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  • 1
    Keywords: RECEPTOR ; CANCER ; GROWTH ; GROWTH-FACTOR ; proliferation ; tumor ; CELL-PROLIFERATION ; PATHWAY ; RISK ; GENE ; GENES ; PROTEIN ; TUMORS ; RELEASE ; PATIENT ; BINDING ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; VARIANTS ; BREAST ; breast cancer ; BREAST-CANCER ; hormone ; COLORECTAL-CANCER ; PROSTATE-CANCER ; cancer risk ; case-control studies ; SOMATOSTATIN ; CANCER PATIENTS ; nutrition ; FACTOR-I ; BINDING PROTEIN ; SERUM ; SINGLE ; IGF-I ; BINDING-PROTEIN ; case-control study ; ASSOCIATIONS ; RE ; VARIANT ; SINGLE NUCLEOTIDE POLYMORPHISMS ; cell proliferation ; development ; GROWTH-FACTOR-I ; BINDING PROTEIN-3 ; LEVEL ; case control studies ; GENOTYPE DATA ; FACTOR (IGF)-I ; PREMENOPAUSAL WOMEN ; IGFBP3 ; insulin-like growth factor ; PLASMA-LEVELS ; SERUM-LEVELS
    Abstract: Insulin-like growth factor-I (IGF-I) stimulates cell proliferation and can enhance the development of tumors in different organs. Epidemiologic studies have shown that an elevated level of circulating IGF-I is associated to increased risk of breast cancer as well as other cancers. Genetic variants affecting the release or biological action of growth hormone (GH), the main stimulator of IGF-I production, may predict circulating levels of IGF-I and have an effect on cancer risk. We tested this hypothesis with a large case-control study of 807 breast cancer patients and 1,588 matched control subjects nested within the European Prospective Investigation into Cancer and Nutrition. We genotyped 22 common single nucleotide polymorphisms in 10 genes involved in GH production and action (GHRH, GHRHR, SST, SSTR1-SSTR5, POU1F1, and GH1), and in parallel, we measured serum levels of IGF-I and IGFBP-3, its major binding protein, in samples of cases and controls. SST and SSTR2 polymorphisms showed weak but statistically significant associations with breast cancer risk. SSTR5 polymorphisms were associated with IGF-I levels, whereas one polymorphism in GHRHR and one in POU1F1 were associated with IGFBP-3 levels. Our conclusion is that common genetic variation in the GH synthesis pathway, as measured by single nucleotide polymorphisms selected in the present study, is not a major determinant of IGF-I and IGFBP-3 circulating levels, and it does not play a major role in altering breast cancer risk
    Type of Publication: Journal article published
    PubMed ID: 16214911
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  • 2
    Keywords: RECEPTOR ; CANCER ; CELLS ; EXPRESSION ; CELL ; LUNG ; LUNG-CANCER ; DEATH ; DISEASE ; RISK ; RISKS ; SITE ; GENE ; GENES ; GENOME ; PROTEIN ; TISSUE ; MARKER ; TISSUES ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; ACID ; COUNTRIES ; REGION ; FRANCE ; EPITHELIAL-CELLS ; RECEPTORS ; SMOKERS ; DEPENDENCE ; SNPs ; NEURONS ; CANDIDATE ; ENGLAND ; GENOME-WIDE ASSOCIATION ; NUCLEOTIDE ; FAGERSTROM TOLERANCE QUESTIONNAIRE ; HAPLOTYPE MAP
    Abstract: Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually(1). To identify genetic factors that modify disease risk, we conducted a genome- wide association study by analysing 317,139 single- nucleotide polymorphisms in 1,989 lung cancer cases and 2,625 controls from six central European countries. We identified a locus in chromosome region 15q25 that was strongly associated with lung cancer ( P= 9 x 10(-10)). This locus was replicated in five separate lung cancer studies comprising an additional 2,513 lung cancer cases and 4,752 controls ( P = 5 x 10(-20) overall), and it was found to account for 14%( attributable risk) of lung cancer cases. Statistically similar risks were observed irrespective of smoking status or propensity to smoke tobacco. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits ( CHRNA5, CHRNA3 and CHRNB4). Such subunits are expressed in neurons and other tissues, in particular alveolar epithelial cells, pulmonary neuroendocrine cells and lung cancer cell lines(2,3), and they bind to N'- nitrosonornicotine and potential lung carcinogens(4). A non- synonymous variant of CHRNA5 that induces an amino acid substitution ( D398N) at a highly conserved site in the second intracellular loop of the protein is among the markers with the strongest disease associations. Our results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets(5)
    Type of Publication: Journal article published
    PubMed ID: 18385738
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  • 3
    Keywords: CANCER ; carcinoma ; INFORMATION ; COHORT ; DEATH ; incidence ; RISK ; SITE ; SITES ; GENE ; INFECTION ; DOWN-REGULATION ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; MOLECULE ; NO ; PROGRESSION ; DIFFERENCE ; PROMOTER ; MUTATION ; smoking ; RATES ; FRANCE ; MUTATIONS ; ADHESION ; case-control studies ; ADHESION MOLECULE ; EPIC ; HELICOBACTER-PYLORI ; nutrition ; SMOKERS ; METHYLATION ; E-cadherin ; ONCOLOGY ; case-control study ; RE ; INCREASE ; gastric cancer ; PROMOTER POLYMORPHISM ; HAPLOTYPE ; prospective ; Helicobacter pylori ; ENGLAND ; block ; GENE POLYMORPHISMS ; GENE POLYMORPHISM ; POSITION ; gastric adenocarcinoma ; CDH1 ; E-CADHERIN GENE
    Abstract: Despite declining incidence rates, gastric cancer (GC) is a major cause of death worldwide. E-Cadherin is an adhesion molecule that is thought to be involved in GC. Germline mutations in the E-Cadherin gene (CDH1) have been identified in hereditary diffuse GC. Also, a promoter polymorphism at position 160 C/A has been suggested to lead to transcriptional down regulation and has been shown to affect GC risk in some studies. However, very little information exists on the GC risk association of other CDH1 polymorphisms and it is unclear whether any associations may be different by GC anatomical sites or histological types. Thus, a case-control study (cases = 245/controls = 950) nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort was conducted to assess the GC risk association of eight CDH1 gene polymorphisms. None of the CDH1 polymorphisms or haplotypes analysed were associated with GC risk and no differences of effect were observed by Helicobacter pylori infection status. However, three CDH1 polymorphisms in the same haplotype block, including the CDH1-160C/A, interacted with smoking to increase GC risk in smokers but not in never smokers. These findings should be confirmed in larger independent studies. (c) 2008 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 18342503
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  • 4
    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
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  • 5
    Keywords: APOPTOSIS ; CANCER ; carcinoma ; CELL ; LUNG ; MODEL ; PATHWAY ; PATHWAYS ; lung cancer ; LUNG-CANCER ; RISK ; GENE ; GENES ; METABOLISM ; CARCINOGENESIS ; ASSOCIATION ; SUSCEPTIBILITY ; VARIANTS ; AGE ; DNA-REPAIR ; smoking ; ADHESION ; CELL-ADHESION ; inflammation ; ONCOLOGY ; case-control study ; REGRESSION ; ASSOCIATIONS ; VARIANT ; CANDIDATE GENES ; METHYLENETETRAHYDROFOLATE REDUCTASE ; INCREASED RISK ; SQUAMOUS-CELL ; CHINESE POPULATION ; XUAN-WEI ; METHYLENE-TETRAHYDROFOLATE REDUCTASE ; GENE POLYMORPHISMS ; Genetic ; CENTRAL-EUROPE ; SEQUENCE VARIANTS
    Abstract: Background. Analysis of candidate genes in individual studies has had only limited success in identifying particular gene variants that are conclusively associated with lung cancer risk. In the International Lung Cancer Consortium (ILCCO), we conducted a coordinated genotyping study of 10 common variants selected because of their prior evidence of an association with lung cancer. These variants belonged to candidate genes from different cancer-related pathways including inflammation (IL1B), folate metabolism (MTHFR), regulatory function (AKAP9 and CAMKK1), cell adhesion (SEZL6) and apoptosis (FAS, FASL, TP53, TP53BP1 and BAT3). Methods. Genotype data from 15 ILCCO case-control studies were available for a total of 8431 lung cancer cases and 11 072 controls of European descent and Asian ethnic groups. Unconditional logistic regression was used to model the association between each variant and lung cancer risk. Results. Only the association between a non-synonymous variant of TP53BP1 (rs560191) and lung cancer risk was significant (OR = 0.91, P = 0.002). This association was more striking for squamous cell carcinoma (OR = 0.86, P = 6 x 10(-4)). No heterogeneity by center, ethnicity, smoking status, age group or sex was observed. In order to confirm this association, we included results for this variant from a set of independent studies (9966 cases/11 722 controls) and we reported similar results. When combining all these studies together, we reported an overall OR = 0.93 (0.89-0.97) (P = 0.001). This association was significant only for squamous cell carcinoma [OR = 0.89 (0.85-0.95), P = 1 x 10(-4)]. Conclusion. This study suggests that rs560191 is associated to lung cancer risk and further highlights the value of consortia in replicating or refuting published genetic associations
    Type of Publication: Journal article published
    PubMed ID: 20106900
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  • 6
    Keywords: LUNG-CANCER ; SUSCEPTIBILITY LOCUS ; NECK-CANCER ; pooled analysis ; FAMILY-HISTORY ; ALCOHOL-DRINKING ; EPIDEMIOLOGY CONSORTIUM ; INTERNATIONAL HEAD ; SENSITIVITY PROTEIN MUS308 ; TOBACCO-RELATED CANCERS
    Abstract: Genome-wide association studies (GWAS) have been successful in identifying common genetic variation involved in susceptibility to etiologically complex disease. We conducted a GWAS to identify common genetic variation involved in susceptibility to upper aero-digestive tract (UADT) cancers. Genome-wide genotyping was carried out using the Illumina HumanHap300 beadchips in 2,091 UADT cancer cases and 3,513 controls from two large European multi-centre UADT cancer studies, as well as 4,821 generic controls. The 19 top-ranked variants were investigated further in an additional 6,514 UADT cancer cases and 7,892 controls of European descent from an additional 13 UADT cancer studies participating in the INHANCE consortium. Five common variants presented evidence for significant association in the combined analysis (p 〈= 5 x 10(-7)). Two novel variants were identified, a 4q21 variant (rs1494961, p = 1 x 10(-8)) located near DNA repair related genes HEL308 and FAM175A (or Abraxas) and a 12q24 variant (rs4767364, p = 2 x 10(-8)) located in an extended linkage disequilibrium region that contains multiple genes including the aldehyde dehydrogenase 2 (ALDH2) gene. Three remaining variants are located in the ADH gene cluster and were identified previously in a candidate gene study involving some of these samples. The association between these three variants and UADT cancers was independently replicated in 5,092 UADT cancer cases and 6,794 controls non-overlapping samples presented here (rs1573496-ADH7, p = 5 x 10(-8); rs1229984-ADH1B, p = 7 x 10(-9); and rs698-ADH1C, p = 0.02). These results implicate two variants at 4q21 and 12q24 and further highlight three ADH variants in UADT cancer susceptibility
    Type of Publication: Journal article published
    PubMed ID: 21437268
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  • 7
    Keywords: METABOLISM ; ethanol ; CONSUMPTION ; NECK-CANCER ; UPPER AERODIGESTIVE TRACT ; pooled analysis ; DOSE-RESPONSE METAANALYSIS ; ACETALDEHYDE PRODUCTION ; COLONIC FLORA ; ADH
    Abstract: BACKGROUND/OBJECTIVES: Heavy alcohol drinking is a risk factor of colorectal cancer (CRC), but little is known on the effect of polymorphisms in the alcohol-metabolizing enzymes, alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) on the alcohol-related risk of CRC in Caucasian populations. SUBJECTS/METHODS: A nested case-control study (1269 cases matched to 2107controls by sex, age, study centre and date of blood collection) was conducted within the European Prospective Investigation into Cancer and Nutrition (EPIC) to evaluate the impact of rs1229984 (ADH1B), rs1573496 (ADH7) and rs441 (ALDH2) polymorphisms on CRC risk. Using the wild-type variant of each polymorphism as reference category, CRC risk estimates were calculated using conditional logistic regression, with adjustment for matching factors. RESULTS: Individuals carrying one copy of the rs1229984(A) (ADH1B) allele (fast metabolizers) showed an average daily alcohol intake of 4.3 g per day lower than subjects with two copies of the rs1229984(G) allele (slow metabolizers) (P-diff〈0.01). None of the polymorphisms was associated with risk of CRC or cancers of the colon or rectum. Heavy alcohol intake was more strongly associated with CRC risk among carriers of the rs1573496(C) allele, with odds ratio equal to 2.13 (95% confidence interval: 1.26-3.59) compared with wild-type subjects with low alcohol consumption P-((interaction)=0.07). CONCLUSIONS: The rs1229984(A) (ADH1B) allele was associated with a reduction in alcohol consumption. The rs1229984 (ADH1B), rs1573496 (ADH7) and rs441 (ALDH2) polymorphisms were not associated with CRC risk overall in Western-European populations. However, the relationship between alcohol and CRC risk might be modulated by the rs1573496 (ADH7) polymorphism.
    Type of Publication: Journal article published
    PubMed ID: 23149980
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  • 8
    Keywords: RECEPTOR ; CANCER ; GROWTH ; PROSTATE ; COHORT ; DISEASE ; RISK ; GENE ; GENES ; BIOMARKERS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; hormone ; HEALTH ; PLASMA ; prostate cancer ; PROSTATE-CANCER ; SWEDEN ; cancer risk ; RECEPTORS ; FACTOR-I ; SINGLE ; SINGLE NUCLEOTIDE POLYMORPHISMS ; GROWTH-FACTOR-I ; BINDING PROTEIN-3 ; biomarker ; EPITHELIUM ; USA ; SOMATOSTATIN ANALOGS ; CANCER-RISK ; CIRCULATING LEVELS ; NORTHERN SWEDEN ; Genetic ; INVESTIGATE
    Abstract: Background: Somatostatin (SST) and its receptors (SSTR1-5) may have a role in prostate cancer by influencing the IGFI hormone axis or through direct effects on prostate epithelia. We have investigated if genetic variation in the SST and SSTR1-5 genes influences prostate cancer risk and/or circulating IGFI and IGFBP3 hormone levels. Materials and Methods: We analyzed 28 haplotype tagging single nucleotide polymorphisms in the SST and SSTR1-5 genes in a case-control/genetic association study to investigate the association between genetic variation and prostate cancer risk. The study included 2863 cases and 1737 controls from the Cancer Prostate in Sweden (CAPS) study. To investigate the genetic influence on circulating hormone levels, plasma concentrations of IGFI and IGFBP3 were analyzed in 874 controls of the CAPS study and 550 male subjects from the Northern Sweden Health and Disease Cohort (NSHDC). Results: No clear association between prostate cancer risk and genetic variation of the SST and SSTR1-5 genes was identified. The SSTR5 missense single nucleotide polymorphism rs4988483 was associated with circulating IGFI (P = 0.002) and IGFBP3 (P = 0.0003) hormone levels in CAPS controls, with a per allele decrease of similar to 11%. This decrease was replicated in NSHDC for circulating IGFBP3 (P = 0.01) but not for IGFI (P = 0.09). Combining CAPS and NSHDC subjects indicated evidence of association between rs4988483 and both IGFBP3 (P = 2 x 10(-5)) and IGFI (P = 0.0004) hormone levels. Conclusions: Our results suggest that genetic variation in the SSTR5 gene and, particularly, the rs4988483 single nucleotide polymorphism influence circulating IGFI and IGFBP3 hormone levels with no measurable effect on prostate cancer risk. (Cancer Epidemiol Biomarkers Prev 2009;18(5):164.4-50)
    Type of Publication: Journal article published
    PubMed ID: 19423539
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  • 9
    Keywords: APOPTOSIS ; CANCER ; CELLS ; GROWTH ; GROWTH-FACTOR ; SURVIVAL ; tumor ; TUMOR-CELLS ; CELL ; PROSTATE ; DIAGNOSIS ; FOLLOW-UP ; SYSTEM ; DEATH ; POPULATION ; RISK ; GENE ; GENES ; PROTEIN ; PROTEINS ; SAMPLE ; SAMPLES ; METABOLISM ; PATIENT ; BINDING ; ASSOCIATION ; LINKAGE ; POLYMORPHISMS ; single nucleotide polymorphism ; VARIANTS ; BREAST-CANCER ; PLASMA ; SNP ; prostate cancer ; PROSTATE-CANCER ; SWEDEN ; BINDING-PROTEINS ; FACTOR-I ; BINDING PROTEIN ; SERUM ; SINGLE ; IGF-I ; VARIANT ; SNPs ; GROWTH-FACTOR-I ; I IGF-I ; LEVEL ; HAPLOTYPE ; FACTOR (IGF)-I ; IGFBP3 ; USA ; HORMONE LEVELS ; INCREASED RISK ; CIRCULATING LEVELS ; FACTOR-BINDING ; SWEDISH ; Genetic ; genetic variation ; ELEVATED LEVELS ; IGFBP-3 LEVELS ; intact IGFBP3 ; TUMOR CHARACTERISTICS
    Abstract: BACKGROUND. Binding proteins regulate bioavailability of insulin-like growth factor-I (IGF-I) in the circulation and affect apoptosis of tumor cells in the prostate. We analyzed genetic variation within genes coding for IGF binding proteins in relation to prostate cancer incidence and survival. We also investigated if circulating IGFBP3 affects prostate cancer-specific survival. MATERIALS AND METHODS. Eleven haplotype tagging SNPs and two single SNPs in the IGFBP1, IGFBP3, and IGFALS genes were genotyped within the CAncer Prostate in Sweden (CAPS) study including 2,774 cases and 1,736 controls. Plasma samples for analyses of total- and intact IGFBP3 levels were available for 1,521 cases and 909 controls. Complete follow-up of vital status was achieved by linkage to the Swedish Cause of Death Register. RESULTS. We found no clear association between the genetic variants and prostate cancer incidence or survival. The rare allele of the IGFBP3 SNP rs2854744 was associated with elevated plasma levels of total IGFBP3 (P-trend = 9 x 10(-8)), but not intact IGFBP3 (P-trend = 0.16). Elevated levels of total- (P-trend = 0.03) and intact IGFBP3 (P-trend = 6 x 10(-14)) were associated with increased risk of prostate cancer specific death. Treatment and tumor characteristics accounted for the association with total IGFBP3, whereas the association with intact IGFBP3 was attenuated, but still statistically significant in adjusted analysis (Ptrend-adjusted = 0.0004). Elevated intact IGFBP3 was also significantly associated with increased risk of prostate cancer-specific death among patients who were chemically or surgically castrated (Ptrend-adjusted = 0.0003), and among patients who had not been treated (Ptrend-adjusted = 0.02). CONCLUSIONS. Circulating levels of intact IGFBP3 Measured after diagnosis is associated with increased risk of prostate cancer-specific death. Prostate 69: 1281-1291, 2009. (C) 2009 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 19455605
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  • 10
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