Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
  • 1
    Keywords: CANCER ; Germany ; EPIDEMIOLOGY ; incidence ; RISK ; RISKS ; GENE ; GENES ; SUSCEPTIBILITY ; SUSCEPTIBILITY GENES ; BREAST ; breast cancer ; BREAST-CANCER ; IDENTIFICATION ; prevention ; DESIGN ; DIFFERENCE ; AGE ; BRCA1 ; WOMEN ; SWEDEN ; DATABASE ; REGION ; MUTATIONS ; MORPHOLOGY ; SIR ; familial risk ; NATIONWIDE ; FAMILY-CANCER DATABASE ; RELATIVES ; familial risk,half sisters,risk factors,sibling risk ; INTERPRETING FAMILY ; SUSCEPTIBILITY GENE
    Abstract: Purpose. The familial risk of female breast cancer is somewhat less than 2.0 when a first-degree relative is diagnosed with breast cancer, but it is not known to what extent heritable or environmental factors explain the familial clustering. Such data would be valuable for prevention and gene identification strategies.Experimental design. We used the nation-wide Swedish Family-Cancer Database on 10.2 million individuals and 190,000 mothers' and 26,000 daughters' breast cancers to calculate familial standardised incidence ratios (SIRs), for all invasive breast cancers in daughters, who were 0-66 years old. Over 5500 familial breast cancers were recorded.Results. The familial SIR for all invasive breast cancer was 1.71 by breast cancer in the mother only, 1.95 by breast cancer in a sister only, and 2.75 by breast cancer in both a mother and sister. The SIRs did not change when adjustments were done for period, age at first birth, parity, socio-economic status and region. Age difference between sisters showed a small variation in risk for breast cancer but the highest SIR was found for those whose age difference was from 6 to 10 years. Half sisters showed an excess of familial risks exactly half of full sisters, the SIR being 1.44.Conclusions. These data suggest that familial aggregation of breast cancer is mainly due to heritable causes. Because the known susceptibility genes only explain about a quarter of the familial aggregation, the remaining majority offers a challenge to new genomic approaches
    Type of Publication: Journal article published
    PubMed ID: 14672399
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    Keywords: APOPTOSIS ; CANCER ; Germany ; NEW-YORK ; POPULATION ; RISK ; GENE ; ASSOCIATION ; polymorphism ; SUSCEPTIBILITY ; BREAST ; breast cancer ; BREAST-CANCER ; DELETION ; NO ; PROMOTER ; REDUCED RISK ; cancer risk ; REGION ; case-control studies ; ONCOLOGY ; case-control study ; RE ; VARIANT ; PROMOTER POLYMORPHISM ; USA ; caspases ; PROMOTER REGION ; CANCER-RISK ; COMMON VARIANT ; breast cancer risk ; Sp1 binding site ; CASP8-652 6N del
    Abstract: A recent study on an Asian population reported a six-nucleotide insertion-deletion polymorphism (-652 6N del) in the CASP8 promoter region to be strongly associated with a decreased risk of multiple types of cancer, including breast cancer (BC). Here, we investigate the effect of this deletion in four independent large European BC case-control studies, including data from a total of 7,753 cases and 7,921 controls. The combined per allele odds ratio (OR) was 0.97 (95% confidence interval (CI), 95% CI = 0.93-1.02). The present result indicates that the CASP8 -652 6N del variant has no significant effect on BC risk in Europeans
    Type of Publication: Journal article published
    PubMed ID: 17891485
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    Keywords: CANCER ; SURVIVAL ; tumor ; Germany ; FOLLOW-UP ; DEATH ; DISEASE ; NEW-YORK ; RISK ; DISTINCT ; TIME ; PATIENT ; MECHANISM ; FAMILY ; prognosis ; mechanisms ; MEMBERS ; ASSOCIATION ; POLYMORPHISMS ; SUSCEPTIBILITY ; BREAST ; breast cancer ; BREAST-CANCER ; METASTASIS ; SWEDEN ; DATABASE ; PROGNOSTIC-FACTORS ; MAMMOGRAPHY ; PROGNOSTIC FACTORS ; familial risk ; PROGNOSTIC FACTOR ; TRENDS ; heredity ; ONCOLOGY ; RE ; FAMILIES ; overall survival ; PROGNOSTIC-FACTOR ; analysis ; USA ; familial breast cancer ; FAMILY-MEMBERS ; SWEDISH ; heritability of survival
    Abstract: Several earlier studies have assessed survival in breast cancer based on familial risk of this disease. The results have been conflicting and suggest that the risk and prognostic factors of cancer are largely distinct. As a novel concept, we searched for familial clustering of survival, i.e., concordance of survival among family members. We used the nation-wide Swedish Family-Cancer Database to estimate hazard ratios (HRs) for cause-specific and overall survival in invasive breast cancer. HR shows the probability of death in the study group compared the reference group. The study covered 1277 mother-daughter pairs with familial breast cancer. Their median follow-up times for survival ranged from 96 to 122 months. When the survival in daughters was analyzed according to the mothers' length of survival, there was a concordance of prognosis. The HR was 0.65 in daughters whose mothers had survived 〉 = 120 months compared to daughters whose mothers had survived less than 36 months (P-value for trend 0.02). When the analysis was reversed and HRs were derived for mothers, the results were essentially similar (P-value for trend 0.02). The survival did not differ between patients with familial or sporadic breast cancer. The results are consistent in showing that both good and poor survival in breast cancer aggregates in families, which is a novel population-level finding for any cancer. The consistency of the results suggests that the prognosis in breast cancer is in part heritable which is likely to be explained by yet unknown genetic mechanisms
    Type of Publication: Journal article published
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    Keywords: CANCER ; IONIZING-RADIATION ; Germany ; neoplasms ; THERAPY ; COHORT ; HISTORY ; incidence ; NEW-YORK ; POPULATION ; RISK ; RISKS ; SITE ; SITES ; radiation ; DNA ; FAMILY ; primary ; SIGNAL ; SUSCEPTIBILITY ; BREAST ; breast cancer ; BREAST-CANCER ; family history ; WOMEN ; COLORECTAL-CANCER ; RATES ; chemotherapy ; leukemia ; ABERRATIONS ; DAMAGE ; DATABASE ; HIGH-RISK ; DNA-DAMAGE ; BRCA2 MUTATIONS ; multiple primaries ; heredity ; 2ND PRIMARY CANCERS ; ONCOLOGY ; RE ; FAMILIES ; THERAPIES ; CHEK2 ; LEVEL ; familial aggregation ; DNA damage ; FAMILY-HISTORY ; USA ; CANCERS ; familial breast cancer ; modification ; neoplasm ; chromosomal aberrations ; SWEDISH ; second primary ; subsequent cancer ; GENETIC RISK ; GENETIC-IMPLICATIONS
    Abstract: An increased risk of second primary cancers may depend on many reasons, including therapy for the first cancer and heritable causation. Population level data are not available exploring the risks of subsequent cancers after breast cancer considering a familial history of breast cancers. We used the nation-wide Swedish Family-Cancer Database to investigate such risks, based on 43,398 first invasive female breast cancers. Standardized incidence ratios (SIRs) were calculated for the second cancer after breast cancer using rates for first cancer as a reference. Many cancers at discordant sites were increased after breast cancer. SIRs for subsequent neoplasms in women who had a family history of breast cancer were increased for ovarian (2.0) and endometrial (1.8) cancers and for acute lymphoid leukemia (12.7) and myelofibrosis (9.4). The data suggest that the familial aggregation of breast and endometrial cancers may be explained by yet unidentified heritable causes. The remarkably high risks for second acute lymphoid leukemia and myelofibrosis, both characterized by chromosomal aberrations, in women with a family history of breast cancer may signal heritable defects in the ability to process DNA damage caused by ionizing radiation and chemotherapy
    Type of Publication: Journal article published
    PubMed ID: 17899363
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    Keywords: CANCER ; GROWTH ; GROWTH-FACTOR ; BLOOD ; DENSITY ; COHORT ; NEW-YORK ; RISK ; GENE ; SAMPLE ; SAMPLES ; TISSUE ; primary ; RISK-FACTORS ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; BREAST ; breast cancer ; BREAST-CANCER ; CARE ; DESIGN ; WOMEN ; SNP ; risk factors ; PROSTATE-CANCER ; cancer risk ; RECRUITMENT ; BINDING-PROTEINS ; NETHERLANDS ; POSTMENOPAUSAL WOMEN ; menopause ; SERUM ; ONCOLOGY ; RE ; INCREASE ; SINGLE NUCLEOTIDE POLYMORPHISMS ; SNPs ; GROWTH-FACTOR-I ; ALLELES ; LEVEL ; methods ; HAPLOTYPE ; GENOTYPE DATA ; USA ; PREMENOPAUSAL ; prospective study ; mammographic density ; RISK-FACTOR ; CANCER-RISK ; CIRCULATING LEVELS ; MULTIETHNIC COHORT ; Insulin-Like Growth Factor I ; NOV ; postmenopausal ; quantitative ; block ; breast density ; IGF1 ; breast cancer risk ; NUCLEOTIDE ; APOLIPOPROTEIN-E ISOFORMS ; Prospect-EPIC
    Abstract: Introduction High breast density is one of the strongest known risk factors for developing breast cancer. Insulin-like growth factor I (IGF-I) is a strong mitogen and has been suggested to increase breast cancer risk by increasing the amount of dense tissue in the female breast. Objectives We wanted to investigate the effect of common variation in the IGF-1 gene on serum IGF-I levels and on breast density. Design and methods Mammograms and blood samples of 1,928 premenopausal participants of the Dutch Prospect-EPIC cohort were collected at baseline. Using a haplotype tagging approach, 16 single nucleotide polymorphisms (SNP) from three blocks covering the IGF-1 gene were genotyped in all study participants. Breast density was assessed using a quantitative computer-assisted method. For a subgroup of women, who went through menopause within 5 years after recruitment (n = 656), premenopausal IGF-I levels and additionally postmenopausal breast density were determined. False positive report probabilities (FPRP) for statistically significant relations were calculated using the Wacholder method. Results The minor alleles of five SNPs in block 3 were significantly associated with elevated levels of IGF-I (rs9989002, rs2033178, rs7136446, rs978458, rs6220; P-values: 0.01-0.04). The same SNPs were related with modestly higher percent breast density before menopause and-in the subgroup of women that became postmenopausal during follow-up-with a modestly higher percent breast density after menopause. The most significant result, i.e. the relation between rs6220 and IGF-I levels, had an FPRP 〈 0.5 assuming prior probabilities of 0.01 and higher. Conclusion Common genetic variation in the IGF-1 gene is related to circulating levels of IGF-I, but the relationship with breast density is indecisive
    Type of Publication: Journal article published
    PubMed ID: 18064566
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    Keywords: CANCER ; DIAGNOSIS ; COHORT ; RISK ; ASSOCIATION ; breast cancer ; BREAST-CANCER ; WOMEN ; OBESITY ; SWEDEN ; POSTMENOPAUSAL WOMEN ; leptin ; IGF-I ; case-control study ; WEIGHT ; GROWTH-FACTOR-I ; OVERWEIGHT ; prospective ; C-PEPTIDE ; SERUM ADIPONECTIN ; Adiponectin ; NORTHERN SWEDEN ; GLUCOSE-HOMEOSTASIS ; Glycated haemoglobin
    Abstract: It is hypothesized that insulin resistance and related metabolic factors may influence breast cancer risk, however the epidemiological evidence remains inconclusive. We conducted a case-control study nested in a prospective cohort in Northern Sweden, to clarify the associations of body mass index (BMI), leptin, adiponectin, C-peptide, and glycated haemoglobin (HbA1c) with breast cancer risk. We also investigated whether these associations may be modified by age at diagnosis, tumour stage, and oestrogen and progesterone receptor status. During follow-up, 561 women developed invasive breast cancer and 561 matched controls were selected. Conditional logistic regression was used to calculate odds ratios (OR) as estimates of relative risk, and 95% confidence intervals (CI). The associations of BMI, leptin and HbA1c with breast cancer risk differed significantly according to whether the tumour was diagnosed as stage I or stage II-IV (P (heterogeneity) all 〈 0.05). These factors were significantly inversely associated with risk in the group of stage I tumours, with ORs for top vs. bottom tertile for BMI of 0.48 (95% CI, 0.30-0.78, P (trend) = 0.004); leptin, 0.64 (95% CI, 0.41-1.00, P (trend) = 0.06); and HbA1c, 0.47 (95% CI, 0.28-0.80, P (trend) = 0.005). For stage II-IV tumours, there was a suggestion of an increased risk with higher levels of these factors. There were no significant differences in the associations of BMI, leptin, adiponectin, C-peptide and HbA1c with breast cancer risk in subgroups of age at diagnosis or tumour receptor status. This prospective study suggests that BMI, leptin and HbA1c influence breast tumour initiation and progression
    Type of Publication: Journal article published
    PubMed ID: 18330696
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
  • 9
    Abstract: Polymorphisms in genes involved in DNA repair, steroid hormone biosynthesis/metabolism/signaling, folate metabolism as well as cell growth are prime candidates for possible associations with breast and ovarian cancer risk in women with an inherited predisposition. We investigated 29 polymorphisms in 20 genes encoding key proteins of the above four biological pathways for their breast and ovarian cancer risk modifying effect in Polish women harboring BRCA1 founder mutations. Of the analyzed genes, ERCC2, XRCC1, XRCC2, XRCC3 and Lig4 participate in DNA repair, TP53 in cell cycle check point control, AIB1, AR, COMT, CYP11A1, CYP17A1, CYP19A1, HSD17 and PGR in steroid hormone biosynthesis/metabolism/signaling, TYMS in folate metabolism and HER2, IL6, LRP1, TGFB and TGFBR1 affect cell growth. Using validated methods, we genotyped 319 breast cancer cases, 146 ovarian cancer cases and 290 unaffected controls, all of whom harbored one of three causative mutations in BRCA1. Our results revealed no association of any of the investigated polymorphisms with BRCA1-associated breast or ovarian cancer risk. Thus, it appears that these polymorphisms do not influence disease risk in Polish women carrying one of the three common BRCA1 founder mutations.
    Type of Publication: Journal article published
    PubMed ID: 19360465
    Signatur Availability
    BibTip Others were also interested in ...
  • 10
    Keywords: RECEPTOR ; CANCER ; EXPRESSION ; tumor ; CELL ; Germany ; THERAPY ; DISEASE ; HISTORY ; RISK ; GENE ; GENES ; COMPLEX ; COMPLEXES ; MECHANISM ; FAMILY ; mechanisms ; ASSOCIATION ; POLYMORPHISMS ; SUSCEPTIBILITY ; BREAST ; breast cancer ; BREAST-CANCER ; hormone ; NUMBER ; STRESS ; ovarian cancer ; OVARIAN-CANCER ; smoking ; ORAL-CONTRACEPTIVES ; OXIDATIVE STRESS ; body mass index ; glutathione-S-transferase ; PHASE-II ; ONCOLOGY ; ASSOCIATIONS ; LIGHT ; PHASE ; GENOTYPE ; FAMILY-HISTORY ; GLUTATHIONE S-TRANSFERASES ; BODY-MASS ; breast cancer risk ; COLLECTION ; hormone therapy ; Metabolizing enzymes ; METABOLIZING GENES ; GSTs
    Abstract: Breast cancer is a complex disease and in recent years a number of breast cancer susceptibility genes have been identified, but the role of low penetrance susceptibility genes has not been completely resolved. Glutathione S-transferases (GSTs) are phase II xenobiotic metabolizing enzymes involved in the detoxification of chemical carcinogens and environmental pollutants and play an important role in cell defense mechanisms against oxidative stress. They have been in the spot light for the investigation of a potential association with breast cancer risk but so far, sparse or even no data for a potential contribution of GSTA2, GSTM2, GSTO, and GSTZ to breast cancer risk are available. We genotyped GSTA2_448_C 〉 G (rs2180314), GSTA2_742_A 〉 C (rs6577), GSTM2_-832_T 〉 C (rs638820), GSTO1_-1242_G 〉 A (rs2164624), GSTO1_419_A 〉 C (rs4925), GSTO2_-183_A 〉 G (rs2297 235), GSTO2_342_A 〉 G (rs156697), GSTZ1_-4378_A 〉 G (rs1046428), and GSTZ1_94_G 〉 A (rs3177427) by MAL DI-TOF MS in the German GENICA breast cancer case-control collection of 1021 cases and 1015 controls and performed breast cancer risk association in general and with respect to the stratifications: menopausal status, family history of breast or ovarian cancer, use of oral contraceptives, use of hormone therapy, body mass index, and smoking as well as histopathological tumor characteristics including hormone receptor status, grade, histology, and node status. We did not observe any breast cancer risk associations and conclude that it is unlikely that glutathione S-transferases GSTA2, GSTM2, GSTO1, GSTO2, and GSTZ1 participate in breast cancer susceptibility
    Type of Publication: Journal article published
    PubMed ID: 19859803
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...