Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
  • 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
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    Keywords: CANCER ; GROWTH ; SURVIVAL ; carcinoma ; KINASE ; MODEL ; PATHWAY ; PATHWAYS ; DISEASE ; GENE ; PROTEIN ; ACTIVATION ; BASE ; protein kinase ; PROTEIN-KINASE ; treatment ; ASSOCIATION ; FREQUENCY ; polymorphism ; SIGNAL ; FREQUENCIES ; ACID ; STAGE ; DESIGN ; MUTATION ; MELANOMA ; METASTATIC MELANOMA ; SWEDEN ; MUTATIONS ; PARAMETERS ; MULTIVARIATE ; MALIGNANT-MELANOMA ; CANCER-RESEARCH ; B-RAF ; BRAF ; HIGH-FREQUENCY ; KINASE PATHWAYS ; N-RAS
    Abstract: Purpose: The RAS-RAF-mitogen-activated protein kinase pathways mediate the cellular response to growth signals. In melanocytes, BRAF is involved in cAMP-dependent growth signals. Recently, activating mutations in the BRAF gene, were reported in a large proportion of melanomas. We have studied mutations in the BRAF gene and their association with clinical parameters. Experimental Design: We analyzed exons 1, 11, and 15 of the BRAF gene and exons 1 and 2 of the N-ras gene for mutations in 38 metastatic melanomas by PCR-single-strand conformation polymorphism and direct sequencing. Kaplan-Meier survival and multivariate analyses were used to correlate mutations with various clinical parameters. Results: Mutations in exon 15 of the BRAF gene were detected in 26 (68%) melanomas. In 25 cases, mutation involved the "hot spot" codon 600(2) of the BRAF gene. Three melanomas without a BRAF mutation carried amino acid substituting base changes at codon 61 of the N-ras gene. In a multivariate proportional hazard (Cox) model, BRAF mutation, along with the stage of metastatic melanomas, showed a statistically significant hazard ratio of 2.16 (95% confidence interval 1.02-4.59; chi(2) for the model 6.94, degrees of freedom 2, P = 0.03) for diminished duration of response to the treatment. In a Kaplan-Meier survival model, cases with BRAF mutation showed longer disease-free survival (median of 12 months) than cases without mutation (median of 5 months), although this association was not statistically significant (Log-rank test P = 0.13). Conclusions: Our results, besides confirming the high frequency of BRAF mutations in metastatic melanomas, also underline the potential importance of these mutations in disease outcome
    Type of Publication: Journal article published
    PubMed ID: 12960123
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    Keywords: CANCER ; SURVIVAL ; MODEL ; MODELS ; GENERATION ; DISEASE ; DISEASES ; MORTALITY ; POPULATION ; RISKS ; TIME ; FAMILY ; PHENOTYPES ; MELANOMA ; SWEDEN ; PHENOTYPE ; CHILDHOOD ; FRAMEWORK ; FAMILIES ; heritability ; familial aggregation ; TWINS ; function ; ONSET ; CANCERS ; population-based ; modelling ; RARE ; CHILD ; SURVIVAL-DATA ; ENVIRONMENTAL-FACTORS ; GIBBS SAMPLING APPROACH ; GLMM ; hierarchical likelihood ; quantitative genetics ; VARIANCE-COMPONENTS
    Abstract: Estimation of genetic and environmental contributions to cancers falls in the framework of generalized linear mixed modelling with several random effect components. Computational challenges remain, however, in dealing with binary or survival phenotypes. In this paper, we consider the analysis of melanoma onset in a population of 2.6 million nuclear families in Sweden, for which none of the current survival-based methodologies is feasible. We treat the disease outcome as a binary phenotype, so that the standard proportional hazard model leads to a generalized linear model with the complementary-log link function. For rare diseases this link is very close to the probit link, and thus allows the use of marginal likelihood for the estimation of the variance components. We correct for the survival length bias by censoring the parent generation within each family at the time they attain the same cumulative hazard as the child generation, thus improving the validity of the estimates. Our finding that childhood shared environment in addition to genetic factors had a considerable effect on the development of melanoma is consistent with epidemiological studies. Copyright (c) 2005 John Wiley & Sons, Ltd
    Type of Publication: Journal article published
    PubMed ID: 16372390
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    Keywords: CANCER ; carcinoma ; neoplasms ; RISK ; RISKS ; TIME ; FAMILY ; tumour ; SKIN ; ASSOCIATION ; SUSCEPTIBILITY ; IN-SITU ; MELANOMA ; SWEDEN ; DATABASE ; SIR ; CUTANEOUS MELANOMA ; Bowen's disease ; in situ carcinoma ; multiple skin cancer ; multiple skin cancers ; NUCLEOTIDE EXCISION-REPAIR ; OCULAR MELANOMA ; PRIMARY CANCERS
    Abstract: We used the updated nation-wide Swedish Family-Cancer Database to examine familial risks in data from 1961 to 1998 on 1252 invasive and 2474 in situ squamous cell carcinoma (SCC) of the skin among offspring, and over 10 times more among parents. In 259 families a parent and an offspring had skin SCC. The familial standardised incidence ratios (SIRs) were 2.72 for invasive and 2.40 for in situ skin cancers in offspring. Multiple skin cancers in parents were associated with increased SIRs for invasive SCC in offspring, being 2.55 for one and up to 14.93 for two invasive and two in situ cancers in parents; the corresponding in situ SCC risks were 2.28 and 7.49. The population attributable fraction for any familial skin SCC, invasive or in situ, was 4.1%. Melanoma was the only discordant tumour that was associated with invasive and in situ skin SCC. These results provide evidence that there is an underlying hereditary susceptibility for at least a part of the familial clustering for skin SCC. (C) 2003 Cancer Research UK
    Type of Publication: Journal article published
    PubMed ID: 12778064
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
    Keywords: CANCER ; tumor ; carcinoma ; CELL ; LUNG ; PROSTATE ; COMMON ; GENERATION ; incidence ; RISK ; RISKS ; SITE ; SITES ; TUMORS ; TIME ; PATIENT ; kidney ; FAMILY ; primary ; renal ; ASSOCIATION ; LYMPHOMA ; MALIGNANCIES ; EXPERIENCE ; MALES ; leukemia ; BLADDER ; SWEDEN ; DATABASE ; MUTATIONS ; HIGH-RISK ; SIR ; 2ND PRIMARY MALIGNANCIES ; adenocarcinoma ; DUPLICATION ; familial risk ; GERMLINE ; kidney,carcinoma,renal cell,carcinoma,papillary,genetic diseases,inborn,neoplasms,second primary ; NATIONWIDE ; TRACT
    Abstract: Purpose: Familial risks in papillary renal cell carcinoma and association with second primary malignancies were studied using the nationwide Swedish Family Cancer Data Base.Materials and Methods: Cancer data obtained from the Swedish Cancer Registry from 1961 to 1998 included 1,733 cases of papillary renal cell carcinoma. The standardized incidence ratio was used to measure cancer risk.Results: Only 5 families were identified in which a parent had papillary renal cell carcinoma and an offspring had kidney cancer (nonsignificant SIR 1.51 for offspring). Discordant tumor sites associated with papillary renal cell carcinoma in the 2 generations were the upper aerodigestive tract and bladder (SIR 2.53, 95% CI 1.08 to 4.58 and 2.14, 95% CI 1.02 to 3.68, respectively). There was an overall increase in the risk of second primary malignancies of the lung, prostate and bladder and for nonHodgkin's lymphoma and leukemia in patients with papillary renal cell carcinoma. The risk for a second primary tumor of the bladder associated with papillary renal cell carcinoma during the followup of 1 to 10 years was about 15 times higher than that associated with adenocarcinoma, which is the most common histological type of kidney cancer. The SIR was significantly higher in females than in males (59.67, 95% CI 40.23 to 82.94 versus 18.76, 95% Cl 14.51 to 23.56).Conclusions: In addition to the familial association of these 2 cancer sites, the high risk of a second primary cancer of the bladder in patients with papillary renal cell carcinoma may reflect a common genetic alteration
    Type of Publication: Journal article published
    PubMed ID: 12629341
    Signatur Availability
    BibTip Others were also interested in ...
  • 9
    Keywords: CANCER ; MASK ; POPULATION ; RISK ; RISKS ; SITE ; SITES ; IN-SITU ; AGE ; WOMEN ; DNA-REPAIR ; MEN ; RATES ; CDKN2A ; MELANOMA ; SWEDEN ; DATABASE ; gene-environment interaction ; HEAD ; NECK ; SIR ; familial risk ; MALIGNANT-MELANOMA ; CUTANEOUS MELANOMA ; MELANOCYTIC NEVI ; head and neck ; germline mutations ; INCIDENCE RATES ; FAMILY-CANCER DATABASE ; CANCER DATABASE ; familial cancer ; heredity ; MELANOCORTIN-1 RECEPTOR MC1R ; parent-offspring risks ; RED HAIR ; sibling risks
    Abstract: We studied incidence trends, age-incidence relationships and familial risks in invasive and in situ cutaneous melanoma, based on the Swedish Family-Cancer Database of more than 10 million individuals. Offspring were 0-66 years of age. Cancers were obtained from the Swedish Cancer Registry from years 1961- 98. The study was based on 9,771 offspring and 22,888 parents with invasive melanoma and 2,446 offspring and 5,017 parents with in situ melanoma. Incidence rates increased markedly for invasive melanoma in the trunk. For in situ melanoma, trunk and head and neck were affected, and, in addition, legs for women. The maximal incidence was around age 80 years, independent of the type or site in men; in women early onset superficially spreading melanoma shifted the age for maximal incidence to about 60 years. For in situ melanoma, lentigo maligna was the main histogenetic type in the head and neck but in the trunk and legs superficially spreading melanoma was somewhat more common. Standardized incidence ratios (SIR) were calculated for familial risk at exposed and covered sites. The combined familial risks for invasive and in situ melanoma were higher at covered (SIR 3.56 from parents) than sun-exposed (1.92 from parents) sites and they agreed when familiality was defined between parents and offspring or between siblings; the sibling SIRs were 3.90 at covered and 2.53 at exposed sites. The data suggest that the higher melanoma density at exposed sites masks familial effects. Furthermore, sun exposure does not appear to reinforce the familial effect. (C) 2003 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 12640685
    Signatur Availability
    BibTip Others were also interested in ...
  • 10
    Keywords: carcinoma ; CELL ; RISK ; smoking ; SWEDEN ; RISK FACTOR ; squamous cell carcinoma ; TRENDS ; CELL CARCINOMA
    Type of Publication: Journal article published
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...