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  • 1
    Keywords: CANCER ; FOLLOW-UP ; lung cancer ; LUNG-CANCER ; COHORT ; MORTALITY ; POPULATION ; RISK ; RISKS ; SITE ; SITES ; TIME ; SKIN ; IN-SITU ; MALIGNANCIES ; WOMEN ; smoking ; skin cancer ; bladder cancer ; BLADDER-CANCER ; SWEDEN ; cancer risk ; SQUAMOUS-CELL CARCINOMA ; CANCER RISKS ; COSMETOLOGISTS ; hair dyes ; hairdressers ; HEMATOPOIETIC NEOPLASMS ; NECK ; OCCUPATIONAL RISKS ; SAFETY ; SIR ; UNITED-STATES
    Abstract: More than a decade ago, an increased risk for bladder cancer among male hairdressers was established. Frequent changes of hair dye formulations together with their widespread use call for safety guarantees. We carried out a follow-up study of a cohort of 38,866 female and 6,824 male hairdressers from Sweden and analyzed all of their malignancies over a period of 39 years. Standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) for 28 cancer sites were calculated using the economically active population as a reference. During the years 1960-1998 a total of 1,043 cancer cases were recorded in male hairdressers. Excess risks for cancers of the upper aerodigestive tract and lung and colorectal adenocarcinoma were observed. Additionally, male hairdressers working in 1960 had an increased risk for urinary bladder cancer, which was highest in the 1960s with an SIR of 2.56 (95% CI 1.36-4.39) and decreased with the follow-up time. A total of 2,858 cancers were recorded in female hairdressers. An increased risk was observed for cancers of the pancreas, lung and cervix and in situ cancer of the skin. The increased risk for in situ skin cancer specifically affected the scalp and neck, sites of contact for hair dyes, with an SIR of 2.43 (95% CI 1.14-4.44). The increase in lung cancer, the only site for which cancer was increased in either sex, may depend on confounding from smoking. Bladder cancer was not increased among hairdressers in the recent decades and is therefore not likely to be associated with modern hair dyes. (C) 2003 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 12672039
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  • 2
    Keywords: RISK ; MELANOMA ; DATABASE ; MUTATIONS ; CANCER RISKS ; AUSTRALIA ; INCIDENCE RATES ; SPOUSES
    Type of Publication: Journal article published
    PubMed ID: 12873883
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  • 3
    Keywords: CANCER ; LUNG-CANCER ; RISK ; SITES ; TIME ; SKIN ; lifestyle ; WOMEN ; risk factors ; MELANOMA ; DATABASE ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; ATTRIBUTABLE RISKS ; CARCINOID-TUMORS ; causes of cancer ; ENDOMETRIAL CANCER ; environmental risks ; EPSTEIN-BARR-VIRUS ; LIFE-STYLE ; sociol factors ; SWEDISH POPULATION
    Abstract: It is well known that certain cancers have shown clustering in socioeconomic groups, but limited data are available on recent results and time trends in such clustering. We determined standardized incidence ratios (SIR) for cancer, adjusted for age, period, region, parity and age at first childbirth among men and women in 6 socioeconomic groups based on the Swedish Family-Cancer Database. Persons had to be identified with the same socioeconomic status in the census of years 1960 and 1970, or of years 1960, 1970 and 1980; the comparison group was all people according to the same censuses. Cancers were followed from years 1970 to 1998 or from 1980 to 1998. Both increased and decreased SIRs were found, and a consistent pattern emerged, although the overall SIRs for cancer did not differ much, the lowest being for farmers (0.8S) and the highest for professional men (1.07) and women (1.11). At individual sites, manual workers were at risk of tobacco-, alcohol- and occupation- and human papilloma virus-related cancers and at a decreased risk at most other cancers. Manual workers and farmers showed an excess of stomach cancer; professionals had an excess of melanoma and squamous cell skin cancer. Male and female SIRs correlated highly for manual and blue-collar workers and for professionals. The overall population- attributable fraction for selected sites was 16.7% for men and 10.9% for women and it was highest, over 50%, for lung cancer in both genders
    Type of Publication: Journal article published
    PubMed ID: 12740920
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  • 4
    Keywords: CANCER ; NEW-YORK ; RISK ; SKIN ; ASSOCIATION ; BREAST-CANCER ; IN-SITU ; RATES ; MELANOMA ; SWEDEN ; DATABASE ; SQUAMOUS-CELL CARCINOMA ; NATIONWIDE ; CUTANEOUS MELANOMA ; OCULAR MELANOMA ; FAMILY-CANCER DATABASE ; 2ND PRIMARY CANCERS ; MALIGNANT- MELANOMA
    Type of Publication: Journal article published
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  • 5
    Keywords: CANCER ; CELL ; Germany ; LUNG ; neoplasms ; PROSTATE ; COMMON ; lung cancer ; LUNG-CANCER ; DISEASE ; HISTORY ; incidence ; NEW-YORK ; RISK ; RISKS ; SITE ; SITES ; renal ; SKIN ; SUSCEPTIBILITY ; BREAST ; BREAST-CANCER ; AGE ; genetics ; etiology ; PROSTATE-CANCER ; leukemia ; SWEDEN ; DATABASE ; SIR ; familial risk ; NATIONWIDE ; ATTRIBUTABLE RISKS ; FAMILY-CANCER DATABASE ; NONPOLYPOSIS COLORECTAL-CANCER ; MULTIPLE-MYELOMA ; GUIDELINES ; familial cancers,heritable cancer,clinical counseling,familial risk ; GENOMIC MEDICINE ; HODGKINS-LYMPHOMA ; TESTICULAR CANCER
    Abstract: Familial risks for cancer are important for clinical counseling and understanding cancer etiology. Medically verified data on familial risks have not been available for all types of cancer. The nationwide Swedish Family-Cancer Database includes all Swedes born in 1932 and later (0-to 68-year-old offspring) with their parents, totaling over 10.2 million individuals. Cancer cases were retrieved from the Swedish Cancer Registry up to year 2000. Standardized incidence ratios (SIR) and 95% confidence limits (Cl) were calculated for age-specific familial risk in offspring by an exact proband status. The familial risks for offspring cancer were increased at 24/25 sites from concordant cancer in only the parent, at 20/21 sites from a sibling proband and at 12/12 sites from a parent and sibling proband. The highest SIRs by parent were for Hodgkin's disease (4.88) and testicular (4.26), non-medullary thyroid (3.26), ovarian (3.15) and esophageal (3.14) cancer and for multiple myeloma (3.33). When a sibling was affected, even prostate, renal, squamous cell skin, endocrine, gastric and lung cancer and leukemia showed SIRs in excess of 3.00. The highest cumulative risks were found for familial breast (5.5%) and prostate (4.2%) cancers. We identified reliable familial risks for 24 common neoplasms, most of which lack guidelines for clinical counseling or action level. If, for example, a familial SIR of 2.2 would be use as an action level, counseling would be needed for most cancers at some diagnostic age groups. The present data provide the basis for clinical counseling. (C) 2003 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 14618624
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  • 6
    Keywords: EXPRESSION ; transcription ; CHROMATIN ; WOMEN ; REVEALS ; susceptibility loci ; GENOME-WIDE ASSOCIATION ; AFRICAN-AMERICAN ; ESTROGEN-RECEPTOR BINDING ; DETERMINANT
    Abstract: The 10q26 locus in the second intron of FGFR2 is the locus most strongly associated with estrogen-receptor-positive breast cancer in genome-wide association studies. We conducted fine-scale mapping in case-control studies genotyped with a custom chip (iCOGS), comprising 41 studies (n = 89,050) of European ancestry, 9 Asian ancestry studies (n = 13,983), and 2 African ancestry studies (n = 2,028) from the Breast Cancer Association Consortium. We identified three statistically independent risk signals within the locus. Within risk signals 1 and 3, genetic analysis identified five and two variants, respectively, highly correlated with the most strongly associated SNPs. By using a combination of genetic fine mapping, data on DNase hypersensitivity, and electrophoretic mobility shift assays to study protein-DNA binding, we identified rs35054928, rs2981578, and rs45631563 as putative functional SNPs. Chromatin immunoprecipitation showed that FOXA1 preferentially bound to the risk-associated allele (C) of rs2981578 and was able to recruit ER alpha to this site in an allele-specific manner, whereas E2F1 preferentially bound the risk variant of rs35054928. The risk alleles were preferentially found in open chromatin and bound by Ser5 phosphorylated RNA polymerase II, suggesting that the risk alleles are associated with changes in transcription. Chromatin conformation capture demonstrated that the risk region was able to interact with the promoter of FGFR2, the likely target gene of this risk region. A role for FOXA1 in mediating breast cancer susceptibility at this locus is consistent with the finding that the FGFR2 risk locus primarily predisposes to estrogen-receptor-positive disease.
    Type of Publication: Journal article published
    PubMed ID: 24290378
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  • 7
    Keywords: COHORT ; VARIANTS ; WOMEN ; HEIGHT ; METAANALYSIS ; bias ; ESTROGEN ; GENOME-WIDE ASSOCIATION ; PROGESTERONE-RECEPTOR STATUS ; INOSITOL POLYPHOSPHATES
    Abstract: A large genotyping project within the Breast Cancer Association Consortium (BCAC) recently identified 41 associations between single nucleotide polymorphisms (SNPs) and overall breast cancer (BC) risk. We investigated whether the effects of these 41 SNPs, as well as six SNPs associated with estrogen receptor (ER) negative BC risk are modified by 13 environmental risk factors for BC. Data from 22 studies participating in BCAC were pooled, comprising up to 26,633 cases and 30,119 controls. Interactions between SNPs and environmental factors were evaluated using an empirical Bayes-type shrinkage estimator. Six SNPs showed interactions with associated p-values (p(int)) 〈1.1 x 10(-3). None of the observed interactions was significant after accounting for multiple testing. The Bayesian False Discovery Probability was used to rank the findings, which indicated three interactions as being noteworthy at 1% prior probability of interaction. SNP rs6828523 was associated with increased ER-negative BC risk in women 170 cm (OR = 1.22, p = 0.017), but inversely associated with ER-negative BC risk in women 〈160 cm (OR = 0.83, p = 0.039, p(int) = 1.9 x 10(-4)). The inverse association between rs4808801 and overall BC risk was stronger for women who had had four or more pregnancies (OR = 0.85, p = 2.0 x 10(-4)), and absent in women who had had just one (OR = 0.96, p = 0.19, p(int) = 6.1 x 10(-4)). SNP rs11242675 was inversely associated with overall BC risk in never/former smokers (OR = 0.93, p = 2.8 x 10(-5)), but no association was observed in current smokers (OR = 1.07, p = 0.14, p(int) = 3.4 x 10(-4)). In conclusion, recently identified BC susceptibility loci are not strongly modified by established risk factors and the observed potential interactions require confirmation in independent studies. What's new? The recent discovery of 47 susceptibility loci associated with all or estrogen receptor-negative breast cancer provided new opportunities for genetic risk prediction but it remained unclear how exposure levels of environmental (non-genetic) risk factors influenced the risk assessment. In this gene-environment study, the international team examined interactions between the single nucleotide polymorphisms and 13 established environmental risk factors including parity, height and alcohol consumption. Notably, relative risks of breast cancer associated with the susceptibility loci were not strongly modified by environmental risk factors, a finding that, if confirmed, has important implications for the risk assessment in breast cancer.
    Type of Publication: Journal article published
    PubMed ID: 25227710
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  • 8
    Keywords: PROSTATE ; prevention ; WOMEN ; SUBTYPES ; FAMILY-HISTORY ; susceptibility loci ; GENOME-WIDE ASSOCIATION ; CONSORTIUM
    Abstract: BACKGROUND: Data for multiple common susceptibility alleles for breast cancer may be combined to identify women at different levels of breast cancer risk. Such stratification could guide preventive and screening strategies. However, empirical evidence for genetic risk stratification is lacking. METHODS: We investigated the value of using 77 breast cancer-associated single nucleotide polymorphisms (SNPs) for risk stratification, in a study of 33 673 breast cancer cases and 33 381 control women of European origin. We tested all possible pair-wise multiplicative interactions and constructed a 77-SNP polygenic risk score (PRS) for breast cancer overall and by estrogen receptor (ER) status. Absolute risks of breast cancer by PRS were derived from relative risk estimates and UK incidence and mortality rates. RESULTS: There was no strong evidence for departure from a multiplicative model for any SNP pair. Women in the highest 1% of the PRS had a three-fold increased risk of developing breast cancer compared with women in the middle quintile (odds ratio [OR] = 3.36, 95% confidence interval [CI] = 2.95 to 3.83). The ORs for ER-positive and ER-negative disease were 3.73 (95% CI = 3.24 to 4.30) and 2.80 (95% CI = 2.26 to 3.46), respectively. Lifetime risk of breast cancer for women in the lowest and highest quintiles of the PRS were 5.2% and 16.6% for a woman without family history, and 8.6% and 24.4% for a woman with a first-degree family history of breast cancer. CONCLUSIONS: The PRS stratifies breast cancer risk in women both with and without a family history of breast cancer. The observed level of risk discrimination could inform targeted screening and prevention strategies. Further discrimination may be achievable through combining the PRS with lifestyle/environmental factors, although these were not considered in this report.
    Type of Publication: Journal article published
    PubMed ID: 25855707
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  • 9
    Keywords: CANCER ; Germany ; PROSTATE ; DISEASE ; HISTORY ; incidence ; NEW-YORK ; POPULATION ; RISK ; RISKS ; SITE ; SITES ; GENE ; GENES ; PATIENT ; kidney ; FAMILY ; MEMBER ; MEMBERS ; SUSCEPTIBILITY ; BREAST-CANCER ; etiology ; PROSTATE-CANCER ; SWEDEN ; DATABASE ; SIR ; familial risk ; NATIONWIDE ; FAMILY-CANCER DATABASE ; GUIDELINES ; GENOMIC MEDICINE ; TESTICULAR CANCER ; CELL TUMORS ; familial cancers,heritable cancer,clinical counseling,urology ; LINDAU-DISEASE
    Abstract: Familial risks for cancer are important for clinical counseling and understanding cancer etiology. The nationwide Swedish Family-Cancer Database includes all Swedes born in 1932 and later (0 to 68-year-old offspring) with their parents, totaling over 10.2 million individuals. Urological cancer cases were retrieved from the Swedish Cancer Registry up to year 2000. Standardized incidence ratios (SIR) and 95% confidence limits (CI) were calculated for age-specific familial risk in offspring by an exact proband status. The familial risks for offspring cancer were increased at all urological sites from concordant cancer in the parent and in a sibling proband. The highest SIRs by parent were for testicular and prostate cancer (4.26 and 2.45). When a sibling was affected, even kidney cancer (4.74) showed a high SIR. For kidney cancers, and also for prostate and testicular cancers, the SIRs were higher among siblings than among offspring and parents, which may indicate the involvement of recessive effects. Family members of patients with prostate cancer or von Hippel Lindau disease can expect organized clinical counseling, but family members of patients with other urological cancers are probably not counseled. Guidelines for clinical counseling or action level should be developed for all urological cancers because of the established familial risks. Urological cancers also offer a challenge to molecular geneticists attempting to identify the susceptibility genes underlying the familial clustering
    Type of Publication: Journal article published
    PubMed ID: 14615900
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  • 10
    Keywords: RECEPTOR ; CANCER ; CELLS ; EXPRESSION ; tumor ; CELL ; RISK ; PROTEIN ; transcription ; DIFFERENTIATION ; TUMORS ; TRANSCRIPTION FACTOR ; MARKER ; REDUCTION ; BIOMARKERS ; ASSOCIATION ; LINKAGE ; polymorphism ; single nucleotide polymorphism ; SUSCEPTIBILITY ; BREAST ; breast cancer ; BREAST-CANCER ; BRCA1 ; WOMEN ; MUTATION ; SNP ; MARKERS ; cancer risk ; LINKAGE DISEQUILIBRIUM ; PROGENITOR CELLS ; CARRIERS ; case-control studies ; PROJECT ; MORPHOGENESIS ; ER ; ESTROGEN-RECEPTOR ; SINGLE ; case control study ; case-control study ; BRCA2 ; TUMOR-SUPPRESSOR ; VARIANT ; MAMMARY-GLAND ; MUTATION CARRIERS ; ESTROGEN ; biomarker ; estrogen receptor ; pooled analysis ; USA ; CANCER-RISK ; CONSORTIUM ; tumor suppressor ; 3 ; Genetic ; TRANSCRIPTION-FACTOR ; BRCA1 and BRCA2 ; GATA3 ; LUMINAL CELL FATE
    Abstract: GATA-binding protein 3 (GATA3) is a transcription factor that is crucial to mammary gland morphogenesis and differentiation of progenitor cells, and has been suggested to have a tumor suppressor function. The rs570613 single nucleotide polymorphism (SNP) in intron 4 of GATA3 was previously found to be associated with a reduction in breast cancer risk in the Cancer Genetic Markers of Susceptibility project and in pooled analysis of two case-control studies from Norway and Poland (P (trend) = 0.004), with some evidence for a stronger association with estrogen receptor (ER) negative tumours [Garcia-Closas M et al. (2007) Cancer Epidemiol Biomarkers Prev 16:2269-2275]. We genotyped GATA3 rs570613 in 6,388 cases and 4,995 controls from the Breast Cancer Association Consortium (BCAC) and 5,617 BRCA1 and BRCA2 carriers from the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA). We found no association between this SNP and breast cancer risk in BCAC cases overall (ORper-allele = 1.00, 95% CI 0.94-1.05), in ER negative BCAC cases (ORper-allele = 1.02, 95% CI 0.91-1.13), in BRCA1 mutation carriers RRper-allele = 0.99, 95% CI 0.90-1.09) or BRCA2 mutation carriers (RRper-allele = 0.93, 95% CI 0.80-1.07). We conclude that there is no evidence that either GATA3 rs570613, or any variant in strong linkage disequilibrium with it, is associated with breast cancer risk in women
    Type of Publication: Journal article published
    PubMed ID: 19082709
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