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  • colorectal  (15)
  • 1
    Keywords: CANCER ; Germany ; DIAGNOSIS ; FOLLOW-UP ; HISTORY ; RISK ; REDUCTION ; colon ; cancer prevention ; prevention ; HEALTH ; AGE ; WOMEN ; colorectal cancer ; MEN ; COLORECTAL-CANCER ; COST-EFFECTIVENESS ; RANDOMIZED-TRIAL ; ONCOLOGY ; RE ; INCREASE ; LEVEL ; biomarker ; case control studies ; cancer research ; ENDOSCOPY ; FLEXIBLE SIGMOIDOSCOPY ; colorectal ; ASYMPTOMATIC ADULTS ; LINE FINDINGS ; POLYPECTOMY ; SCREENING TRIAL
    Abstract: We aimed to estimate the proportions of colorectal cancer cases that might be prevented by sigmoidoscopy compared with colonoscopy among women and men. In a population-based case control study conducted in Germany, 540 cases with a first diagnosis of primary colorectal cancer and 614 controls matched for age, sex, and county of residence were recruited. A detailed lifetime history of endoscopic examinations of the large bowel was obtained by standardized personal interviews, validated by medical records, and compared between cases and controls, paying particular attention to location of colorectal cancer and sex differences. Overall, 39%, 77%, and 64% of proximal, distal, and total colorectal cancer cases were estimated to be preventable by colonoscopy. The estimated proportion of total colorectal cancer cases preventable by sigmoidoscopy was 45% among both women and men, assuming that sigmoidoscopy reaches the junction of the descending and sigmoid colon only and findings of distal polyps are not followed by colonoscopy. Assuming that sigmoidoscopy reaches the splenic flexure and colonoscopy is done after detection of distal polyps, estimated proportions of total colorectal cancer preventable by sigmoidoscopy increase to 50% and 55% (73% and 91% of total colorectal cancer preventable by primary colonoscopy) among women and men, respectively. We conclude that colonoscopy provides strong protection against colorectal cancer among both women and men. The proportion of this protection achieved by sigmoidoscopy with follow-up colonoscopy in case of distal polyps may be larger than anticipated. Among men, this regimen may be almost as effective as colonoscopy, at least at previous performance levels of colonoscopy
    Type of Publication: Journal article published
    PubMed ID: 17337649
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  • 2
    Keywords: CANCER ; Germany ; INFORMATION ; EXPOSURE ; RISK ; GENE ; METABOLISM ; PATIENT ; HETEROCYCLIC AMINES ; ASSOCIATION ; polymorphism ; SUSCEPTIBILITY ; AGE ; CIGARETTE-SMOKING ; colorectal cancer ; smoking ; COLORECTAL-CANCER ; cancer risk ; genetic polymorphism ; CARCINOGENS ; case-control studies ; TOBACCO ; INDIVIDUALS ; CONSUMPTION ; meat ; ONCOLOGY ; case-control study ; REGRESSION ; RE ; ALLELE ; CARCINOGEN ; SUBSTRATE ; case control studies ; INTERVAL ; ENZYME ; analysis ; GENOTYPE ; MEAT CONSUMPTION ; USA ; odds ratio ; RISK-FACTOR ; CANCER-RISK ; colorectal ; LOGISTIC-REGRESSION ; N-ACETYLTRANSFERASE-1 ; NAT2 GENETIC POLYMORPHISMS ; SULFOTRANSFERASE 1A1 ; SULT1A1
    Abstract: Several procarcinogens that are present in cooked red meat and tobacco smoke are substrates for sulfotransferase 1A1 (SULT1A1). The association between environmental exposures and colorectal cancer risk may be modified by individual differences in the metabolism. Thus, we investigated the effect of a common polymorphism in the SULT1A1 gene associated with decreased enzyme activity on the susceptibility to colorectal cancer in a population-based case-control study. Patients (505) and 604 age- and sex-matched controls provided detailed risk factor information and were genotyped for SULT1A1 G638A using a fluorescence-based melting curve analysis method. Multivariate logistic regression analysis was used to estimate colorectal cancer risk associated with environmental exposures by SULT1A1 genotype. SULT1A1 genotype was not an independent risk factor for colorectal cancer. Risk of colorectal cancer associated with frequent consumption of red meat was significantly elevated among carriers of the SULT1A1*2 allele but not increased among subjects with the SULT1A1*1/*1 genotype (odds ratio (OR) 2.1, 95% confidence interval (CI) 1.1-4.1 and OR 1.0, 95% CI 0.5-2.1, respectively). Colorectal cancer risk associated with 30+ pack-years of active smoking was higher among carriers of the SULT1A1*2 allele (OR 1.7, 95 % CI 1.0-3.2) than among individuals with the SULT1A1*1/*1 genotype (OR 1.1, 95% CI 0.6-2.1). Our results do not support a main effect of SULT1A1 genotype with regard to colorectal cancer but suggest that individuals with the low activity SULT1A1*2 allele may be at higher risk following carcinogen exposure than those with the SULT1A1*1/*1 genotype. (c) 2006 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17013894
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  • 3
    Keywords: RECEPTOR ; APOPTOSIS ; CANCER ; GROWTH ; GROWTH-FACTOR ; proliferation ; CELL ; CELL-PROLIFERATION ; Germany ; PATHWAY ; RISK ; SITE ; GENE ; GENES ; PROTEIN ; PROTEINS ; transcription ; DIFFERENTIATION ; SERA ; BINDING ; ASSOCIATION ; LINKAGE ; polymorphism ; POLYMORPHISMS ; BREAST-CANCER ; NO ; SNP ; colorectal cancer ; COLORECTAL-CANCER ; PROSTATE-CANCER ; REGION ; REGIONS ; LINKAGE DISEQUILIBRIUM ; case-control studies ; BINDS ; BINDING PROTEIN ; insulin ; CELL-GROWTH ; signaling ; SERUM ; SINGLE ; ONCOLOGY ; BINDING-PROTEIN ; case control study ; case-control study ; RE ; SNPs ; cell proliferation ; PROMOTER POLYMORPHISM ; GROWTH-FACTOR-I ; LEVEL ; case control studies ; methods ; HAPLOTYPE ; HAPLOTYPES ; single-nucleotide ; IGFBP3 ; SERUM-LEVELS ; HAPLOTYPE RECONSTRUCTION ; CIRCULATING LEVELS ; ENGLAND ; IGFBP-3 ; MULTIETHNIC COHORT ; colorectal ; case control ; UPSTREAM ; REPEAT ; IGF1 ; CASCADE ; GENETIC-VARIATION ; IGF ; INSULIN-LIKE ; cell growth ; BONE-MINERAL DENSITY ; INSULIN-LIKE-GROWTH-FACTOR-1
    Abstract: Background: The insulin-like growth factor1 (IGF1) pathway plays a significant role in both the normal and malignant cell growth. IGF1 binds to the IGF1 receptor and starts a signaling cascade that regulates cell proliferation, differentiation, and apoptosis. The bioavailability of IGF1 is regulated by the binding protein IGFBP3. A CA repeat polymorphism, in the IGF1 gene, which is located 969 bp upstream from the transcription start site and the rs2854744 and rs2854746 single nucleotide polyrnorphisms (SNPs) in the IGFBP3 gene have been associated with the serum levels of the respective proteins and colorectal cancer (CRC), but the results are inconsistent. We wanted to study if these polymorphisms or any haplotypes of the IGF1 and the IGFBP3 genes are associated with CRC. Methods: High linkage disequilibrium was seen in these gene regions. Therefore, the CA repeat along with two SNPs in the IGF1 gene, and rs2854744 (A-202C), rs2854746 (Ala32Gly) and two additional SNPs in the IGFBP3 gene were selected to cover the whole gene regions. A case-control study was carried out using 661 German CRC cases and 607 matched controls. Results: We did not find any association between the CA repeat length or any of the SNPs in the IGF1 and the IGFBP3 genes and the risk of CRC. Nor did the haplotypes of these genes affect the risk of CRC. Conclusion: Our study suggests no major role of the assessed genetic variation within the IGF1 and the IGFBP3 genes in CRC risk. (c) 2007 International Society for Preventive Oncology. Published by Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 18031946
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  • 4
    Keywords: APOPTOSIS ; CANCER ; proliferation ; CELL ; Germany ; EXPOSURE ; RISK ; RISKS ; GENE ; PROTEIN ; DRUG ; DIFFERENTIATION ; NF-KAPPA-B ; DNA ; GENETIC POLYMORPHISMS ; cell cycle ; CELL-CYCLE ; CYCLE ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; VARIANTS ; PROGRESSION ; DNA-REPAIR ; REPAIR ; genetics ; colorectal cancer ; COLORECTAL-CANCER ; p53 ; TUMOR-SUPPRESSOR GENE ; cancer risk ; GENOTYPES ; gene-environment interaction ; genetic polymorphism ; MULTIVARIATE ; CARRIERS ; case-control studies ; aspirin ; NONSTEROIDAL ANTIINFLAMMATORY DRUGS ; heredity ; DNA repair ; ARREST ; case control study ; case-control study ; REGRESSION ; RE ; VARIANT ; ALLELE ; genomics ; interaction ; case control studies ; INTERVAL ; analysis ; methods ; GENOTYPE ; HAPLOTYPE ; HAPLOTYPES ; USA ; LINKAGE PHASE ; DRUGS ; odds ratio ; CANCER-RISK ; genomic ; microbiology ; colorectal ; LOGISTIC-REGRESSION ; FUNCTIONAL-ANALYSIS ; ANTIINFLAMMATORY DRUGS ; COLON ADENOCARCINOMA CELLS ; nonsteroidal anti-inflammatory drugs ; P53 POLYMORPHISMS ; SULINDAC SULFIDE ; TP53 gene
    Abstract: Objective Substantial evidence indicates that nonsteroidal anti-inflammatory drugs protect against colorectal cancer by altering cell cycle progression and/or inducing apoptosis, whereas p53 protein is crucial to maintaining cell-cycle arrest and regulating DNA repair, differentiation, and apoptosis. Genetic variants in TP53 gene might therefore influence colorectal cancer risk and modify the effects of nonsteroidal anti-inflammatory drugs. We assessed the association of TP53 Arg72Pro and p53PIN3 polymorphisms with colorectal cancer risk and their possible interaction with nonsteroidal antiinflammatory drug use. Methods We included 467 cases and 563 controls from a population-based case-control study. Multivariate logistic regression analysis was used to estimate the association between genotypes, environmental exposures and colorectal cancer risk, adjusting for potential confounders. Results Odds ratios of colorectal cancer were 0.75 (95% confidence interval, 0.57-0.99) for TP53 72Pro carriers compared with those homozygous for the TP53 72Arg allele and 0.78 (95% confidence interval, 0.58-1.05) for p53PIN3 A2 carriers compared with p53PIN3 A1A1. Risks differed by nonsteroidal anti -inf lam matory drug use. For both investigated TP53 polymorphisms, we found that the colorectal cancer risk associated with regular nonsteroidal anti-inflammatory drug use was statistically significantly modified by the TP53 genotype (P values for interaction=0.049 and 0.034, respectively), whereby a substantial protective effect of nonsteroidal antiinflammatory drug use was observed for homozygous carriers of the 72Arg allele and of the PIN3 Al allele (odds ratio 0.44; 95% confidence interval, 0.30-0.65 and odds ratio, 0.45; 95% confidence interval, 0.31-0.65). The interaction between nonsteroidal anti-inflammatory drugs and TP53 genetic polymorphisms was confirmed by haplotype analysis. Conclusions These data suggest that the TP53 genotype may modify the influence of nonsteroidal anti-inflammatory drug use on the risk of colorectal cancer. A direct proof of functional analysis is warranted to confirm these findings. Pharmacogenetics and Genomics 17:639-645 (C) 2007 Lippincott Williams & Wilkins
    Type of Publication: Journal article published
    PubMed ID: 17622940
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  • 5
    Keywords: CANCER ; COMBINATION ; Germany ; COHORT ; cohort study ; DISEASE ; POPULATION ; RISK ; DRUG ; IMPACT ; REDUCTION ; ASSOCIATION ; TRIAL ; TRIALS ; ADENOMAS ; prevention ; HEALTH ; colorectal cancer ; PROSPECTIVE COHORT ; COLORECTAL-CANCER ; COLON-CANCER ; POPULATIONS ; case-control studies ; aspirin ; NONSTEROIDAL ANTIINFLAMMATORY DRUGS ; chemoprevention ; RANDOMIZED-TRIAL ; SINGLE ; ONCOLOGY ; case control study ; case-control study ; REGRESSION ; RE ; CARDIOVASCULAR-DISEASE ; METAANALYSIS ; case control studies ; INTERVAL ; USA ; prospective ; DRUGS ; odds ratio ; colorectal ; cardiovascular disease ; LONG-TERM USE ; LOGISTIC-REGRESSION ; statins
    Abstract: Recent research has drawn attention to protective effects of statins on colorectal cancer (CRC) and possible joint effects with other drugs. Because statins are often administered in combination With low-dose aspirin for the prevention of cardiovascular disease, the aim of our study was to investigate individual and combined effects of statins and low-dose aspirin on CRC risk. We assessed use of statins and low-dose aspirin in 540 cases with histologically confirmed incident CRC and 614 control subjects in a populations based case-control study in Germany. Multiple logistic regression. was used to estimate the impact of regular use of either low-dose aspirin or statins, and of both drugs combined on CRC risk. We found modest risk reduction of CRC for regular use of low-dose aspirin (adjusted odds ratio 0.77, 95% confidence interval 0.551.07) and a stronger association with regular use of statins (OR 0.65, 95% CI 0.43-0.99) or use of both drugs (OR 0.63, 95% CI 0.36-1.10). Combined use of low-dose aspirin and statins was associated with risk reduction by 62% after 5 or more years (OR 0.38, 95% CI 0.15-0.97). Combinational chemoprevention with low-dose aspirin and statins might provide stronger risk reduction than either of the single drugs after at least 5 years use, but confirmation is needed, preferably in prospective cohort studies and eventually by randomized controlled trials. (c) 2007 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17487832
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  • 6
    Keywords: CANCER ; Germany ; HISTORY ; MORTALITY ; RISK ; validation ; FAMILY ; REDUCTION ; NO ; prevention ; HEALTH ; AGE ; family history ; colorectal cancer ; COLORECTAL-CANCER ; EFFICACY ; cancer risk ; case-control studies ; aspirin ; sensitivity ; specificity ; VALIDITY ; SCREENING SIGMOIDOSCOPY ; case control study ; case-control study ; RE ; FAMILIES ; colonoscopy ; case control studies ; INTERVAL ; FAMILY-HISTORY ; USA ; reproducibility of results ; odds ratio ; CANCER-RISK ; colorectal neoplasms ; ENDOSCOPY ; colorectal ; POLYPECTOMY ; KAPPA ; mass screening ; MEDICAL-RECORD AUDIT ; reporting ; validation studies ; VETERANS
    Abstract: Large-bowel endoscopy with removal of polyps strongly reduces colorectal cancer risk. In epidemiologic studies, ascertainment of large-bowel endoscopies often relies on self-reports and might be prone to imperfect recall. In 2003-2004, the authors assessed the validity of self-reported colorectal endoscopies in a population-based case-control study including 540 cases and 614 controls from southwest Germany and calculated odds ratios of colorectal cancer risk according to self-reports and medical records. They sought to obtain all medical records for the last self-reported endoscopy and for a subsample of 100 subjects reporting no previous endoscopy. In total, 377 of 483 records could be obtained (78%). Sensitivity of self-reports was 100%, and specificity ranged from 93% to 98% among subgroups defined by age, gender, education, family history of colorectal cancer, and case-control status. The odds ratios for colorectal cancer risk after previous colonoscopy were 0.31 (95% confidence interval: 0.21, 0.45) using self-reports and 0.31 (95% confidence interval: 0.20, 0.47) using medical records. However, agreement between self-reports and medical records was poor regarding type of endoscopy (colonoscopy, sigmoicloscopy, or rectoscopy; kappa = 0.22), moderate concerning polypectomy (kappa = 0.58), and reasonable for year of examination (kappa = 0.70). Self-reports of previous colorectal endoscopies agreed well with medical records, but validation appears to be essential with respect to details of the examination
    Type of Publication: Journal article published
    PubMed ID: 17456475
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  • 7
    Keywords: CANCER ; Germany ; THERAPY ; RISK ; INDEX ; REDUCTION ; CONTRAST ; ASSOCIATION ; BREAST-CANCER ; hormone ; WOMEN ; colorectal cancer ; HORMONE REPLACEMENT THERAPY ; COLORECTAL-CANCER ; COLON-CANCER ; UNITED-STATES ; case-control studies ; BODY ; POSTMENOPAUSAL WOMEN ; menopause ; MASS INDEX ; MASSES ; BODIES ; ONCOLOGY ; case control study ; case-control study ; RE ; THERAPIES ; interaction ; colonoscopy ; METAANALYSIS ; case control studies ; INTERVAL ; MASS ; RANDOMIZED CONTROLLED-TRIAL ; OVERWEIGHT ; HORMONES ; ESTROGEN PLUS PROGESTIN ; REPLACEMENT THERAPY ; odds ratio ; population-based ; ENGLAND ; REPLACEMENT ; colorectal ; case control ; NOV ; postmenopausal ; BODY-MASS ; BODY-MASS-INDEX ; German ; case-control ; body mass
    Abstract: Previous studies have reported inconsistent results regarding the modifying effect of hormone replacement therapy (HRT) on the association of body mass index (BMI) and the risk of colorectal cancer (CRC) among postmenopausal women. We assessed the use of HRT and BMI in 208 postmenopausal women with histologically confirmed incident CRC and 246 controls in a population-based case-control study in Germany (DACHS study). Ever use of HRT was strongly associated with reduction of CRC risk (adjusted odds ratio 0.41, 95% confidence interval 0.25-0.67). Among nonusers of HRT, risk of CRC was strongly increased in women with BMI 27 to 〈 30 kg m(-2) (2.76, 1.07-7.12) and obese women (3.30, 1.25-8.72), when compared with women with BMI 〈 23 kg m(-2) (P for trend 〈 0.01). BMI was not associated with risk of CRC among HRT users (P for interaction 〈 0.01). In contrast to most other studies, a positive association of BMI and CRC risk was found among nonusers of HRT, but not among users of HRT. The reasons for the inconsistency of results regarding the potential risk modifying effect of postmenopausal hormones in the association of BMI with CRC remain inconclusive and require further study
    Type of Publication: Journal article published
    PubMed ID: 17987040
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  • 8
    Keywords: CANCER ; Germany ; screening ; TOOL ; POPULATION ; RISK ; IMPACT ; ADENOMAS ; prevention ; AGE ; WOMEN ; colorectal cancer ; MEN ; COLORECTAL-CANCER ; CERVICAL-CANCER ; RATES ; DATABASE ; EUROPE ; colonoscopy ; RANDOMIZED CONTROLLED-TRIAL ; colorectal ; POLYPECTOMY ; CRC ; REMOVAL
    Abstract: In late 2002, colonoscopy was introduced as a primary screening tool for colorectal cancer (CRC) in Germany We aimed to estimate the expected reduction in case numbers and incidence of CRC between 2003 and 2010 by detection and removal of advanced adenomas. Data from 1,875,708 women and men included in the national screening colonoscopy database were combined with estimates of transition rates of advanced adenomas and with national population projections. Despite relatively low screening participation, incident CRC cases are expected to be reduced by more than 15,000 between 2003 and 2010. The impact is expected to be largest in age groups 55-59, 60-64 and 65-69 in whom total case numbers in 2010 are expected to be reduced by 13%, 19% and 14% among women, and by 11%, 15% and 12%, respectively, among men. our results forecast a major rapid reduction of the CRC burden in Germany by screening colonoscopy. (c) 2009 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 19289271
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  • 9
    Keywords: CANCER ; Germany ; screening ; EPIDEMIOLOGY ; MORTALITY ; POPULATION ; DIFFERENTIATION ; TIME ; NEOPLASIA ; prevention ; PATTERNS ; AGE ; WOMEN ; colorectal cancer ; MEN ; COLORECTAL-CANCER ; COUNTRIES ; US ; POPULATIONS ; UNITED-STATES ; INITIATION ; GUIDELINES ; ONCOLOGY ; RE ; ELDERLY-PATIENTS ; colonoscopy ; HORMONE-REPLACEMENT THERAPY ; LEVEL ; cancer registry ; EXTENT ; colorectal ; BENEFITS ; MILLION WOMEN ; sigmoidoscopy
    Abstract: There is some variation regarding age at initiation of screening for colorectal cancer (CRC) between countries, but the same age of initiation is generally recommended for women and men within countries, despite important gender differences in the epidemiology of CRC. We have explored whether, and to what extent, these differences would be relevant regarding age at initiation of CRC screening. Using population-based cancer registry data from the US and national mortality statistics from different countries, we looked at cumulative 10-year incidence and mortality of CRC reached among men at ages 50, 55, and 60, and found that women mainly reached equivalent levels when 4 to 8 years older. The gender differences were remarkably constant across populations and over time. These patterns suggest that gender differentiation of age at initiation may be worthwhile to utilise CRC-screening resources more efficiently
    Type of Publication: Journal article published
    PubMed ID: 17311019
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  • 10
    Keywords: RECEPTOR ; CANCER ; EXPRESSION ; Germany ; human ; PATHWAY ; screening ; RISK ; GENE ; GENES ; PROTEIN ; PROTEINS ; TIME ; PATIENT ; LIGAND ; CARCINOGENESIS ; colon ; DOWN-REGULATION ; ASSOCIATION ; SUSCEPTIBILITY ; TARGET ; NO ; PROGRESSION ; colorectal cancer ; COLORECTAL-CANCER ; BLADDER-CANCER ; HETEROZYGOSITY ; cancer risk ; COLON-CANCER ; LIGANDS ; CARCINOMAS ; CARRIERS ; INDIVIDUALS ; beta-catenin ; RECEPTORS ; WNT ; signaling ; ONCOLOGY ; RE ; VARIANT ; HUMAN CANCER ; TUMORIGENESIS ; FAMILIAL BREAST-CANCER ; INTERVAL ; TARGET GENES ; rectal cancer ; HUMAN CANCERS ; INCREASED RISK ; CANCERS ; CANCER-RISK ; colorectal ; SFRP1
    Abstract: The Wnt-beta-catenin pathway plays a central role in colorectal tumorigenesis. Frizzled-related protein (FRZB, also termed secreted frizzled-related protein 3, sFRP3) antagonizes the signaling of wingless (Wnt) ligands through the frizzled membrane-bound receptors, resulting in beta-catenin destabilization thereby suppressing the expression of target genes. Recently, the FRZB Gly324 variant has been shown to have an attenuated ability to antagonize Wnt signaling and to be associated with an increased osteoarthritis risk. Here, we investigated, for the first time, the role of Arg324Gly (970C〉G) along with Arg200Trp (598C〉T) on colorectal cancer (CRC) risk by analyzing 659 patients and 607 control individuals drawn from the German DACHS (Darmkrebs: Chancen der Verhu " tung durch Screening) study. Although Arg200Trp showed no effect on CRC risk, we found homozygous carriers of Gly324 more frequent in cases than in controls, leading to a significantly increased risk for CRC [odds ratio (OR) = 5.1, 95% confidence interval (95% CI) = 1.74-14.71, P 〈 0.001]. The association was stronger in rectal cancer (OR = 7.52, 95% CI = 2.40-23.25, P 〈 0.0001) than in colon cancer (OR = 3.66, 95% CI = 1.14-11.76, P 〈 0.05). Since modified Wnt signaling and down-regulation of frizzled-related proteins have been observed in many human cancers, this variant may also affect the susceptibility to other cancers
    Type of Publication: Journal article published
    PubMed ID: 17420170
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