast implants for cosmetic purposes and those with no implants and to evaluate whether cosmetic breast augmentation before the detection of breast cancer is a predictor of post-diagnosis survival. Design Systematic review of observational studies with two meta-analyses. Data sources Systematic search of the literature published before September 2012 conducted in Medline, Embase, Global health, CINAHL, IPAB, and PsycINFO. Study selection Eligible publications were those that included women diagnosed as having breast cancer and who had had augmentation mammaplasty for cosmetic purposes. Results The overall odds ratio of the first meta-analysis based on 12 studies was 1.26 (95% confidence interval 0.99 to 1.60; P=0.058; I2=35.6%) for a non-localized stage of breast cancer at diagnosis comparing women with implants who had breast cancer and women without implants who had breast cancer. The second meta-analysis, based on five studies, evaluated the relation between cosmetic breast implantation and survival. This meta-analysis showed reduced survival after breast cancer among women who had implants compared with those who did not (overall hazard ratio for breast cancer specific mortality 1.38, 95% confidence interval 1.08 to 1.75). Conclusions The research published to date suggests that cosmetic breast augmentation adversely affects the survival of women who are subsequently diagnosed as having breast cancer. These findings should be interpreted with caution, as some studies included in the meta-analysis on survival did not adjust for potential confounders. Further investigations are warranted regarding diagnosis and prognosis of breast cancer among women with breast implants.

Cancer of the small intestine is very uncommon. There are 4 main histological subtypes: adenocarcinomas, carcinoid tumors, lymphoma and sarcoma. The incidence of small intestine cancer has increased over the past several decades with a four-fold increase for carcinoid tumors, less dramatic rises for adenocarcinoma and lymphoma and stable sarcoma rates. Very little is known about its etiology. An increased risk has been noted for individuals with Crohn’s disease, celiac disease, adenoma, familial adenomatous polyposis and Peutz-Jeghers syndrome. Several behavioral risk factors including consumption of red or smoked meat, saturated fat, obesity and smoking have been suggested. The prognosis for carcinomas of the small intestine cancer is poor (5 years relative survival < 30%), better for lymphomas and sarcomas, and best for carcinoid tumors. There has been no significant change in long-term survival rates for any of the 4 histological subtypes. Currently, with the possible exceptions of obesity and cigarette smoking, there are no established modifiable risk factors which might provide the foundation for a prevention program aimed at reducing the incidence and mortality of cancers of the small intestine. More research with better quality and sufficient statistical power is needed to get better understanding of the etiology and biology of this cancer. In addition, more studies should be done to assess not only exposures of interest, but also host susceptibility.