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  • DKFZ Publication Database  (1,743)
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  • DKFZ Publication Database  (1,743)
Keywords
  • 101
    Keywords: RECEPTOR ; APOPTOSIS ; CANCER ; proliferation ; CELL-PROLIFERATION ; Germany ; DISEASE ; RISK ; SITE ; GENE ; GENES ; PROTEIN ; transcription ; DIFFERENTIATION ; GENETIC POLYMORPHISMS ; BINDING ; ASSOCIATION ; FREQUENCY ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY GENES ; BREAST ; breast cancer ; BREAST-CANCER ; PROMOTER ; AGE ; BRCA1 ; WOMEN ; PROSTATE-CANCER ; cancer risk ; LENGTH ; CARRIERS ; SERIES ; BINDING PROTEIN ; BINDING-PROTEIN ; case-control study ; RE ; VARIANT ; FACTOR-BINDING PROTEIN-3 ; interaction ; cell proliferation ; GROWTH-FACTOR-I ; ALLELES ; CARRIER ; IGFBP3 ; SERUM-LEVELS ; IGF-1 ; SEQUENCE REPEAT
    Abstract: Binding of IGF-1 to the type I IGF receptor starts a signalling cascade that plays an important role in regulating cell proliferation, differentiation and apoptosis. The interaction between the IGF-1 and its receptor is mainly regulated by a binding protein, IGFBP3. We studied a CA repeat polymorphism 969 bp upstream of the transcription start site in the IGF-1 gene and an A-202C polymorphism in the IGFBP3 gene and tested their association with breast cancer risk using four case-control series with a total of 787 cases and 900 controls. We did not find any association between the breast cancer risk and the IGF-1 repeat length (19 versus non-19) or the IGFBP3 A-202C polymorphism in the postmenopausal breast cancer series or in women diagnosed for breast cancer under the age of 50. In the familial breast cancer series we observed a non-significantly increased odds-ratio (OR) in homozygotes for the non-19 alleles of the IGF-1 gene (OR 1.51, 95% CI 0.96-2.39, p=0.07). Similarly, in the familial breast cancer series we detected an increased frequency of the IGFBP3 -202C allele carriers (OR 1.50, 95% CI 1.05-2.14, p=0.03). The association was stronger in individuals homozygous for these alleles (OR 3.76, 95% CI 1.44-9.81, p=0.006). Thus, the polymorphisms in the IGF-1 and IGFBP3 genes associated with an increased risk of breast cancer in familial cases carrying the variant alleles
    Type of Publication: Journal article published
    PubMed ID: 15986122
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  • 102
    Keywords: CANCER ; Germany ; PATHWAYS ; RISK ; ACTIVATED PROTEIN-KINASE ; BETA ; INTEGRIN ; RE ; HOMOZYGOSITY
    Type of Publication: Journal article published
    PubMed ID: 15900047
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  • 103
    Keywords: Germany ; THERAPY ; CLASSIFICATION ; RISK ; PATIENT ; treatment ; LESIONS ; EXPERIENCE ; REPAIR ; HIGH-RISK ; SELECTION ; RECONSTRUCTION ; MANAGEMENT ; SURGICAL-TREATMENT ; ABDOMINAL AORTIC-ANEURYSM ; aneurysm ; ARTERY ANEURYSMS ; endograft ; endovascular ; ENDOVASCULAR TREATMENT ; GRAFTS ; iliac artery ; MIDTERM EXPERIENCE
    Abstract: Isolated iliac aneurysms (IIA) are uncommon lesions that require surgical repair to prevent rupture. The aim of this article is to give an update on the current surgical management of IIA. This report also evaluates the application of endovascular repair in IIA, based on a recent Pubmed search and on our own experience in the interventional field: Open reconstruction achieves good longterm results and still represents the golden standard in surgical treatment of IIA. Transluminally placed endovascular stent grafts can be successfully used to exclude isolated iliac aneurysms in selected high risk patients with suitable anatomy. A classification based on aneurysm morphology is useful for patient selection. The value of endovascular therapy has yet to be determined
    Type of Publication: Journal article published
    PubMed ID: 16485205
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  • 104
    Keywords: CANCER ; Germany ; human ; MODEL ; COHORT ; RISK ; ASSOCIATION ; MEN ; COUNTRIES ; DIETARY ; ALCOHOL ; CONSUMPTION ; EPIC ; nutrition ; VEGETABLES ; CALIBRATION ; RELATIVE RISK ; REGRESSION ; ASSOCIATIONS ; LEVEL ; INTERVAL ; FRUITS ; fruits and vegetables ; prospective ; prospective study ; RECOMMENDATIONS ; EUROPEAN COUNTRIES ; CANCERS ; VARIABLES ; root vegetables ; SUBGROUPS ; upper aero-digestive cancer
    Abstract: Epidemiologic studies suggest that a high intake of fruits and vegetables is associated with decreased risk of cancers of the upper aero-digestive tract. We studied data from 345,904 subjects of the prospective European Investigation into Cancer and Nutrition (EPIC) recruited in seven European countries, who had completed a dietary questionnaire in 1992-1998. During 2,182,560 person years of observation 352 histologically verified incident squamous cell cancer (SCC) cases (255 males; 97 females) of the oral cavity, pharynx, larynx, and esophagus were identified. Linear and restricted cubic spline Cox regressions were fitted on variables of intake of fruits and vegetables and adjusted for potential confounders. We observed a significant inverse association with combined total fruits and vegetables intake (estimated relative risk (RR) = 0.91; 95% confidence interval (95% CI) 0.83-1.00 per 80 g/d of consumption), and nearly significant inverse associations in separate analyses with total fruits and total vegetables intake (RR: 0.97 (95% CI: 0.92-1.02) and RR = 0.89 (95% CI: 0.78-1.02) per 40 g/d of consumption). Overall, vegetable subgroups were not related to risk with the exception of intake of root vegetables in men. Restricted cubic spline regression did not improve the linear model fits except for total fruits and vegetables and total fruits with a significant decrease in risk at low intake levels (〈 120 g/d) for fruits. Dietary recommendations should consider the potential benefit of increasing fruits and vegetables consumption for reducing the risk of cancers of the upper aero-digestive tract, particularly at low intake
    Type of Publication: Journal article published
    PubMed ID: 16841263
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  • 105
    Keywords: Germany ; THERAPY ; FOLLOW-UP ; SYSTEM ; SYSTEMS ; MORTALITY ; RISK ; computed tomography ; SURGERY ; PATIENT ; treatment ; DESIGN ; AGE ; REPAIR ; RATES ; tomography ; COMPUTED-TOMOGRAPHY ; COMPLICATIONS ; DISSECTION ; STROKE ; THORACIC AORTA ; THROMBOSIS ; methods ; Male ; VARIABLES ; endovascular ; GRAFTS ; ANEURYSM REPAIR ; DISSECTIONS ; PHANTOMS ; PULSATILE FLOW ; SINGLE-CENTER ; STENT-GRAFT PLACEMENT ; TRUE-LUMEN COLLAPSE
    Abstract: Objective: To outline the complications after endovascular repair in patients with acute symptomatic and chronic expanding Stanford type B aortic dissections. Methods: Between 1997 and 2004, of 125 patients with acute and chronic aortic type B dissections, 88 were treated conservatively. Thirty-seven patients ( 29 male, mean age 58 years, range 30-82 years) underwent endovascular repair (30%) using 44 stent grafts of 3 different designs: Excluder ( W. L. Gore & Associates, Inc, Flagstaff, Ariz), Talent ( Medtronic Vascular, Santa Rosa, Calif), and Endofit (Endomed, Inc, Phoenix, Ariz). Indications for treatment were acute symptomatic type B dissection in 15 patients, chronic expanding aortic dissection greater than 55 mm in 14, rupture in 3, and simultaneous type A repair in 5 patients. Twenty-two operations were performed on an emergency basis. Patient characteristics, procedural variables, outcome, and complications were prospectively recorded. All patients underwent follow-up by computed tomography before discharge, at 6 and 12 months, and annually thereafter ( mean follow-up: 24 months). Results: Correct deployment was achieved in 97% of cases. There were no instances of primary conversion, paraplegia, or stroke. Complete false lumen thrombosis was observed in 11 patients (44%). Perioperative complication rate was 22%. Thirty-day mortality rate in acute and chronic dissections was 19% and 0%, respectively. Freedom from aortic reintervention was 81%, 73%, and 68%, freedom from late rupture was 97%, 90%, and 80%, and overall success rate was 76%, 65%, and 57% at 1, 2, and 5 years, respectively. Results for patients with chronic dissections are significantly ( P =.038) better than results in those with acute dissections. Conclusions: Despite the minimally invasive approach, the complication and mortality rates for endovascular therapy of aortic dissections are still high. Frank reporting of these sequelae is if great importance to clarify the recent limitations of the method
    Type of Publication: Journal article published
    PubMed ID: 16872963
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  • 106
    Keywords: human ; DISEASE ; POPULATION ; RISK ; CLONING ; GENOME ; DNA ; INFECTION ; FAMILY ; papillomavirus ; ASSOCIATION ; antibodies ; antibody ; LESIONS ; PCR ; human papillomavirus ; HPV ; BENIGN ; HUMAN-PAPILLOMAVIRUS ; case-control studies ; L1 ; CHILDREN ; PREVALENCE ; BIOPSY ; ORAL-MUCOSA ; SERUM ; ELISA ; FEATURES ; case-control study ; REQUIREMENT ; LEVEL ; case control studies ; PERSISTENCE ; population-based ; COMMUNITY ; Colombia ; Embera-Chami ; FEH ; focal epithelial hyperplasia ; HECKS DISEASE ; HPV 13 ; HUMAN-PAPILLOMAVIRUS TYPE-13 ; SOUTH-AFRICANS
    Abstract: Background: Focal epithelial hyperplasia is a benign proliferative condition that is more frequently found in children of certain ethnic groups. Human papillomavirus 13 and 32 DNA has been consistently detected in these lesions. Objective: To demonstrate the epidemiological association of HPV 13 with FEH in the Embera-Chami community of Antioquia, Colombia. Methods: A population-based, case-control study was conducted. One hundred and thirty-eight children were screened and 17 clinical and histologically-confirmed cases were sex and age-matched with 27 controls. Biopsies from FEH lesions and mouth washes from controls were obtained for DNA analysis. HPV 13 DNA was identified using a previously described type-specific PCR test. HPV 13 VLPs were produced by cloning of L1 from the HPV 13 cloned genome and seroreactivity against HPV 13 VLPs of sera from cases and controls were evaluated by ELISA. Results: Among the whole population the prevalence of FEH was 13%. One-hundred-percent of the cases and 29.6% of the controls were HPV 13 positive. There was a significant difference in HPV DNA status between cases and controls (one-tailed Fisher exact test: P 〈 0.0001). Antibodies against HPV 13 VLPs were found in 58.8% of cases and in 33.3% of controls, this difference was not statistically significant (P = 0.089 Fisher exact test). However, the median of the ODs of the ELISA positive sera of the cases was 0.596 (interquartile range: 0.5075-0.8245) versus 0.452 (interquartile range: 0.337-0.479) in the controls and this was significantly different (P = 0.0041 Man-Whitney test). Conclusions: We demonstrated a risk for association of FEH with infection with HPV 13. The higher level of antibodies against HPV 13 VLPs in cases may suggest the requirement of higher viral load or viral persistence for disease development
    Type of Publication: Journal article published
    PubMed ID: 16793332
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  • 107
    Keywords: PEPTIDE ; EXPRESSION ; INVASION ; Germany ; human ; COHORT ; DISEASE ; DISEASES ; POPULATION ; RISK ; GENE ; GENOME ; HYBRIDIZATION ; PATIENT ; DNA ; INDUCTION ; colon ; polymorphism ; COMPARATIVE GENOMIC HYBRIDIZATION ; COPY NUMBER ; NUMBER ; HUMAN GENOME ; PEPTIDES ; POLYMERASE-CHAIN-REACTION ; INDIVIDUALS ; ULCERATIVE-COLITIS ; inflammation ; INFLAMMATORY-BOWEL-DISEASE ; CLUSTER ; DNA-SEQUENCE ; INTERVAL ; LOCUS ; chronic inflammation ; DEFICIENT ; SEGMENTAL DUPLICATIONS ; odds ratio ; genomic ; ALPHA-DEFENSIN ; DEFENSIN DEFICIENCY ; healthy individuals ; NOD2 ; PANETH CELLS ; RESIDENT INTESTINAL FLORA
    Abstract: Defensins are endogenous antimicrobial peptides that protect the intestinal mucosa against bacterial invasion. It has been suggested that deficient defensin expression may underlie the chronic inflammation of Crohn disease ( CD). The DNA copy number of the beta-defensin gene cluster on chromosome 8p23.1 is highly polymorphic within the healthy population, which suggests that the defective beta-defensin induction in colonic CD could be due to low beta-defensin gene copy number. Here, we tested this hypothesis, using genomewide DNA copy number profiling by array-based comparative genomic hybridization and quantitative polymerase-chain-reaction analysis of the human beta-defensin 2 (HBD-2) gene. We showed that healthy individuals, as well as patients with ulcerative colitis, have a median of 4 ( range 2 - 10) HBD-2 gene copies per genome. In a surgical cohort with ileal or colonic CD and in a second large cohort with inflammatory bowel diseases, those with ileal resections/disease exhibited a normal median HBD-2 copy number of 4, whereas those with colonic CD had a median of only 3 copies per genome ( for the surgical cohort; P = .008 P = .032 for the second cohort). Overall, the copy number distribution in colonic CD was shifted to lower numbers compared with controls ( for both the surgical cohort and the cohort with inflammatory bowel diseases). Individuals with P = .002 〈= 3 copies have a significantly higher risk of developing colonic CD than did individuals with 〉= 4 copies ( odds ratio 3.06; 95% confidence interval 1.46 - 6.45). An HBD-2 gene copy number of 〈 4 was associated with diminished mucosal HBD-2 mRNA expression (P = 0.033). In conclusion, a lower HBD-2 gene copy number in the beta-defensin locus predisposes to colonic CD, most likely through diminished beta-defensin expression
    Type of Publication: Journal article published
    PubMed ID: 16909382
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  • 108
    Keywords: CANCER ; EXPRESSION ; Germany ; PATHWAY ; RISK ; GENE ; transcription ; PATIENT ; FAMILY ; TRANSCRIPTION FACTOR ; MARKER ; ASSOCIATION ; VARIANTS ; BREAST ; breast cancer ; BREAST-CANCER ; SNP ; cancer risk ; COLORECTAL CANCERS ; case-control studies ; INDIVIDUALS ; beta-catenin ; C-MYC ; TYPE-2 ; WNT ; CYCLIN D1 ; signaling ; case-control study ; RE ; FAMILIES ; VARIANT ; case control studies ; ROLES ; CANCER-RISK ; FAMILIAL BREAST ; familial breast cancer ; GENETIC ALTERATION ; Wnt signaling ; type 2 diabetes
    Abstract: Background: The transcription factor 7-like 2 (TCF7L2) is a critical component of the Wnt/beta-catenin pathway. Aberrant TCF7L2 expression modifies Wnt signaling and mediates oncogenic effects through the upregulation of c-MYC and cyclin D. Genetic alterations in TCF7L2 may therefore affect cancer risk. Recently, TCF7L2 variants, including the microsatellite marker DG10S478 and the nearly perfectly linked SNP rs12233372, were identified to associate with type 2 diabetes. Methods: We investigated the effect of the TCF7L2 rs12255372 variant on familial breast cancer ( BC) risk by means of TaqMan allelic discrimination, analyzing BRCA1/2 mutation-negative index patients of 592 German BC families and 735 control individuals. Results: The T allele of rs12255372 showed an association with borderline significance ( OR = 1.19, 95% C. I. = 1.01-1.42, P = 0.04), and the Cochran-Armitage test for trend revealed an allele dose-dependent association of rs12255372 with BC risk ( P-trend = 0.04). Conclusion: Our results suggest a possible influence of TCF7L2 rs12255372 on the risk of familial BC
    Type of Publication: Journal article published
    PubMed ID: 17109766
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  • 109
    Keywords: CANCER ; SURVIVAL ; Germany ; neoplasms ; DIAGNOSIS ; COHORT ; DISEASE ; DISEASES ; MORTALITY ; POPULATION ; RISK ; RISKS ; PATIENT ; RISK-FACTORS ; BREAST ; LYMPHOMA ; NUMBER ; CLINICAL-TRIALS ; risk factors ; case-control studies ; INHIBITORS ; case-control study ; case control studies ; INTERVAL ; DRUGS ; RISK-FACTOR ; PRAVASTATIN ; PROTEIN GERANYLGERANYLATION
    Abstract: Background: Statins, drugs used to treat dyslipidemia, may have anticancer properties. We have evaluated lymphoma risk associated with regular statin use in an international case-control study. Methods: This case-control study included 2,362 cases of incident B- and T-cell lymphoma from Czech Republic, France, Germany, Ireland, Italy, and Spain and 2,206 hospital or population controls. Information on drug use, diagnosis at admission (for hospital controls), and putative risk factors for lymphoma was collected with personal interviews. Hospital controls admitted for diseases possibly entailing use of statins were excluded from the analysis. Results: The odds ratio for regular statin use was 0.61 (95% confidence interval, 0.45-0.84); all major lymphoma subtypes showed similarly decreased risks. Decreased risks were observed in all centers. Duration of statin use was not associated with a greater reduction in the risk of lymphoma. Use of other lipid lowering drugs, such as fibrates, did not significantly modify the risk of lymphoma (odds ratio, 0.75; 95% confidence interval, 0.44-1.27). Conclusion: Statin use was associated with an important reduction in lymphoma risk, adding to the growing evidence of anticancer properties of this group of drugs. These results are reassuring for the increasing number of patients taking statins on a regular basis
    Type of Publication: Journal article published
    PubMed ID: 16702371
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  • 110
    Keywords: CANCER ; tumor ; FOLLOW-UP ; COHORT ; RISK ; RISKS ; TUMORS ; colon ; ASSOCIATION ; ENERGY ; WOMEN ; etiology ; MEN ; COLORECTAL-CANCER ; cancer risk ; COLON-CANCER ; DOSE-RESPONSE ; UNITED-STATES ; BODY ; body mass index ; nutrition ; dietary fiber ; LEISURE-TIME ; physical activity ; RECTAL-CANCER ; MASS INDEX ; ASSOCIATIONS ; colon cancer ; PHYSICAL-ACTIVITY ; INTERVAL ; PARTICIPANTS ; BODY-MASS INDEX ; ENERGY-BALANCE ; prospective ; BMI ; CANCERS ; CANCER-RISK ; ACTIVITY QUESTIONNAIRE ; ANATOMIC SUBSITE ; intake ; LARGE-BOWEL-CANCER ; OCCUPATIONAL RISK
    Abstract: We investigated several aspects of the role of physical activity in colon and rectal cancer etiology that remain unclear in the European Prospective Investigation into Nutrition and Cancer. This cohort of 413,044 men and women had 1,094 cases of colon and 599 cases of rectal cancer diagnosed during an average of 6.4 years of follow-up. We analyzed baseline data on occupational, household, and recreational activity to examine associations by type of activity, tumor subsite, body mass index (BMI), and energy intake. The multivariate hazard ratio for colon cancer was 0.78 [95% confidence interval (95% CI), 0.59-1.03] among the most active participants when compared with the inactive, with evidence of a dose-response effect (P-trend = 0.04). For right-sided colon tumors, the risk was 0.65 (95% CI, 0.43-1.00) in the highest quartile of activity with evidence of a linear trend (P-trend=0.004). Active participants with a BMI under 25 had a risk of 0.63 (95% CI, 0.39-1.01) for colon cancer compared with the inactive. Finally, an interaction between BMI and activity (P-interaction=0.03) was observed for right-sided colon cancers; among moderately active and active participants with a BMI under 25, a risk of 0.38 (95% CI, 0.21-0.68) was found as compared with inactive participants with BMI 〉 30. No comparable decreased risks were observed for rectal cancer for any type of physical activity for any subgroup analyses or interactions considered. We found that physical activity reduced colon cancer risk, specifically for right-sided tumors and for lean participants, but not rectal cancer
    Type of Publication: Journal article published
    PubMed ID: 17164362
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  • 111
    Keywords: CELL ; Germany ; RISK ; RISKS ; DRUG ; COMPLEXES ; NUCLEI ; ERYTHROPOIETIN ; RE ; XENOPUS-LAEVIS OOCYTES
    Type of Publication: Journal article published
    PubMed ID: 16815349
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  • 112
    Keywords: CANCER ; Germany ; human ; PROSTATE ; ALGORITHM ; ALGORITHMS ; DIAGNOSIS ; COHORT ; RISK ; GENE ; GENES ; TIME ; PATIENT ; FAMILY ; treatment ; ASSOCIATION ; MALIGNANCIES ; AGE ; MUTATION ; REPAIR ; colorectal cancer ; COLORECTAL-CANCER ; prostate cancer ; PROSTATE-CANCER ; COLON-CANCER ; HEREDITARY ; MISMATCH REPAIR ; MUTATIONS ; CANCER-PATIENTS ; UNITED-STATES ; INDIVIDUALS ; CANCER PATIENTS ; GASTRIC-CANCER ; germline mutations ; NONPOLYPOSIS COLORECTAL-CANCER ; GENE-MUTATIONS ; RECTAL-CANCER ; MALIGNANCY ; ONCOLOGY ; FAMILIES ; MUTATION CARRIERS ; HNPCC ; gastric cancer ; MLH1 ; analysis ; methods ; MISMATCH-REPAIR ; correlation ; Male ; CANCERS ; colorectal ; hereditary nonpolyposis colorectal cancer ; MISMATCH-REPAIR-GENE ; PROSTATE CANCERS ; DNA-MISMATCH-REPAIR ; MUIR-TORRE-SYNDROME ; SYNDROME-II ; TUMOR SPECTRUM
    Abstract: Purpose Lynch syndrome is linked to germline mutations in mismatch repair genes. We analyzed the genotype-phenotype correlations in the largest cohort so far reported. Patients and Methods Following standard algorithms, we identified 281 of 574 unrelated families with deleterious germline mutations in MLH1 (n = 124) or MSH2 (n = 157). A total of 988 patients with 1,381 cancers were included in this analysis. Results We identified 181 and 259 individuals with proven or obligatory and 254 and 294 with assumed MLH1 and MSH2 mutations, respectively. Age at diagnosis was younger both in regard to first cancer (40 v 43 years; P 〈.009) and to first colorectal cancer (CRC; 41 v 44 years; P =.004) in MLH1 (n = 435) versus MSH2 (n = 553) mutation carriers. In both groups, rectal cancers were remarkably frequent, and the time span between first and second CRC was smaller if the first primary occurred left sided. Gastric cancer was the third most frequent malignancy occurring without a similarly affected relative in most cases. All prostate cancers occurred in MSH2 mutation carriers. Conclusion The proportion of rectal cancers and shorter time span to metachronous cancers indicates the need for a defined treatment strategy for primary rectal cancers in hereditary nonpolyposis colorectal cancer patients. Male MLH1 mutation carriers require earlier colonoscopy beginning at age 20 years. We propose regular gastric surveillance starting at age 35 years, regardless of the familial occurrence of this cancer. The association of prostate cancer with MSH2 mutations should be taken into consideration both for clinical and genetic counseling practice
    Type of Publication: Journal article published
    PubMed ID: 16908935
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  • 113
    Keywords: CANCER ; RISK ; INFECTION ; STOMACH ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; STOMACH-CANCER ; UNIT ; RISK-FACTOR ; Helicobacter pylori ; stomach cancer
    Type of Publication: Journal article published
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  • 114
    Keywords: CANCER ; Germany ; human ; neoplasms ; RISK ; TIME ; ASSOCIATION ; LYMPHOMA ; MALIGNANCIES ; WOMEN ; MEN ; leukemia ; cancer risk ; CARCINOGENS ; hair dyes ; case-control studies ; NON-HODGKINS-LYMPHOMA ; MALIGNANCY ; PRODUCTS ; HUMAN CANCER ; INCREASE ; INTERVAL ; odds ratio ; population-based ; CANCER-RISK ; lymphatic system
    Abstract: Hair dyes have been evaluated as possibly being mutagenic and carcinogenic in animals. Studies of the association between human cancer risk and use of hair dyes have yielded inconsistent results. The authors evaluated the risk of lymphoid malignancies associated with personal use of hair dyes. The analysis included 2,302 incident cases of lymphoid neoplasms and 2,417 hospital- or population-based controls from the Czech Republic, France, Germany, Ireland, Italy, and Spain (1998-2003). Use of hair dyes was reported by 74% of women and 7% of men. Lymphoma risk among dye users was significantly increased by 19% in comparison with never use (odds ratio (OR) = 1.19, 95% confidence interval (CI): 1.00, 1.41) and by 26% among persons who used hair dyes 12 or more times per year (OR = 1.26, 95% CI: 1.00, 1.60; p for linear trend = 0.414). Lymphoma risk was significantly higher among persons who had started coloring their hair before 1980 (OR = 1.37, 95% CI: 1.09, 1.72) and persons who had used hair dyes only before 1980 (OR = 1.62, 95% CI: 1.10, 2.40). Personal use of hair dyes is associated with a moderate increase in lymphoma risk, particularly among women and persons who used dyes before 1980. Specific compounds associated with this risk remain to be elucidated
    Type of Publication: Journal article published
    PubMed ID: 16731576
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  • 115
    Keywords: CANCER ; MODEL ; MODELS ; FOLLOW-UP ; COHORT ; DISEASE ; MORTALITY ; RISK ; RISKS ; AGE ; WOMEN ; OBESITY ; smoking ; COUNTRIES ; TOBACCO ; GLUCOSE ; BODY ; DIABETES-MELLITUS ; nutrition ; pancreatic cancer ; RELATIVE RISK ; physical activity ; MASS INDEX ; PANCREATIC-CANCER ; PHYSICAL-ACTIVITY ; HEIGHT ; WAIST ; INTERVAL ; pancreatic ; INSULIN-RESISTANCE ; PARTICIPANTS ; anthropometry ; prospective ; RISK-FACTOR ; BODY-FAT DISTRIBUTION ; hip ; MALE SMOKERS
    Abstract: Tobacco smoking is the only established risk factor for pancreatic cancer. Results from several epidemiologic studies have suggested that increased body mass index and/or lack of physical activity may be associated with an increased risk of this disease. We examined the relationship between anthropometry and physical activity recorded at baseline and the risk of pancreatic cancer in the European Prospective Investigation into Cancer and Nutrition (n = 438,405 males and females age 19-84 years and followed for a total of 2,826,070 person-years). Relative risks (RR) were calculated using Cox proportional hazards models stratified by age, sex, and country and adjusted for smoking and self-reported diabetes and, where appropriate, height. In total, there were 324 incident cases of pancreatic cancer diagnosed in the cohort over an average of 6 years of follow-up. There was evidence that the RR of pancreatic cancer was associated with increased height [RR, 1.74; 95% confidence interval (95% CI), 1.20-2.52] for highest quartile compared with lowest quartile (P-trend = 0.001). However, this trend was primarily due to a low risk in the lowest quartile, as when this group was excluded, the trend was no longer statistically significant (P = 0.27). A larger waist-to-hip ratio and waist circumference were both associated with an increased risk of developing the disease (RR per 0.1, 1.24; 95% CI, 1.04-1.48; P-trend = 0.02 and RR per 10 cm, 1.13; 95% CI, 1.01-1.26; P-trend = 0.03, respectively). There was a nonsignificant increased risk of pancreatic cancer with increasing body mass index (RR, 1.09; 95% CI, 0.95-1.24 per 5 kg/m(2)), and a nonsignificant decreased risk with total physical activity (RR, 0.82; 95% CI, 0.50-1.35 for most active versus inactive). Future studies should consider including measurements of waist and hip circumference, to further investigate the relationship between central adiposity and the risk of pancreatic cancer
    Type of Publication: Journal article published
    PubMed ID: 16702364
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  • 116
    Keywords: RECEPTOR ; CANCER ; RISK ; GENE ; ASSOCIATION ; polymorphism ; BREAST-CANCER ; PROMOTER ; ENDOMETRIAL CANCER ; insulin ; ENDOMETRIAL ; GROWTH-FACTOR-I ; HORMONES ; OVARIAN ; ENDOGENOUS HORMONES ; FUNCTIONAL POLYMORPHISM
    Type of Publication: Journal article published
    PubMed ID: 16835347
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  • 117
    Keywords: human ; MODEL ; MODELS ; PATHWAY ; PATHWAYS ; RISK ; ENZYMES ; METABOLISM ; ACTIVATION ; RAT ; animals ; HPLC ; METABOLITES ; carcinogenicity ; HEALTH ; HUMANS ; OXIDATION ; rodent ; cytochrome P450 ; RECOMBINANT ; PRODUCTS ; CARCINOGEN ; LEVEL ; ENZYME ; methods ; SEPARATION ; carcinogenic ; EXTRAPOLATION ; PARTICIPATION ; animal
    Abstract: OBJECTIVES: The detoxifying metabolism of a potent rodent carcinogen, 2-nitroanisole (2-NA) by human, rabbit and rat cytochromes P450 (P450) was investigated. Comparison between P450s of experimental animals and humans is essential for the extrapolation of animal carcinogenicity data to the human situation and to assess health risk. METHODS: HPLC with UV detection was employed for the separation and characterization of 2-NA metabolites formed by hepatic microsomes, human recombinant P450s and purified rat and rabbit P450s. RESULTS: An O-demethylated metabolite of 2-NA, 2-nitrophenol (2-NP), and two oxidation products of this metabolite [2,5-dihydroxynitrobenzene (2,5-DNB) and 2,6-dihydroxynitrobenzene (2,6-DNB)] were generated by microsomes and P450s from the species investigated, but at different levels. All the metabolites are detoxication products. 2-NP is the major metabolite generated by rabbit and rat microsomes, but 2,5-DNB is the predominant product in human microsomes. Using human recombinant P450s and purified rodent P450s, we found that human P450 2E1, 1A1 and 2B6 as well as orthologous animal P450s were the most efficient enzymes oxidizing 2-NA to 2-NP, while P450 2E1 and 1A1 were the most effective in the formation of 2,5-DNB and 2,6-DNB. In human hepatic microsomes, 2-NA was oxidized mainly by P4502E1. 2-NA and its reductive metabolite o-anisidine induced rat hepatic and renal P450 1A1/2 and NAD(P)H:quinone oxidoreductase (NQO1), thus modifying their own detoxication and/or activation pathways. CONCLUSIONS: The data demonstrated the participation of orthologous P450s in 2-NA oxidation by all species and indicated that the rat and rabbit might serve as suitable models to mimic 2-NA oxidation in man
    Type of Publication: Journal article published
    PubMed ID: 17159769
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  • 118
    Keywords: CANCER ; Germany ; COHORT ; cohort studies ; cohort study ; RISK ; GENES ; familial risk ; MULTIPLE-SCLEROSIS ; RE ; multiple sclerosis
    Type of Publication: Journal article published
    PubMed ID: 16554342
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  • 119
    Keywords: CANCER ; tumor ; Germany ; DISEASE ; incidence ; RISK ; RISKS ; GENE ; GENES ; TUMORS ; SUSCEPTIBILITY ; IDENTIFICATION ; IN-SITU ; AGE ; WOMEN ; cervical cancer ; CERVICAL-CANCER ; DATABASE ; familial risk ; FAMILY-CANCER DATABASE ; CANCER DATABASE ; RE ; AGGREGATION ; familial aggregation ; TWINS ; CANCERS ; VARIABLES
    Abstract: Many studies have shown familial aggregation for cervical cancer, but they have been unable to distinguish between shared environmental and genetic effects. Full and half-siblings were identified from the nationwide Swedish Family-Cancer Database, including invasive and in situ cervical cancers in women up to age 70 years. Half-siblings were defined through a common father or mother. Standardized incidence ratios, adjusted for several variables, were calculated for proband-wise risks between full and half-siblings. The familial risk for full siblings was 1.84, compared with 1.40 for maternal and 1.27 for paternal half-siblings. These data were used to apportion familial risk for cervical tumors in full siblings into a heritable component, accounting for 64%, and an environmental component, accounting for 36% of the total risk. No evidence for gene-environment interactions was found. The intractable difficulty in separating cervical cancer causation will be an obstacle for a successful identification of susceptibility genes
    Type of Publication: Journal article published
    PubMed ID: 16835346
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  • 120
    Keywords: CANCER ; Germany ; CLASSIFICATION ; DISEASE ; DISEASES ; RISK ; RISKS ; DISTINCT ; GENE ; GENES ; MECHANISM ; mechanisms ; treatment ; SUSCEPTIBILITY ; IDENTIFICATION ; etiology ; SWEDEN ; DATABASE ; TWIN ; familial risk ; MULTIPLE-SCLEROSIS ; HOSPITALIZATION ; MOLECULAR-BASIS ; DISORDERS ; GENETIC EPIDEMIOLOGY ; RE ; AGGREGATION ; SUBTYPES ; familial aggregation ; SIZE ; epilepsy ; SAMPLE-SIZE ; CEREBRAL-PALSY ; MUSCULAR-DYSTROPHIES ; MIGRAINE ; SLEEP
    Abstract: Recent successes in identifying the underlying genetic mechanisms for neurological diseases, particularly for their Mendelian forms, have had profound implications for their diagnostics, treatment and classification. However, there has never been an attempt to compare familial risks in a systematic way among and between the main neurological diseases. Familial risks were here defined for siblings who were hospitalized because of a neurological disease in Sweden. A nationwide database for neurological diseases was constructed by linking the Multigeneration Register of 0- to 69-year-old siblings to the Hospital Discharge Register for the years 1987 to 2001. Standardized risk ratios were calculated for affected sibling pairs by comparing them to those whose siblings had no neurological disease. There were three main results. First, it was shown that all disease groups had a familial risk, with the exception of transient ischemic attacks, and the risks could be ranked from the highest (3451) for Huntington's disease to the lowest (2.1) for inflammatory diseases. Second, increased familial risks were shown for disease subtypes for which susceptibility genes or familial clustering have not been demonstrated previously, including multiple sclerosis, sleep apnea, nerve, nerve root and plexus disorders, and cerebral palsy. Third, based on the available sample size there was no convincing evidence for familial comorbidity between the disease groups, suggesting that the factors causing familial aggregation, probably usually heritable genes, are distinct for each subtype. The high familial risks for neurological disease imply heritable etiology and opportunities for identification of further susceptibility genes
    Type of Publication: Journal article published
    PubMed ID: 16899166
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  • 121
    Keywords: BLOOD ; Germany ; human ; CLASSIFICATION ; FOLLOW-UP ; COHORT ; DEATH ; DISEASE ; EPIDEMIOLOGY ; RISK ; PROTEIN ; PROTEINS ; HEART ; PATIENT ; INFECTION ; ASSOCIATION ; antibodies ; antibody ; HUMANS ; meta-analysis ; etiology ; risk factors ; C-REACTIVE PROTEIN ; MYOCARDIAL-INFARCTION ; DIABETES-MELLITUS ; INFECTIONS ; COMPLICATIONS ; STROKE ; SERUM ; ADULT ; PROGRAM ; INCREASE ; CARDIOVASCULAR-DISEASE ; prospective studies ; CORONARY-HEART-DISEASE ; METAANALYSIS ; analysis ; methods ; PARTICIPANTS ; EVENTS ; prospective ; prospective study ; Chlamydophila pneumoniae ; microbiology ; Aged ; Middle Aged ; Antibodies,Bacterial ; cardiovascular disease ; cardiovascular diseases ; Chaperonin 60 ; Chlamydophila Infections ; Coronary Disease ; Diabetes Mellitus ; myocardial infarction ; Proportional Hazards Models ; rehabilitation
    Abstract: BACKGROUND: There have been suggestions of an association between Chlamydia pneumoniae, chlamydial heat shock protein (Ch-hsp) 60 and human heat shock protein (h-hsp) 60 infection sero-status and development of secondary cardiovascular events. Patients with diabetes might be at higher risk since they are prone to infections. The objective of this study was to investigate prospectively the role of Chlamydia pneumoniae (CP), chlamydial heat shock protein (Ch-hsp) 60 and a possible intermediate role of human heat shock protein (h-hsp) 60 sero-status in the development of secondary cardiovascular disease (CVD) events in patients with coronary heart disease (CHD) under special consideration of diabetes mellitus. METHODS: Patients aged 30-70 undergoing an in-patient rehabilitation program after acute manifestation of coronary heart disease (International Classification of Disease, 9th Rev. pos. 410-414) between January 1999 and May 2000 in one of two participating rehabilitation clinics in Germany were included in this analysis. Chlamydia pneumoniae (CP), chlamydial heat shock protein (Ch-hsp) 60 and human heat shock protein (h-hsp) 60 status at baseline were measured by serum immunoglobulin G and A antibodies. Secondary CVD events (myocardial infarction, stroke, and cardiovascular death) were recorded during a mean follow-up period of 33.5 months (response = 87%). RESULTS: Among the 1052 subjects 37.4% and 39.3% were sero-positive to CP IgA and IgG respectively, 22.2% were sero-positive to Ch-hsp 60 IgG and 8.4% were positive to h-hsp 60 IgG at baseline. During follow-up, secondary CVD events occurred among 71 (6.8%) participants. Occurrence of a secondary CVD event was more common among CP (IgA) and CP (IgG) sero-positive than among sero-negative patients (p-values 0.04 and 0.1, respectively). The risk of secondary CVD events was increased among patients with both a positive CP sero-status and diabetes compared to infection negative, non-diabetic patients and in general, sero-positivity added a hazard to diabetes. The interaction term between infection sero-status and diabetes was not statistically significant. We were not able to show an intermediate role of human heat shock protein (h-hsp) 60 sero-status in the development of secondary CVD events in patients with CHD. CONCLUSION: Results from this cohort of 1052 patients with pre-existing CHD cannot exclude a possible moderate increase in risk of secondary CVD events among patients with a positive infection sero-status. However, our study showed no intermediate role of human heat shock protein (h-hsp) 60 sero-status in the development of secondary CVD events in patients with CHD. Larger studies or meta-analysis of multiple studies are needed to address the interaction between infection sero-status and diabetes with adequate power
    Type of Publication: Journal article published
    PubMed ID: 16608530
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  • 122
    Keywords: CANCER ; FOLLOW-UP ; COHORT ; EXPOSURE ; RISK ; NITRIC-OXIDE ; INFECTION ; ASSOCIATION ; antibodies ; antibody ; PLASMA ; NUMBER ; cancer risk ; DIETARY ; INDIVIDUALS ; CARDIA ; CONSUMPTION ; EPIC ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; nutrition ; DIETARY-INTAKE ; INCREASE ; IRON ; LEVEL ; prospective ; MEAT INTAKE ; RED MEAT ; CANCER-RISK ; Helicobacter pylori ; N-NITROSO COMPOUNDS ; HEME ; processed meat
    Abstract: The risk of gastric cancer (GC) associated with dietary intake of nitrosodimethylamine (NDMA) and endogenous formation of nitroso compounds (NOCs) was investigated in the European Prospective Investigation into Cancer and Nutrition (EPIC). The study included 521 457 individuals and 314 incident cases of GC that had occurred after 6.6 average years of follow-up. An index of endogenous NOC (ENOC) formation was estimated using data of the iron content from meat intake and faecal apparent total NOC formation according to previous published studies. Antibodies to Helicobacter pylori and vitamin C levels were measured in a sub-sample of cases and matched controls included in a nested case-control within the cohort. Exposure to NDMA was 〈 1 mu g on average compared with 93 mu g on average from ENOC. There was no association between NDMA intake and GC risk (HR, 1.00; 95% CI, 0.7-1.43). ENOC was significantly associated with non-cardia cancer risk (HR, 1.42; 95% CI, 1.14-1.78 for an increase of 40 mu g/day) but not with cardia cancer (HR, 0.96; 95% CI, 0.69-1.33). Although the number of not infected cases is low, our data suggest a possible interaction between ENOC and H.pylori infection (P for interaction = 0.09). Moreover, we observed an interaction between plasma vitamin C and ENOC (P 〈 0.02). ENOC formation may account for our previously reported association between red and processed meat consumption and gastric cancer risk
    Type of Publication: Journal article published
    PubMed ID: 16571648
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  • 123
    Keywords: CANCER ; CELL ; DISEASE ; DISEASES ; incidence ; liver ; RISK ; RISKS ; GENE ; kidney ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; AGE ; MELANOMA ; SWEDEN ; DATABASE ; MUTATIONS ; familial risk ; CHILDREN ; FAMILY-CANCER DATABASE ; CHONDROSARCOMA ; CHILDHOOD ; ASSOCIATIONS ; AGGREGATION ; LI-FRAUMENI-SYNDROME ; Ewing's sarcoma ; osteosarcoma ; familial aggregation ; BONE ; CANCERS ; PROBAND ; familial disease ; KIDNEY CANCER ; HISTOLOGICAL TYPE ; bone cancer ; EARLY-ONSET ; EWINGS-SARCOMA ; giant cell sarcoma ; NEUROECTODERMAL TUMORS ; soft-tissue sarcoma
    Abstract: We used the nation-wide Swedish Family-Cancer Database to examine the familial risks of histology-specific bone cancers in offspring by parental or sibling probands. Adjusted standardised incidence ratios (SIRS) were used to measure the risk. Among the 1327 offspring bone cancers, only two parent-offspring pairs and one sibling pair were noted with concordant bone cancer but the SIRS were not significant. Significant associations were observed in specific histological types or specific age groups, some of which may be chance findings arising from multiple comparisons. However, the risk of early-onset (〈 25 years) osteosarcoma in offspring was significantly increased when mothers presented with breast cancer (1.7) and melanoma (2.9), suggesting that Li-Fraumeni syndrome could partly explain this familial aggregation. Other associations, such as childhood osteosarcoma with parental liver cancer, Ewing's sarcoma with kidney cancer and giant cell sarcoma with maternal breast cancer, were novel findings and may be related to other familial diseases. (c) 2006 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16859907
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  • 124
    Keywords: CANCER ; tumor ; carcinoma ; human ; CLASSIFICATION ; EXPOSURE ; RISK ; SITE ; PROTEIN ; PROTEINS ; TUMORS ; PATIENT ; DNA ; INFECTION ; FAMILY ; RISK-FACTORS ; SKIN ; MR ; papillomavirus ; ASSOCIATION ; antibodies ; IN-SITU ; risk factors ; PATHOGENESIS ; human papillomavirus ; VIRUS-LIKE PARTICLES ; HUMAN-PAPILLOMAVIRUS ; CARCINOMAS ; case-control studies ; squamous cell carcinoma ; INDIVIDUALS ; sensitivity ; RENAL-TRANSPLANT RECIPIENTS ; basal cell carcinoma ; glutathione-S-transferase ; CELL CARCINOMA ; case-control study ; population-based case-control study ; ASSOCIATIONS ; case control studies ; INTERVAL ; TECHNOLOGY ; RISK-FACTOR ; CANCERS ; population-based ; IMMUNOCOMPETENT INDIVIDUALS ; E6 PROTEIN ; multiplex serology ; PLUCKED EYEBROW HAIRS
    Abstract: Background. Although infection with human papillomaviruses (HPVs) is a major risk factor for several epithelial cancers, an etiologic relationship between HPV and keratinocyte cancers, such as squamous cell carcinomas (SCCs) and basal cell carcinomas (BCCs), remains unclear. Methods: In a population-based case-control study of 252 SCC case patients, 525 BCC case patients, and 461 control subjects, we used multiplex serology to detect antibodies in plasma samples against 16 HPV types from phylogenetic genera alpha, beta, and mu. Multiplex serology is a new method that is based on fluorescent bead technology and allows simultaneous detection of antibodies against up to 100 different in situ affinity-purified recombinant HPV proteins. Data on sun sensitivity, outdoor exposure, and other risk factors for keratinocyte cancers were collected through personal interviews. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated via unconditional logistic regression models. Results: Overall, we detected HPV antibodies more frequently in SCC patients than in control subjects (OR = 1.6, 95% CI = 1.2 to 2.3), but we found no difference in HPV seropositivity between BCC case patients and control subjects (OR = 0.8, 95% CI = 0.6 to 1.1). Among HPV types, seropositivity to HPV types in genus beta (OR = 1.5,95% CI = 1.0 to 2.1), particularly HPV 5 (OR = 1.8,95% CI = 1.0 to 3.1), was associated with SCC risk. Individuals with tumors on chronically sun exposed sites were more likely to be seropositive for beta HPV types than individuals with SCC at other anatomic sites. The highest SCC risk was associated with positivity for multiple HPV types and, among individuals seropositive for HPV beta, a tendency to sunburn; however, the associations had limited statistical precision. Conclusions: Our findings support a role for HPV types from the genus beta in the pathogenesis of SCC
    Type of Publication: Journal article published
    PubMed ID: 16537831
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  • 125
    Keywords: CANCER ; GROWTH ; GROWTH-FACTOR ; BLOOD ; COHORT ; DISEASE ; RISK ; PROTEIN ; RISK-FACTORS ; INTERVENTION ; BINDING ; ASSOCIATION ; BREAST-CANCER ; hormone ; HEALTH ; PLASMA ; AGE ; WOMEN ; MEN ; risk factors ; PRESSURE ; cholesterol ; GLUCOSE ; BLOOD-PRESSURE ; MYOCARDIAL-INFARCTION ; BODY ; HYPERTENSION ; PROJECT ; body mass index ; FACTOR-I ; CARDIOVASCULAR RISK-FACTORS ; BINDING PROTEIN ; insulin ; MASS INDEX ; IGF-I ; ASSOCIATIONS ; RE ; ARRAY ; CARDIOVASCULAR-DISEASE ; GROWTH-FACTOR-I ; LEVEL ; INTERVAL ; analysis ; methods ; HORMONES ; odds ratio ; BMI ; RISK-FACTOR ; CANCERS ; cross-sectional studies ; Aged ; IGFBP-1 ; IGFBP-3 ; NUTRITIONAL REGULATION ; cardiovascular disease ; cardiovascular risk factors ; COLORECTAL-CANCER RISK ; FACTOR-BINDING-PROTEINS ; insulin-like growth factor binding proteins ; Insulin-Like Growth Factor I ; ISCHEMIC-HEART-DISEASE ; LEFT-VENTRICULAR HYPERTROPHY
    Abstract: PURPOSE: Elevated circulating insulin-like growth factor I (IGF-I) levels increasingly are being implicated as a potential risk factor for the development of some cancers; however, relatively few epidemiologic Studies have focused on potential relationships between circulating IGF-I levels an cardiovascular risk factors or cardiovascular disease. Hence, our objective is to examine relationships between IGF-I levels; body mass index (BMI); fasting insulin level; IGF binding protein 1 (IGFBP-1), IGFBP-2, and IGFBP-3 levels; and an array of traditional cardiovascular risk factors. METHODS: Our analysis included 715 men and women aged 30 to 62 years who participated in the Vasterbotten Intervention Project cohort. IGF-1 and IGFBP-1, -2, and -3 were measured in stored plasma samples. Cardiovascular risk factors of interest included glucose level (fasting and 2-hour postload). lipid levels (total cholesterol, high-density lipoprotein cholesterol, and triglycerides), blood pressure (systolic and diastolic), and hypertension status. All presented results were adjusted for age, sex, and laboratory batch. RESULTS: IGF-1 quartile was associated inversely with 2-hour glucose level and diastolic blood pressure. There was a stepwise inverse graded association between increasing IGF-I quartile and hypertension, with an odds ratio of 0.51 (95% confidence interval, 0.29-0.90) for hypertension comparing the fourth IGF-I quartile with the first. Further adjusting for BMI and IGFBP-3 level simultaneously strengthened the inverse association, with an odds ratio of 0.42 (95% confiderice interval, 0.22-0.80) for hypertension comparing the fourth With the first IGF-I quartile. CONCLUSIONS: Contrary to positive associations between IGF-I levels and some cancers, Our results suggest that IGF-I level may be related inversely to prevalent hypertension, a risk factor for cardiovascular disease
    Type of Publication: Journal article published
    PubMed ID: 16431135
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  • 126
    Keywords: COHORT ; POPULATION ; RISK ; GENE ; DIFFERENTIATION ; AIR-POLLUTION ; SKIN ; T-CELLS ; ASSOCIATION ; polymorphism ; DESIGN ; PREVALENCE ; asthma ; ATOPY ; CYTOKINE ; REGISTRY ; IL-18 ; INTERVAL ; single-nucleotide ; single-nucleotide polymorphism ; haplotype-tagging ; allergic rhinitis ; cohort analysis ; RISK-FACTOR ; population-based ; general population ; BRONCHIAL-ASTHMA ; IGE LEVELS ; IL18 GENE ; LUNG-DISEASES
    Abstract: IL-18 is a pleiotrophic cytokine involved in both, T-helper type 1 (Th1) and Th2 differentiation. Recently genetic variants in the IL-18 gene have been associated with increased risk of atopy and asthma. To examine the relationship of a genetic, haplotype-tagging promotor variant -137G/C in the IL-18 gene with atopic asthma in a large, well-characterized and population-based study of adults. Prospective cohort study design was used to collect interview and biological measurement data at two examination time-points 11 years apart. Multivariate logistic regression analysis was used to assess the association of genotype with asthma and atopy. The G-allele of the IL-18 promotor variant (-137G/C) was associated with a markedly increased risk for the prevalence of physician-diagnosed asthma with concomitant skin reactivity to common allergens. Stratification of the asthma cases by skin reactivity to common allergens revealed an exclusive association of IL-18 -137 G-allele with an increased prevalence of atopic asthma (adjusted odds ratio (OR): 3.63; 95% confidence interval: (1.64-8.02) for GC or GG carriers vs. CC carriers), and no according association with asthma and concomitant negative skin reactivity (adjusted OR: 1.13; 0.66-1.94). The interaction between IL-18 -137G/C genotype and positive skin prick test was statistically significant (P=0.029). None of 74 incident asthma cases with atopy at baseline exhibited the CC genotype. Our results strongly suggest that this variant of the IL-18 gene is an important genetic determinant involved in the development of atopic asthma
    Type of Publication: Journal article published
    PubMed ID: 16433859
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  • 127
    Keywords: CANCER ; radiotherapy ; SURVIVAL ; tumor ; carcinoma ; SYSTEM ; DISEASE ; incidence ; RISK ; RISKS ; SITE ; SITES ; TISSUE ; TUMORS ; PATIENT ; SKIN ; treatment ; ASSOCIATION ; BREAST ; BREAST-CANCER ; NERVOUS-SYSTEM ; LYMPHOMA ; MALIGNANCIES ; AGE ; CERVIX ; leukemia ; MELANOMA ; SWEDEN ; DATABASE ; squamous cell carcinoma ; FAMILY-CANCER DATABASE ; LONG-TERM SURVIVORS ; CHILDHOOD-CANCER ; CELL CARCINOMA ; MALIGNANCY ; ASSOCIATIONS ; LI-FRAUMENI-SYNDROME ; GLAND ; SURVIVORS ; PRIMARY NEOPLASMS ; BONE ; INCREASED RISK ; CANCERS ; fibrosarcoma ; PRIMARY MALIGNANCIES ; second malignancies ; LEIOMYOSARCOMA ; rhabdomyosarcoma ; SARCOMAS ; second primary malignancies ; soft tissue tumors
    Abstract: Survival from soft tissue tumors (STTs) has been improved because of the successful treatment. One of the late sequelae in STT survivors is the development of a second malignancy. The present study aimed at quantifying risks for second malignancies in patients with STTs, and risks for second STTs after other primary malignancies. Adjusted standardized incidence ratios (SIRs), calculated from the Swedish Family-Cancer Database, were used as a measure of risk. Among 6,671 primary STT patients, a total of 650 second malignancies occurred. Besides second STTs, other cancer sites with an increased SIR were the nervous system, endocrine glands, skin (melanoma and squamous cell carcinoma) and prostate; the risk for non-Hodgkin lymphoma (NHL) was also increased. The overall risk of second malignancies decreased in the following order: fibrosarocma (1.63) 〉 myxosarcoma (1.48) 〉 leiomyosarcoma (1.44) 〉 liposarcoma (1.21). An increased risk of second sTTs after primary cancers of the bone, ovary, nervous system, cervix, thyroid gland, skin, endometrium, breast. upper aero-digestive tract, and after Hodgkin disease, NHL and leukemia was also noted. This study showed that the incidence of second primary malignancies in patients with STTs was increased, but the SIRs varied among specific cancer sites. Besides therapeutic effects, the associations between STTs and bone and nervous system tumors suggested that cancer syndromes, such as neurofibromatosis type I and Li-Fraumeni syndrome, may partly explain the excesses. The associations of STTS with cancers of the skin (squamous cell carcinoma and melanoma) and with NHL may be related to immunodeficiency. (c) 2006 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16557572
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  • 128
    Keywords: CANCER ; FOLLOW-UP ; follow-up studies ; COHORT ; cohort studies ; cohort study ; EPIDEMIOLOGY ; incidence ; occupation ; POPULATION ; RISK ; WORKERS ; FAMILY ; RISK-FACTORS ; TRANSPORT ; AGE ; MEN ; risk factors ; SWEDEN ; DATABASE ; REGION ; adenocarcinoma ; CONSTRUCTION ; CARDIA ; ESOPHAGUS ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; STOMACH-CANCER ; FAMILY-CANCER DATABASE ; gastric cancer ; INTERVAL ; INCREASED RISK ; RISK-FACTOR ; CANCERS ; TRANSMISSION ; EXPOSURES ; stomach cancer ; cardia cancer ; CEMENT ; corpus cancer ; MAJOR CANCERS
    Abstract: The effects of socio-economic/occupational factors on gastric cancer at various subsites (including corpus, cardia and unspecified cancers) are not well known. To investigate this issue, we carried out a follow-up study on the economically active Swedish population, based on the Swedish Family-Cancer Database. We calculated standardized incidence ratios and 95% confidence intervals for different occupational groups, adjusted for age, period, region and socio-economic status. The reference group was all the economically active population. Manual workers and farmers were at an increased risk of stomach cancer. An increased risk of corpus cancer was observed for male miners and quarry workers, fishermen, construction workers, packers, loaders and warehouse workers, clerical workers and female assistant nurses and postal workers. For cardia cancer, significantly increased standardized incidence ratios were observed for gardeners, transport workers, bricklayers and chemical process workers among men. Only male miner and quarry workers showed significantly increased risk of unspecified cancer. In conclusion, the present study indicates that socio-economic groups differ in risk by almost a factor of two for corpus and unspecified cancers, and less for cardia cancers. Cement and mineral dusts appear as major occupational risk factors
    Type of Publication: Journal article published
    PubMed ID: 16912567
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  • 129
    Keywords: BLOOD ; Germany ; human ; RISK ; RISK-FACTORS ; CONTRAST ; MAGNETIC-RESONANCE ; METABOLITES ; ACID ; risk factors ; mass spectrometry ; NMR ; MASS-SPECTROMETRY ; LIGNANS ; BREAST-CANCER RISK ; SERUM ; RE ; ARRAY DETECTION ; technique ; ENTEROLACTONE ; phytoestrogens ; RISK-FACTOR ; LIQUID ; H1 ; (+)-enterodiol ; (+)-enterolactone ; (-)-enterodiol monoglucuronide ; (-)-enterolactone monoglucuronide ; (-)-secoisolariciresinol diglucoside ; CHROMATOGRAPHY MASS-SPECTROMETRY ; enterolignans ; ISOTOPE-DILUTION ; linseeds ; MAMMALIAN LIGNANS ENTEROLACTONE ; PLANT LIGNANS ; PLASMA ENTEROLACTONE ; SECOISOLARICIRESINOL DIGLUCOSIDE ; spectroscopic analysis ; TIME-RESOLVED FLUOROIMMUNOASSAY
    Abstract: A method involving the coupling of high-performance liquid chromatography with electrospray ionisation mass spectrometry (HPLC-ESI-MS) for the quantitative determination of the mammalian lignans enterolactone and enterodiol in human blood and urine has been developed. In contrast to techniques previously published, the method allows direct measurement of free enterolignans as well as their monoglucuronide conjugates in human biofluids with minimal sample preparation. Thereby the method is suitable for large-scale intervention, case-control and epidemiologic studies. Comprehensive, high-precision H-1 and C-13 nuclear magnetic resonance data (CD3OD as solvent) obtained at 11.7 T in combination with polarimetric data show that the major form of lignan precursor in the linseeds used is (-)-secoisolariciresinol diglucoside ((2R,3R)-2,3-bis(4'-hydroxy-3'-methoxy-benzyl)- 1,4-butanediyl-bis-beta-D-glucopyrano side) which is transformed by human intestinal bacteria into (+)-enterodiol and (+)-enterolactone. However, these metabolites are mono-glucuronidated after absorption and are detected as (-)enterodiol 3'-beta-D-glucuronide = (2R,3R)-2-(3'-O-(beta-D-glucopyranosyluronic acid)benzyl)-3-(3"-hydroxybenzyl)-butane-1,4,diol and (-)-enterolactone 3'-beta-D-glucuronide = (2R,3R)-2-(3'-O-(beta-D-glucopyranosyluronic acid) benzyl)-3-(3"-hydroxybenzyl)-beta-butyrolactone in blood and urine. (c) 2006 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16488523
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  • 130
    Keywords: CANCER ; BLOOD ; Germany ; RISK ; METABOLISM ; RISK-FACTORS ; BREAST ; breast cancer ; BREAST-CANCER ; TRIAL ; WOMEN ; risk factors ; mass spectrometry ; MASS-SPECTROMETRY ; PARAMETERS ; DIETARY ; chemoprevention ; VEGETABLES ; LIGNANS ; DIETARY-INTAKE ; BREAST-CANCER RISK ; SERUM ; RE ; INCREASE ; PHYTO-ESTROGENS ; LEVEL ; PARTICIPANTS ; ENTEROLACTONE ; phytoestrogens ; RISK-FACTOR ; LIQUID ; enterolignans ; linseeds ; PLANT LIGNANS ; CONSUMING FLAXSEED POWDER ; CONTROLLED-TRIAL ; enterodiol ; ENTEROLACTONE CONCENTRATION ; flaxseeds ; GUT MICROFLORA ; ISOFLAVONOID EXCRETION ; LIGNAN EXCRETION
    Abstract: Linseeds are a rich source of lignans, secondary plant substances which are suggested to possess chemopreventive effects inter alia with regard to breast cancer. In a randomised controlled trial 40 German women were informed about "5-a-day" and encouraged to increase their dietary intake of fruit and vegetables. Moreover 19 participants were randomly assigned to an intervention group supplemented with ground linseeds (20 g/d) over a 2-month period. Before and after intervention, urine and blood samples were collected after an overnight fast. Analysis was by intention-to-treat and the outcome parameters of interest were enterolignan concentrations. After linseed supplementation, enterolignan concentrations (mean) measured as their glucuronides by a newly developed high performance liquid chromatography electrospray mass spectrometry (HPLC-ESI-MS) in serum (122 nmol/l) as well as in urine (72 mu mol/l) showed a significant increase (P 〈 0.01) compared to pre-intervention values (47 nmol/l and 29 mu mol/l). In the control group enterolignan levels were raised slightly but did not reach significance. Serum and urinary enterolignans of the whole collective showed a good pairwise correlation. (c) 2006 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16494982
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  • 131