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  • 1
    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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  • 2
    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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  • 3
    Keywords: EXPRESSION ; GENE ; BREAST-CANCER ; OVARIAN-CANCER ; PROSTATE-CANCER ; telomere length ; COMMON VARIANT ; susceptibility loci ; GENOME-WIDE ASSOCIATION ; FUNCTIONAL VARIATION
    Abstract: Several studies have reported associations between multiple cancer types and single-nucleotide polymorphisms (SNPs) on chromosome 5p15, which harbours TERT and CLPTM1L, but no such association has been reported with endometrial cancer. To evaluate the role of genetic variants at the TERT-CLPTM1L region in endometrial cancer risk, we carried out comprehensive fine-mapping analyses of genotyped and imputed SNPs using a custom Illumina iSelect array which includes dense SNP coverage of this region. We examined 396 SNPs (113 genotyped, 283 imputed) in 4,401 endometrial cancer cases and 28,758 controls. Single-SNP and forward/backward logistic regression models suggested evidence for three variants independently associated with endometrial cancer risk (P = 4.9 x 10(-6) to P = 7.7 x 10(-5)). Only one falls into a haplotype previously associated with other cancer types (rs7705526, in TERT intron 1), and this SNP has been shown to alter TERT promoter activity. One of the novel associations (rs13174814) maps to a second region in the TERT promoter and the other (rs62329728) is in the promoter region of CLPTM1L; neither are correlated with previously reported cancer-associated SNPs. Using TCGA RNASeq data, we found significantly increased expression of both TERT and CLPTM1L in endometrial cancer tissue compared with normal tissue (TERT P = 1.5 x 10(-18), CLPTM1L P = 1.5 x 10(-19)). Our study thus reports a novel endometrial cancer risk locus and expands the spectrum of cancer types associated with genetic variation at 5p15, further highlighting the importance of this region for cancer susceptibility.
    Type of Publication: Journal article published
    PubMed ID: 25487306
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  • 4
    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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  • 5
    Keywords: CANCER ; EXPRESSION ; DISEASE ; RISK ; GENE ; GENES ; ASSOCIATION ; SUSCEPTIBILITY ; BREAST ; breast cancer ; BREAST-CANCER ; genetics ; familial risk ; USA ; LOCI ; GENOME-WIDE ASSOCIATION ; CONFER SUSCEPTIBILITY ; Genetic ; 33 ; COMMON VARIANTS ; Genome-wide association studies
    Abstract: Genome-wide association studies (GWAS) have identified seven breast cancer susceptibility loci, but these explain only a small fraction of the familial risk of the disease. Five of these loci were identified through a two-stage GWAS involving 390 familial cases and 364 controls in the first stage, and 3,990 cases and 3,916 controls in the second stage(1). To identify additional loci, we tested over 800 promising associations from this GWAS in a further two stages involving 37,012 cases and 40,069 controls from 33 studies in the CGEMS collaboration and Breast Cancer Association Consortium. We found strong evidence for additional susceptibility loci on 3p (rs4973768: per-allele OR 1.11, 95% CI = 1.08-1.13, P = 4.1 x 10(-23)) and 17q (rs6504950: per-allele OR 0.95, 95% CI = 0.92-0.97, P = 1.4 x 10(-8)). Potential causative genes include SLC4A7 and NEK10 on 3p and COX11 on 17q
    Type of Publication: Journal article published
    PubMed ID: 19330027
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  • 6
    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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  • 7
    Keywords: RECEPTOR ; APOPTOSIS ; CANCER ; HISTORY ; RISK ; SAMPLE ; TUMOR-NECROSIS-FACTOR ; FAMILY ; BIOMARKERS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; FREQUENCIES ; BREAST ; breast cancer ; BREAST-CANCER ; HEALTH ; AGE ; WOMEN ; SNP ; cancer risk ; GENOTYPES ; HETEROGENEITY ; FAMILIES ; VARIANT ; SINGLE NUCLEOTIDE POLYMORPHISMS ; ESTROGEN ; SINGLE-NUCLEOTIDE POLYMORPHISMS ; ALLELES ; biomarker ; GENOTYPE ; FAMILY-HISTORY ; USA ; CANCER-RISK ; Sample Size ; CONSORTIUM ; ERCC4 ; RECEPTOR STATUS ; PROGESTERONE-RECEPTOR GENE ; CASP8
    Abstract: Previous studies have suggested that minor alleles for ERCC4 rs744154, TNF rs361525, CASP10 rs13010627, PGR rs1042838, and BID rs8190315 may influence breast cancer risk, but the evidence is inconclusive due to their small sample size. These polymorphisms were genotyped in more than 30,000 breast cancer cases and 30,000 controls, primarily of European descent, from 30 studies in the Breast Cancer Association Consortium. We calculated odds ratios (OR) and 95% confidence intervals (95% CI) as a measure of association. We found that the minor alleles for these polymorphisms were not related to invasive breast cancer risk overall in women of European descent: ECCR4 per-allele OR (95% CI) = 0.99 (0.97-1.02), minor allele frequency = 27.5%; TNF 1.00 (0.95-1.06), 5.0%; CASP10 1.02 (0.98-1.07), 6.5%; PGR 1.02 (0.99-1.06), 15.3%; and BID 0.98 (0.86-1.12), 1.7%. However, we observed significant between-study heterogeneity for associations with risk for single-nucleotide polymorphisms (SNP) in CASP10, PGR, and BID. Estimates were imprecise for women of Asian and African descent due to small numbers and lower minor allele frequencies (with the exception of BID SNP). The ORs for each copy of the minor allele were not significantly different by estrogen or progesterone receptor status, nor were any significant interactions found between the polymorphisms and age or family history of breast cancer. In conclusion, our data provide persuasive evidence against an overall association between invasive breast cancer risk and ERCC4 rs744154, TNF rs361525, CASPIO rs13010627, PGR rs1042838, and BID rs8190315 genotypes among women of European descent. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1610-6)
    Type of Publication: Journal article published
    PubMed ID: 19423537
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  • 8
    Keywords: CANCER ; SURVIVAL ; tumor ; DIAGNOSIS ; INFORMATION ; DEATH ; EPIDEMIOLOGY ; MORTALITY ; POPULATION ; RISK ; GENE ; microarray ; TUMORS ; validation ; DNA ; RISK-FACTORS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; SUSCEPTIBILITY ; BREAST ; breast cancer ; BREAST-CANCER ; ASSAY ; microarrays ; OVARIAN-CANCER ; meta-analysis ; SNP ; risk factors ; mass spectrometry ; SPECTROMETRY ; RISK FACTOR ; PROGNOSTIC-FACTORS ; MASS-SPECTROMETRY ; ONCOLOGY ; case-control study ; REGRESSION ; ASSOCIATIONS ; overall survival ; PROGNOSTIC-FACTOR ; METAANALYSIS ; SINGLE-NUCLEOTIDE POLYMORPHISMS ; GENOTYPE ; cancer survival ; INTERNATIONAL CASE-CONTROL ; GENOME-WIDE ASSOCIATION ; GENETIC-VARIATION ; REPAIR GENES ; TUMOR CHARACTERISTICS ; COMMON POLYMORPHISMS ; single nucleotide ; journals ; COX REGRESSION ; ALL-CAUSE ; BRCA1 MUTATIONS
    Abstract: Traditional prognostic factors for survival and treatment response of patients with breast cancer do not fully account for observed survival variation. We used available genotype data from a previously conducted two-stage, breast cancer susceptibility genome-wide association study (ie, Studies of Epidemiology and Risk factors in Cancer Heredity [SEARCH]) to investigate associations between variation in germline DNA and overall survival. We evaluated possible associations between overall survival after a breast cancer diagnosis and 10 621 germline single-nucleotide polymorphisms (SNPs) from up to 3761 patients with invasive breast cancer (including 647 deaths and 26 978 person-years at risk) that were genotyped previously in the SEARCH study with high-density oligonucleotide microarrays (ie, hypothesis-generating set). Associations with all-cause mortality were assessed for each SNP by use of Cox regression analysis, generating a per rare allele hazard ratio (HR). To validate putative associations, we used patient genotype information that had been obtained with 5' nuclease assay or mass spectrometry and overall survival information for up to 14 096 patients with invasive breast cancer (including 2303 deaths and 70 019 person-years at risk) from 15 international case-control studies (ie, validation set). Fixed-effects meta-analysis was used to generate an overall effect estimate in the validation dataset and in combined SEARCH and validation datasets. All statistical tests were two-sided. In the hypothesis-generating dataset, SNP rs4778137 (C 〉 G) of the OCA2 gene at 15q13.1 was statistically significantly associated with overall survival among patients with estrogen receptor-negative tumors, with the rare G allele being associated with increased overall survival (HR of death per rare allele carried = 0.56, 95% confidence interval [CI] = 0.41 to 0.75, P = 9.2 x 10(-5)). This association was also observed in the validation dataset (HR of death per rare allele carried = 0.88, 95% CI = 0.78 to 0.99, P = .03) and in the combined dataset (HR of death per rare allele carried = 0.82, 95% CI = 0.73 to 0.92, P = 5 x 10(-4)). The rare G allele of the OCA2 polymorphism, rs4778137, may be associated with improved overall survival among patients with estrogen receptor-negative breast cancer
    Type of Publication: Journal article published
    PubMed ID: 20308648
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  • 9
    Keywords: RECEPTOR ; CANCER ; EXPRESSION ; GROWTH ; SURVIVAL ; tumor ; KINASE ; DIAGNOSIS ; SUPPORT ; DISEASE ; RISK ; DISTINCT ; PROTEIN ; TUMORS ; PROTEIN-KINASE ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; BREAST ; breast cancer ; BREAST-CANCER ; prevention ; DIFFERENCE ; genetics ; COLORECTAL-CANCER ; PROSTATE-CANCER ; cancer risk ; PROGNOSTIC-FACTORS ; PROGNOSTIC FACTORS ; PROGNOSTIC FACTOR ; heredity ; KERATINOCYTE GROWTH-FACTOR ; HETEROGENEITY ; fibroblast ; SNPs ; overall survival ; GRADE ; PROGNOSTIC-FACTOR ; METAANALYSIS ; ESTROGEN ; USA ; CANCER-RISK ; comparison ; GENOME-WIDE ASSOCIATION ; LOW-GRADE ; FGFR2 ; NUCLEOTIDE ; genetic variants
    Abstract: A three-stage genome-wide association study recently identified single nucleotide polymorphisms ( SNPs) in five loci ( fibroblast growth receptor 2 ( FGFR2), trinucleotide repeat containing 9 ( TNRC9), mitogen-activated protein kinase 3 K1 (MAP3K1), 8q24, and lymphocyte- specific protein 1 ( LSP1)) associated with breast cancer risk. We investigated whether the associations between these SNPs and breast cancer risk varied by clinically important tumor characteristics in up to 23,039 invasive breast cancer cases and 26,273 controls from 20 studies. We also evaluated their influence on overall survival in 13,527 cases from 13 studies. All participants were of European or Asian origin. rs2981582 in FGFR2 was more strongly related to ER- positive ( per- allele OR ( 95%CI) = 1.31 (1.27-1.36)) than ER- negative (1.08 (1.03- 1.14)) disease ( P for heterogeneity = 10-(13)). This SNP was also more strongly related to PR-positive, low grade and node positive tumors (P = 10(-5), 10(-8), 0.013, respectively). The association for rs13281615 in 8q24 was stronger for ER- positive, PR-positive, and low grade tumors (P = 0.001, 0.011 and 10(-4), respectively). The differences in the associations between SNPs in FGFR2 and 8q24 and risk by ER and grade remained significant after permutation adjustment for multiple comparisons and after adjustment for other tumor characteristics. Three SNPs ( rs2981582, rs3803662, and rs889312) showed weak but significant associations with ER- negative disease, the strongest association being for rs3803662 in TNRC9 ( 1.14 ( 1.09-1.21)). rs13281615 in 8q24 was associated with an improvement in survival after diagnosis ( per- allele HR = 0.90 (0.83-0.97). The association was attenuated and non-significant after adjusting for known prognostic factors. Our findings show that common genetic variants influence the pathological subtype of breast cancer and provide further support for the hypothesis that ER- positive and ER- negative disease are biologically distinct. Understanding the etiologic heterogeneity of breast cancer may ultimately result in improvements in prevention, early detection, and treatment
    Type of Publication: Journal article published
    PubMed ID: 18437204
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