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1.
  • Genkinger, J M, et al. (författare)
  • Dairy products and ovarian cancer : A pooled analysis of 12 cohort studies
  • 2006
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA. NYU, Dept Environm Med, Div Epidemiol, New York, NY 10016 USA. Loma Linda Univ, Sch Med, Ctr Hlth Res, Loma Linda, CA USA. SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA. Netherlands Org Appl Sci Res Qual Life, Dept Food & Chem Risk Anal, Zeist, Netherlands. Univ Oslo, Dept Nutr, Oslo, Norway. NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. Natl Inst Environm Med, Div Nutr Epidemiol, Karolinska Inst, Stockholm, Sweden. Amer Canc Soc, Atlanta, GA 30329 USA. Univ Toronto, Fac Med, Dept Publ Hlth Sci, Toronto, ON, Canada. Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA. Maastricht Univ, Dept Epidemiol, Nutr & Toxicol Res Inst, Maastricht, Netherlands. : AMER ASSOC CANCER RESEARCH. - 1055-9965 .- 1538-7755. ; 15:2, s. 364-372
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Dairy foods and their constituents (lactose and calcium) have been hypothesized to promote ovarian carcinogenesis. Although case-control studies have reported conflicting results for dairy foods and lactose, several cohort studies have shown positive associations between skim milk, lactose, and ovarian cancer. Methods: A pooled analysis of the primary data from 12 prospective cohort studies was conducted. The study population consisted of 553,217 women among whom 2,132 epithelial ovarian cases were identified. Study-specific relative risks and 95% confidence intervals were calculated by Cox proportional hazards models and then pooled by a random-effects model. Results: No statistically significant associations were observed between intakes of milk, cheese, yogurt, ice cream, and dietary and total calcium intake and risk of ovarian cancer. Higher lactose intakes comparing >= 30 versus < 10 g/d were associated with a statistically significant higher risk of ovarian cancer, although the trend was not statistically significant (pooled multivariate relative risk, 1.19; 95% confidence interval, 1.01-1.40; P-trend = 0.19). Associations for endometrioid, mucinous, and serous ovarian cancer were similar to the overall findings. Discussion: Overall, no associations were observed for intakes of specific dairy foods or calcium and ovarian cancer risk. A modest elevation in the risk of ovarian cancer was seen for lactose intake at the level that was equivalent to three or more servings of milk per day. Because a new dietary guideline recommends two to three servings of dairy products per day, the relation between dairy product consumption and ovarian cancer risk at these consumption levels deserves further examination.
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2.
  • Koushik, A, et al. (författare)
  • Fruits and vegetables and ovarian cancer risk in a pooled analysis of 12 cohort studies
  • 2005
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA. Brigham & Womens Hosp, Dept Med, Div Prevent Med, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA USA. Harvard Univ, Ctr Canc Prevent, Boston, MA 02115 USA. Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA. NYU, Sch Med, Div Epidemiol, Dept Environm Med, New York, NY USA. NYU, Sch Med, Div Biostat, Dept Environm Med, New York, NY USA. Loma Linda Univ, Sch Med, Ctr Hlth Res, Loma Linda, CA USA. Maastricht Univ, Dept Epidemiol, Maastricht, Netherlands. Mayo Clin & Mayo Fdn, Dept Hlth Sci Res, Coll Med, Rochester, MN 55905 USA. SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA. TNO, Nutr & Food Res Inst, Dept Epidemiol, Zeist, Netherlands. Karolinska Inst, Div Nutr Epidemiol, Natl Inst Environm Med, Stockholm, Sweden. NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. Amer Canc Soc, Atlanta, GA 30329 USA. Univ Toronto, Fac Med, Dept Publ Hlth Sci, Toronto, ON, Canada. Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA. : AMER ASSOC CANCER RESEARCH. - 1055-9965 .- 1538-7755. ; 14:9, s. 2160-2167
  • Tidskriftsartikel (refereegranskat)abstract
    • Because fruits and vegetables are rich in bioactive compounds with potential cancer-preventive actions, increased consumption may reduce the risk of ovarian cancer. Evidence on the association between fruit and vegetable intake and ovarian cancer risk has not been consistent. We analyzed and pooled the primary data from 12 prospective studies in North America and Europe. Fruit and vegetable intake was measured at baseline in each study using a validated food frequency questionnaire. To summarize the association between fruit and vegetable intake and ovarian cancer, study-specific relative risks (RR) were estimated using the Cox proportional hazards model, and then combined using a random-effects model. Among 560,441 women, 2,130 cases of invasive epithelial ovarian cancer occurred during a maximum follow-up of 7 to 22 years across studies. Total fruit intake was not associated with ovarian cancer risk-the pooled multivariate RR for the highest versus the lowest quartile of intake was 1.06 [95% confidence interval (95% CI), 0.92-1.21; P value, test for trend = 0.73; P value, test for between-studies heterogeneity = 0.741. Similarly, results for total vegetable intake indicated no significant association (pooled multivariate RR, 0.90; 95% Cl, 0.78-1.04, for the highest versus the lowest quartile; P value, test for trend = 0.06; P value, test for between-studies heterogeneity = 0.31). Intakes of botanically defined fruit and vegetable groups and individual fruits and vegetables were also not associated with ovarian cancer risk. Associations for total fruits and vegetables were similar for different histologic types. These results suggest that fruit and vegetable consumption in adulthood has no important association with the risk of ovarian cancer.
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3.
  • Larsson, S C, et al. (författare)
  • A prospective study of dietary folate intake and risk of colorectal cancer : Modification by caffeine intake and cigarette smoking
  • 2005
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden. Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA. : AMER ASSOC CANCER RESEARCH. - 1055-9965 .- 1538-7755. ; 14:3, s. 740-743
  • Tidskriftsartikel (refereegranskat)abstract
    • Epidemiologic evidence indicates an inverse association of folate intake with risk of colorectal cancer, but whether this association is modified by intake of caffeine (in coffee and tea) or cigarette smoking-factors that possibly interfere with folate-has not been studied. Thus, we examined whether the association between dietary folate intake and incidence of colorectal cancer is modified by caffeine intake and smoking. Cox proportional hazards modeling was used to estimate rate ratios relating dietary folate intake to colorectal cancer incidence among 61,433 women ages 40 to 75 years at recruitment into the Swedish Mammography Cohort in 1987 to 1990. From March 1987 through June 2004, a total of 805 incident cases of colorectal cancer were diagnosed. After controlling for age and other potential confounders, we observed an inverse association between dietary folate intake and risk of colon cancer (rate ratio for the highest versus the lowest quintile, 0.61; 95% confidence interval, 0.41-0.91; P-trend = 0.02), but not of rectal cancer (rate ratio, 0.93; 95% confidence interval, 0.55-1.56; P-trend = 0.97). The inverse association between dietary folate intake and colon cancer risk was most pronounced among smokers (P-interaction = 0.03). We found no apparent modification of risk by caffeine intake. Findings from this population-based cohort study support an inverse association between dietary folate intake and risk of colon cancer and suggest that smokers might benefit most from a high dietary folate intake.
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4.
  • Lindblad, Per, 1953-, et al. (författare)
  • Diet and risk of renal cell cancer : a population-based case-control study
  • 1997
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - Philadelphia, USA : American Association for Cancer Research. - 1055-9965 .- 1538-7755. ; 6:4, s. 215-223
  • Tidskriftsartikel (refereegranskat)abstract
    • In a few previous studies on diet and renal cell cancer, an inconsistent positive association with meat, milk, and protein and a negative association with vegetable and fruit consumption have been found. Whereas earlier studies have dealt with recent diet only, our study explored the effect of foods consumed both during the usual adult lifetime and 20 years prior to interview. The study included 379 individuals with incident histologically verified renal cell cancer and 350 control subjects residing in eight counties in Sweden between June 1989 and December 1991. Usual adult dietary intake and dietary habits 20 years prior to interview were assessed by a structured face-to-face interview and a self-administered questionnaire, respectively. Odds ratios were estimated through unconditional logistic regression. We have not observed an association of renal cell cancer with milk or total meat consumption per se; however, frequent intake of fried/sauteed meat increased the risk of renal cell cancer by about 60%; frequent consumption of poultry was also associated with an increased risk (P for trend, 0.05). A significantly protective effect on risk of renal cell cancer was observed with increasing consumption of fruit (P for trend, 0.05). When analyzed by smoking status, total fruit and especially citrus fruit consumption among nonsmokers showed an even stronger protective effect; the highest quartiles of total fruit, apple, and citrus fruit consumption entailed a 50-60% reduction in risk of renal cell cancer compared with the lowest quartiles. There was a suggestion of a protective effect of high total vegetable consumption. A protective effect of vitamin C and alpha-tocopherol was also more pronounced in nonsmokers (P for trend, 0.004 and 0.007, respectively). Our study adds to the evidence that diet may have an important role in the etiology of renal cell cancer.
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5.
  • Lindblad, Per, 1953-, et al. (författare)
  • The role of obesity and weight fluctuations in the etiology of renal cell cancer : a population-based case-control study
  • 1994
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - Philadelphia, USA : American Association for Cancer Research. - 1055-9965 .- 1538-7755. ; 3:8, s. 631-9
  • Tidskriftsartikel (refereegranskat)abstract
    • The causes of renal cell cancer (RCC) are poorly understood. Besides smoking, obesity remains the only risk factor that is fairly well established. The association between obesity and RCC appears stronger and more consistent in women than in men. We investigated the question of whether this apparent sex difference could be explained by repeated weight changes (weight cycling), less physical exercise, or pharmacological treatment of obesity in women. Structured face-to-face interviews were carried out with 379 (70% of all eligible) incident cases of RCC and 353 (72% of eligible) controls. The relationships between RCC and adult height, weight, and body mass index (BMI), defined as weight/height, were analyzed. Odds ratios (ORs) were estimated through logistic regression. No association was found between adult height and RCC. In men, weight and BMI appeared at most to be weakly related to risk of RCC. In women, higher adult weight and BMI (usual, highest, and lowest) and also high BMI at ages 30, 40, and 50 years were consistently associated with a significantly increased risk of RCC. Women with an usual adult BMI in the top 5% had a nearly 3-fold increased risk of RCC [OR, 2.67; 95% confidence interval (CI), 1.02-7.01]. Compared with individuals with no weight-loss periods, 2 or more such periods implied an OR of 0.96 (95% CI, 0.32-2.90) in men and 3.87 (95% CI, 1.20-12.45) in women. Physical activity at work reduced the risk of RCC in men but not women. Regular use of diet pills containing amphetamine was associated with an increased risk of RCC (OR, 4.06; 95% CI, 1.35-12.22).(ABSTRACT TRUNCATED AT 250 WORDS)
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6.
  • Terry, P, et al. (författare)
  • A prospective study of major dietary patterns and the risk of breast cancer
  • 2001
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - 1055-9965 .- 1538-7755. ; 10:12, s. 1281-5
  • Tidskriftsartikel (refereegranskat)abstract
    • Our aim was to study the broader eating patterns that potentially reflect many dietary exposures working together in their association with breast cancer risk. Using data from a prospective study of 61,463 women with an average follow-up of 9.6 years and 1,328 incident cases of breast cancer, we conducted a factor analysis to identify major dietary patterns. Proportional hazards regression was used to estimate hazard ratios. We found no association between the "Western" dietary pattern (characterized by such foods as red and processed meats, refined grains, fat, and sweets) or the "healthy" dietary pattern (fruit and vegetables, fish and poultry, low-fat dairy, and whole grains) and breast cancer risk. However, women who were in the highest category of the "drinker" dietary pattern (wine, beer, and spirits) had a moderately increased risk (rate ratio = 1.27; 95% confidence interval, 1.06-1.52; P for trend, 0.002). The positive association was somewhat weaker among women below 50 years of age, a finding not inconsistent with chance. Our results are in agreement with the majority of previous studies that show alcohol consumption moderately increases the risk of breast cancer, but our results do not support any association between breast cancer risk and the "Western" or "healthy" dietary patterns.
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7.
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8.
  • ANDERSSON, SO, et al. (författare)
  • EARLY-LIFE RISK-FACTORS FOR PROSTATE-CANCER - A POPULATION-BASED CASE-CONTROL STUDY IN SWEDEN
  • 1995
  • Ingår i: CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION. - : AMER ASSOC CANCER RESEARCH. - 1055-9965. ; 4:3, s. 187-192
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • We undertook a population-based case-control study to investigate early life risk factors for prostate cancer. Information on dietary habits during childhood and adolescence, childhood environment, pubertal development, and physical activity was collected
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9.
  • Andersson, SO, et al. (författare)
  • Lifestyle factors and prostate cancer risk: A case-control study in Sweden
  • 1996
  • Ingår i: CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION. - : AMER ASSOC CANCER RESEARCH. - 1055-9965. ; 5:7, s. 509-513
  • Tidskriftsartikel (refereegranskat)abstract
    • We examined associations between lifestyle factors and subsequent risk of prostate cancer in a population-based case-control study, Information on smoking and alcohol habits, socioeconomic factors, marital status, family history, and sexual habits were ob
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10.
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