Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • case-control studies  (23)
Collection
Keywords
  • 1
    Keywords: RECEPTOR ; CANCER ; GROWTH ; GROWTH-FACTOR ; proliferation ; tumor ; CELL-PROLIFERATION ; PATHWAY ; RISK ; GENE ; GENES ; PROTEIN ; TUMORS ; RELEASE ; PATIENT ; BINDING ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; VARIANTS ; BREAST ; breast cancer ; BREAST-CANCER ; hormone ; COLORECTAL-CANCER ; PROSTATE-CANCER ; cancer risk ; case-control studies ; SOMATOSTATIN ; CANCER PATIENTS ; nutrition ; FACTOR-I ; BINDING PROTEIN ; SERUM ; SINGLE ; IGF-I ; BINDING-PROTEIN ; case-control study ; ASSOCIATIONS ; RE ; VARIANT ; SINGLE NUCLEOTIDE POLYMORPHISMS ; cell proliferation ; development ; GROWTH-FACTOR-I ; BINDING PROTEIN-3 ; LEVEL ; case control studies ; GENOTYPE DATA ; FACTOR (IGF)-I ; PREMENOPAUSAL WOMEN ; IGFBP3 ; insulin-like growth factor ; PLASMA-LEVELS ; SERUM-LEVELS
    Abstract: Insulin-like growth factor-I (IGF-I) stimulates cell proliferation and can enhance the development of tumors in different organs. Epidemiologic studies have shown that an elevated level of circulating IGF-I is associated to increased risk of breast cancer as well as other cancers. Genetic variants affecting the release or biological action of growth hormone (GH), the main stimulator of IGF-I production, may predict circulating levels of IGF-I and have an effect on cancer risk. We tested this hypothesis with a large case-control study of 807 breast cancer patients and 1,588 matched control subjects nested within the European Prospective Investigation into Cancer and Nutrition. We genotyped 22 common single nucleotide polymorphisms in 10 genes involved in GH production and action (GHRH, GHRHR, SST, SSTR1-SSTR5, POU1F1, and GH1), and in parallel, we measured serum levels of IGF-I and IGFBP-3, its major binding protein, in samples of cases and controls. SST and SSTR2 polymorphisms showed weak but statistically significant associations with breast cancer risk. SSTR5 polymorphisms were associated with IGF-I levels, whereas one polymorphism in GHRHR and one in POU1F1 were associated with IGFBP-3 levels. Our conclusion is that common genetic variation in the GH synthesis pathway, as measured by single nucleotide polymorphisms selected in the present study, is not a major determinant of IGF-I and IGFBP-3 circulating levels, and it does not play a major role in altering breast cancer risk
    Type of Publication: Journal article published
    PubMed ID: 16214911
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    Keywords: CANCER ; BLOOD ; MODEL ; MODELS ; COHORT ; RISK ; RISKS ; PATIENT ; RISK-FACTORS ; BINDING ; CYCLE ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; hormone ; WOMEN ; risk factors ; cancer risk ; case-control studies ; EPIC ; nutrition ; ESTRADIOL ; SERUM ; SINGLE ; DEFICIENCY ; case-control study ; ASSOCIATIONS ; RE ; MAMMARY-GLAND ; ESTROGEN ; case control studies ; INTERVAL ; TESTS ; RANDOMIZED CONTROLLED-TRIAL ; PREMENOPAUSAL WOMEN ; SERUM-LEVELS ; ADRENAL ANDROGENS ; ESTROGEN PLUS PROGESTIN ; FEMALE NOBLE RATS ; HEALTHY POSTMENOPAUSAL WOMEN ; HORMONE LEVELS ; ONE-YEAR PERIOD ; REPLACEMENT THERAPY
    Abstract: Background. Contrasting etiologic hypotheses about the role of endogenous sex steroids in breast cancer development among premenopausal women implicate ovarian androgen excess and progesterone deficiency, estrogen excess, estrogen and progesterone excess, and both an excess or lack of adrenal androgens (dehydroepiandrosterone [DHEA] or its sulfate [DHEAS]) as risk factors. We conducted a case-control study nested within the European Prospective Investigation into Cancer and Nutrition cohort to examine associations among premenopausal serum concentrations of sex steroids and subsequent breast cancer risk. Methods: Levels of DHEAS, (Delta 4-)androstenedione, testosterone, and sex hormone binding globulin (SHBG) were measured in single prediagnostic serum samples from 370 premenopausal women who subsequently developed breast cancer (case patients) and from 726 matched cancer-free control subjects. Levels of progesterone, estrone, and estradiol were also measured for the 285 case patients and 555 matched control subjects who had provided information about the day of menstrual cycle at blood donation. Conditional logistic regression models were used to estimate relative risks of breast cancer by quartiles of hormone concentrations. All statistical tests were two-sided. Results: Increased risks of breast cancer were associated with elevated serum concentrations of testosterone (odds ratio [OR] for highest versus lowest quartile = 1.73, 95% confidence interval [CI] = 1.16 to 2.57; P-trend =.01), androstenedione (OR for highest versus lowest quartile = 1.569 95% CI = 1.05 to 2.32; P-trend =.01), and DHEAS (OR for highest versus lowest quartile = 1.48, 95% CI = 1.02 to 2.14; P-trend =.10) but not SHBG. Elevated serum progesterone concentrations were associated with a statistically significant reduction in breast cancer risk (OR for highest versus lowest quartile = 0.61, 95% CI = 0.38 to 0.98; P-trend =.06). The absolute risk of breast cancer for women younger than 40 followed up for 10 years was estimated at 2.6% for those in the highest quartile of serum testosterone versus 1.5% for those in the lowest quartile; for the highest and lowest quartiles of progesterone, these estimates were 1.7% and 2.6%, respectively. Breast cancer risk was not statistically significantly associated with serum levels
    Type of Publication: Journal article published
    PubMed ID: 15900045
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    Keywords: CANCER ; MODEL ; MODELS ; FOLLOW-UP ; RISK ; METABOLISM ; INDEX ; CARCINOGENESIS ; ASSOCIATION ; BREAST-CANCER ; NO ; hormone ; PLASMA ; NUMBER ; WOMEN ; OBESITY ; cancer risk ; ORAL-CONTRACEPTIVES ; cholesterol ; LIPOPROTEIN ; LOW-DENSITY-LIPOPROTEIN ; case-control studies ; ABNORMALITIES ; BODY ; DIABETES-MELLITUS ; EPIC ; European Prospective Investigation into Cancer and Nutrition ; nutrition ; ENDOMETRIAL CANCER ; RELATIVE RISK ; REGRESSION-MODELS ; CLUSTER ; POSTMENOPAUSAL WOMEN ; MASS INDEX ; MASSES ; BODIES ; ONCOLOGY ; case control study ; case-control study ; REGRESSION ; ASSOCIATIONS ; ENDOMETRIAL ; RE ; INCREASE ; BODY-SIZE ; PHYSICAL-ACTIVITY ; LEVEL ; case control studies ; INTERVAL ; metabolic syndrome ; HORMONES ; prospective ; UNIT ; CANCER-RISK ; C-PEPTIDE ; SET ; case control ; LOGISTIC-REGRESSION ; BODY-MASS ; BODY-MASS-INDEX ; lipid ; HDL-CHOLESTEROL ; LOW-DENSITY ; SERUM-CHOLESTEROL
    Abstract: To clarify the role of metabolic factors in endometrial carcinogenesis, we conducted a case-control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC), and examined the relation between prediagnostic plasma lipids, lipoproteins, and glucose, the metabolic syndrome (MetS; a cluster of metabolic factors) and endometrial cancer risk. Among pre- and postmenopausal women, 284 women developed endometrial cancer during follow-up. Using risk set sampling, 546 matched control subjects were selected. From conditional logistic regression models, high-density lipoprotein cholesterol (HDL-C) levels were inversely associated with risk body mass index (BMI)-adjusted relative risk (FR) for top versus bottom quartile 0.61 (95% confidence intervals (CI) 0.38-0.97), P-trend= 0.02). Glucose levels were positively associated with risk (BMI-adjusted RR top versus bottom quartile 1.69 (95% Cl 0.99-2.90), P-trend, = 0.03), which appeared stronger among postmenopausal women (BMI-adjusted RR top versus bottom tertile 2.61 (95% Cl 1.46-4.66), P-trend=0.0006, P-heterogeneity=0.13) and never-users of exogenous hormones (P-heterogeneity=0-005 for oral contraceptive (OC) use and 0.05 for hormone replacement therapy-use). The associations of HDL-C and glucose with risk were no longer statistically significant after further adjustment for obesity-related hormones. Plasma total cholesterol, Low-density lipoprotein cholesterol (LDL-C), and triglycerides were not significantly related to overall risk. The presence of MetS was associated with risk (RR 2.12 (95% CI 1.51-2.97)), which increased with the number of MetS factors (P-trend=0.02). An increasing number of MetS factors other than waist circumference, however, was marginally significantly associated with risk only in women with waist circumference above the median (P-interaction=0-01). None of the associations differed significantly by fasting status. These findings suggest that metabolic abnormalities and obesity may act synergistically to increase endometrial cancer risk
    Type of Publication: Journal article published
    PubMed ID: 17914105
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    Keywords: RECEPTOR ; CANCER ; BLOOD ; POPULATION ; RISK ; GENE ; GENES ; BIOMARKERS ; colon ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; VARIANTS ; ADENOMAS ; HEALTH ; colorectal cancer ; REDUCED RISK ; COLORECTAL-CANCER ; GENOTYPES ; COLON-CANCER ; POPULATIONS ; UNITED-STATES ; case-control studies ; CALCIUM ; nutrition ; RECTAL-CANCER ; SERUM ; case control study ; case-control study ; REGRESSION ; colon cancer ; VARIANT ; interaction ; LEVEL ; biomarker ; EPIDEMIOLOGIC EVIDENCE ; GENOTYPE ; USA ; prospective ; rectal cancer ; cancer research ; colorectal ; vitamin D ; VITAMIN-D ; LOGISTIC-REGRESSION ; D METABOLITES ; vitamin D receptor ; 25-HYDROXYVITAMIN-D ; RECTAL CANCERS ; Genetic ; VITAMIN ; CONFIDENCE ; CRC ; Logistic regression ; D-RECEPTOR ; DIETARY CALCIUM
    Abstract: Increased levels of vitamin D and calcium may play a protective role in colorectal cancer (CRC) risk. It has been suggested that these effects may be mediated by genetic variants of the vitamin D receptor (VDR) and the calcium sensing receptor (CASR). However, current epidemiologic evidence from European populations for a role of these genes in CRC risk is scarce. In addition, it is not clear whether these genes may modulate CRC risk independently or by interaction with blood vitamin D concentration wild-type bb, the BB genotype of the VDR BsmI polymorphism was associated with a reduced risk of CRC [RR, 0.76; 95% confidence interval (CI), 0.59-0.98). The association was observed for colon cancer (RR, 0.69; 95% CI, 0.45-0.95) but not rectal cancer (RR, 0.97; 95% CI, 0.62-1.49). The Fok1 and CASR genotypes were not associated with CRC risk in thisand level of dietary calcium intake. A case-control study was conducted nested within the European Prospective Investigation into Cancer and Nutrition. CRC cases (1,248) were identified and matched to 1,248 control subjects. Genotyping for the VDR (BsmI: rs1544410; Fok1: rs2228570) and CASR (rs1801725) genes was done by Taqman, and serum vitamin D (25OHD) concentrations were measured. Conditional logistic regression was used to estimate the incidence rate ratio (RR). Compared with the study. No interactions were noted for any of the polymorphisms with serum 25OHD concentration or level of dietary calcium. These results confirm a role for the BsmI polymorphism of the VDR gene in CRC risk, independent of serum 25OHD concentration and dietary calcium intake. (Cancer Epidemiol Biomarkers Prev 2009;18(9):2485-91)
    Type of Publication: Journal article published
    PubMed ID: 19706842
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    Keywords: CANCER ; BLOOD ; RISK ; ENZYMES ; GENE ; GENES ; ACTIVATION ; DNA ; CARCINOGENESIS ; GENETIC POLYMORPHISMS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; AGE ; CIGARETTE-SMOKING ; COUNTRIES ; GENOTYPES ; COLORECTAL CANCERS ; LINKAGE DISEQUILIBRIUM ; adenocarcinoma ; case-control studies ; TOBACCO ; GASTRIC-CANCER ; nutrition ; SMOKERS ; case-control study ; VARIANT ; TOBACCO-SMOKE ; GSTM1 ; GSTT1 ; gastric cancer ; S-TRANSFERASE M1 ; case control studies ; INTERVAL ; ENZYME ; GENETIC-POLYMORPHISM ; LOCUS ; FAMILY-HISTORY ; prospective ; ALLELE FREQUENCIES ; COMPOUND ; EPOXIDE HYDROLASE POLYMORPHISMS ; EUROPEAN COUNTRIES ; HIGH-INCIDENCE AREA ; INCREASED RISK ; NEVER SMOKERS ; odds ratio ; T1 NULL GENOTYPES ; tobacco smoke ; UNIT
    Abstract: Metabolizing enzymes, which often display genetic polymorphisms, are involved in the activation of compounds present in tobacco smoke that may be relevant to gastric carcinogenesis. We report the results of a study looking at the association between risk of gastric adenocarcinoma and polymorphisms in genes CYP1A1, CYP1A2, EPHX1, and GSTT1. A nested case-control study was carried out within the European Prospective Investigation into Cancer and Nutrition, developed in 10 European countries. The study includes 243 newly diagnosed cases of histologically confirmed gastric adenocarcinoma and 946 controls matched by center, age, sex, and date of blood collection. Genotypes were determined in nuclear DNA from WBCs. We found an increased risk of gastric cancer for homozygotes for C (histidine) variant in Y113H of EPHX1 (odds ratio, 1.91; 95% confidence interval, 1.19-3.07) compared with subjects with TC/TT. There was also a significant increased risk for smokers carrying at least one variant allele A in Ex7+129C 〉 A (m4) of CYP1A1 and never smokers with null GSTT1 and allele A in the locus -3859G 〉 A of CYP1A2. Most of these genes are involved in the activation and detoxification of polycyclic aromatic hydrocarbons, suggesting a potential role of these compounds in gastric carcinogenesis
    Type of Publication: Journal article published
    PubMed ID: 17164366
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    Keywords: CANCER ; carcinoma ; FOLLOW-UP ; COHORT ; cohort study ; RISK ; SITE ; INFECTION ; ASSOCIATION ; antibodies ; WOMEN ; MEN ; COUNTRIES ; DIET ; STOMACH ; adenocarcinoma ; case-control studies ; CARDIA ; CONSUMPTION ; EPIC ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; nutrition ; CALIBRATION ; case-control study ; INCREASE ; case control studies ; HELICOBACTER-PYLORI INFECTION ; prospective ; Helicobacter pylori ; intake ; FOODS
    Abstract: It is considered that fruit and vegetable (F&V) protect against oesophagus and gastric cancer (GC). However, 2 recent meta-analyses suggest that the strength of association on GC seems to he weaker for vegetables than for fruit and weaker in cohort than in case-control studies. No evidence exists from cohort studies about adenocarcinoma of oesophagus (ACO). In 521,457 men and women participating in the EPIC cohort in 10 European countries, information of diet and lifestyle was collected at baseline. After an average of 6.5 years of follow-up, a total of 330 GC and 65 ACO, confirmed and classified by a panel of pathologists, was used for the analysis. We examined the relation between F&V intake and GC and ACO. A calibration study in a sub-sample was used to control diet measurement errors. In a sub-sample of cases and a random sample of controls, antibodies against Helicobacter pylori (Hp) were measured and interactions with F&V were examined in a nested case-control study. We observed no association with total vegetable intake or specific groups of vegetables and GC risk, except for the intestinal type, where a negative association is possible regarding total vegetable (calibrated HR 0.66; 95% CI 0.35-1.22 per 100 g increase) and onion and garlic intake (calibrated HR 0.70; 95% CI 0.38-1.29 per 10 g increase). No evidence of association between fresh fruit intake and GC risk was observed. We found a negative but non significant association between citrus fruit intake and the cardia site (calibrated HR 0.77; 95% CI 0.47-1.22 per 100 g increase) while no association was observed with the non-cardia site. Regarding ACO, we found a non significant negative association for vegetable intake and for citrus intake (calibrated HRs 0.72; 95% Cl 0.32-1.64 and 0.77; 95% CI 0.46-1.28 per 100 and 50 g increase, respectively). It seems that lip infection does not modify the effect of F&V intake. Our study supports a possible protective role of vegetable intake in the intestinal type of GC and the ACO. Citrus fruit consumption may have a role in the protection against cardia GC and ACO. (c) 2005 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16380980
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    Keywords: CANCER ; FOLLOW-UP ; COHORT ; POPULATION ; RISK ; INFECTION ; CARCINOGENESIS ; ASSOCIATION ; WOMEN ; MEN ; cancer risk ; DOSE-RESPONSE ; DIETARY ; adenocarcinoma ; ADENOCARCINOMAS ; case-control studies ; CARDIA ; CONSUMPTION ; EPIC ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; nutrition ; case-control study ; DIETARY FACTORS ; ASSOCIATIONS ; INCREASE ; case control studies ; INTERVAL ; prospective ; MEAT INTAKE ; RED MEAT ; JAPANESE ; Helicobacter pylori ; N-NITROSO COMPOUNDS
    Abstract: Background. Dietary factors are thought to have an important role in gastric and esophageal carcinogenesis, but evidence from cohort studies for such a role is lacking. We examined the risks of gastric cancer and esophageal adenocarcinoma associated with meat consumption within the European Prospective Investigation Into Cancer and Nutrition (EPIC) cohort. Methods: A total of 521 457 men and women aged 35-70 years in 10 European countries participated in the EPIC cohort. Dietary and lifestyle information was collected at recruitment. Cox proportional hazard models were used to examine associations between meat intake and risks of cardia and gastric noncardia cancers and esophageal adenocarcinoma. Data from a calibration substudy were used to correct hazard ratios (HRs) and 95% confidence intervals (CIs) for diet measurement errors. In a nested case-control study, we examined interactions between Helicobacter pylori infection status (i.e., plasma H. pylori antibodies) and meat intakes. All statistical tests were two-sided. Results: During a mean follow-up of 6.5 years, 330 gastric adenocarcinoma and 65 esophageal adenocarcinomas were diagnosed. Gastric noncardia cancer risk was statistically significantly associated with intakes of total meat (calibrated HR per 100-g/day increase = 3.52, 95%, CI = 1.96 to 6.34), red meat (calibrated HR per 50-g/day increase = 1.73; 95% CI = 1.03 to 2.88), and processed meat (calibrated HR per 50-g/day increase = 2.45; 95% CI = 1.43 to 4.21). The association between the risk of gastric noncardia cancer and total meat intake was especially large in H. pylori-infected subjects (odds ratio per 100-g/day increase = 5.32; 95% CI = 2.10 to 13.4). Intakes of total, red, or processed meat were not associated with the risk of gastric cardia cancer. A positive but non-statistically significant association was observed between esophageal adenocarcinoma cancer risk and total and processed meat intake in the calibrated model. In this study population, the absolute risk of development of gastric adenocarcinoma within 10 years for a study subject aged 60 years was 0.26% for the lowest quartile of total meat intake and 0.33% for the highest quartile of total meat intake. Conclusion: Total, red, and processed meat intakes were associated with an increased risk of gastric noncardia cancer, especially in H. pylori antibody-positive subjects, but not with cardia gastric cancer
    Type of Publication: Journal article published
    PubMed ID: 16507831
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
    Keywords: CANCER ; SURVIVAL ; BLOOD ; human ; COHORT ; MORTALITY ; RISK ; GENE ; GENES ; ASSOCIATION ; POLYMORPHISMS ; SUSCEPTIBILITY ; VARIANTS ; DESIGN ; genetics ; SNP ; RATES ; case-control studies ; INDIVIDUALS ; pancreatic cancer ; MAPS ; case control study ; case-control study ; WORLDWIDE ; PANCREATIC-CANCER ; VARIANT ; SNPs ; EPIDEMIOLOGIC EVIDENCE ; USA ; prospective ; BASE-LINE CHARACTERISTICS ; BLOOD-GROUP ; GENOME-WIDE ASSOCIATION ; WOMENS HEALTH ; Genetic ; Genome-wide association studies ; ALLERGIES ; CONFIDENCE ; RATIONALE
    Abstract: We conducted a two-stage genome-wide association study of pancreatic cancer, a cancer with one of the lowest survival rates worldwide. We genotyped 558,542 SNPs in 1,896 individuals with pancreatic cancer and 1,939 controls drawn from 12 prospective cohorts plus one hospital-based casecontrol study. We conducted a combined analysis of these groups plus an additional 2,457 affected individuals and 2,654 controls from eight case-control studies, adjusting for study, sex, ancestry and five principal components. We identified an association between a locus on 9q34 and pancreatic cancer marked by the SNP rs505922 (combined P = 5.37 x 10(-8); multiplicative per-allele odds ratio 1.20; 95% confidence interval 1.12-1.28). This SNP maps to the first intron of the ABO blood group gene. Our results are consistent with earlier epidemiologic evidence suggesting that people with blood group O may have a lower risk of pancreatic cancer than those with groups A or B
    Type of Publication: Journal article published
    PubMed ID: 19648918
    Signatur Availability
    BibTip Others were also interested in ...
  • 9
    Keywords: CANCER ; BLOOD ; PROSTATE ; SUPPORT ; RISK ; RISKS ; SAMPLE ; SAMPLES ; ASSOCIATION ; PLASMA ; AGE ; MEN ; prostate cancer ; PROSTATE-CANCER ; case-control studies ; nutrition ; NESTED CASE-CONTROL ; HETEROGENEITY ; isoflavones ; case-control study ; REGRESSION ; GENISTEIN CONTENT ; prospective ; ENTEROLACTONE ; phytoestrogens ; lignan ; DAIDZEIN ; genistein ; JAPANESE MEN ; RECEPTOR-ALPHA ; isoflavone ; SOY PRODUCT
    Abstract: We examined plasma concentrations of phyto-oestrogens in relation to risk for subsequent prostate cancer in a case-control study nested in the European Prospective Investigation into Cancer and Nutrition. Concentrations of isoflavones genistein, daidzein and equol, and that of lignans enterolactone and enterodiol, were measured in plasma samples for 950 prostate cancer cases and 1042 matched control participants. Relative risks (RRs) for prostate cancer in relation to plasma concentrations of these phyto-oestrogens were estimated by conditional logistic regression. Higher plasma concentrations of genistein were associated with lower risk of prostate cancer: RR among men in the highest vs the lowest fifth, 0.71 (95% confidence interval (CI) 0.53-0.96, P trend = 0.03). After adjustment for potential confounders this RR was 0.74 (95% CI 0.54-1.00, P trend = 0.05). No statistically significant associations were observed for circulating concentrations of daidzein, equol, enterolactone or enterodiol in relation to overall risk for prostate cancer. There was no evidence of heterogeneity in these results by age at blood collection or country of recruitment, nor by cancer stage or grade. These results suggest that higher concentrations of circulating genistein may reduce the risk of prostate cancer but do not support an association with plasma lignans. British Journal of Cancer (2009) 100, 1817-1823. doi: 10.1038/sj.bjc.6605073 www.bjcancer.com Published online 12 May 2009 (C) 2009 Cancer Research UK
    Type of Publication: Journal article published
    PubMed ID: 19436304
    Signatur Availability
    BibTip Others were also interested in ...
  • 10
    Keywords: CANCER ; Germany ; LUNG ; MODEL ; FOLLOW-UP ; lung cancer ; LUNG-CANCER ; COHORT ; incidence ; MORTALITY ; NEW-YORK ; POPULATION ; RISK ; RISK-FACTORS ; ASSOCIATION ; AGE ; MEN ; smoking ; COUNTRIES ; cancer risk ; POPULATIONS ; DIET ; DIETARY ; NETHERLANDS ; case-control studies ; CONSUMPTION ; EPIC ; EPIC study ; European Prospective Investigation into Cancer and Nutrition ; FRUIT ; nutrition ; QUESTIONNAIRE ; SMOKERS ; VEGETABLES ; EUROPE ; FOOD ; RELATIVE RISK ; cancer,diet,epidemiology,fruits,vegetables,lung cancer,smoking ; FLAVONOIDS ; NONSMOKING WOMEN
    Abstract: Intake of fruits and vegetables is thought to protect against the development of lung cancer. However, some recent cohort and case-control studies have shown no protective effect. We have assessed the relation between fruit and vegetable intake and lung cancer incidence in the large prospective investigation on diet and cancer, the European Prospective Investigation Into Cancer and Nutrition (EPIC). We studied data from 478,021 individuals that took part in the EPIC study, who were recruited from 10 European countries and who completed a dietary questionnaire during 1992-1998. Follow-up was to December 1998 or 1999, but for some centres with active follow-up to June 2002. During follow-up, 1,074 participants were reported to have developed lung cancer, of whom 860 were eligible for our analysis. We used the Cox proportional hazard model to determine the effect of fruit and vegetable intake on the incidence of lung cancer. We paid particular attention to adjustment for smoking. Relative risk estimates were obtained using fruit and vegetable intake categorised by sex-specific, cohort-wide quintiles. After adjustment for age, smoking, height, weight and gender, there was a significant inverse association between fruit consumption and lung cancer risk: the hazard ratio for the highest quintile of consumption relative to the lowest being 0.60 (95% Confidence Interval 0.46-0.78), p for trend 0.0099. The association was strongest in the Northern Europe centres, and among current smokers at baseline, and was strengthened when the 293 lung cancers diagnosed in the first 2 years of follow-up were excluded from the analysis. There was no association between vegetable consumption or vegetable subtypes and lung cancer risk. The findings from this analysis can be regarded as re-enforcing recommendations with regard to enhanced fruit consumption for populations. However, the effect is likely to be small compared to smoking cessation. (C) 2003 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 14639614
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...