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  • COLORECTAL-CANCER  (38)
  • 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 ; Germany ; screening ; EPIDEMIOLOGY ; incidence ; MORTALITY ; prevention ; AGE ; WOMEN ; colorectal cancer ; MEN ; COLORECTAL-CANCER ; COUNTRIES ; GUIDELINES ; ONCOLOGY ; RE ; aging ; LEVEL ; ENGLAND
    Abstract: We assessed incidence and mortality of colorectal cancer (CRC) at various ages among women and men in 38 European countries. The ages at which defined levels of incidence and mortality were reached varied between 9 and 17 years between countries. This variation requires consideration in the definition of screening guidelines
    Type of Publication: Journal article published
    PubMed ID: 18628760
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  • 6
    Keywords: CANCER ; Germany ; MODEL ; MODELS ; neoplasms ; INFORMATION ; screening ; COHORT ; POPULATION ; RISK ; DESIGN ; AGE ; WOMEN ; colorectal cancer ; MEN ; COLORECTAL-CANCER ; PREVALENCE ; REGRESSION ; PROGRAM ; aging ; colonoscopy ; METAANALYSIS ; BIRTH ; CANCER INCIDENCE ; colorectal neoplasms ; PARTICIPATION ; POLYPS ; COHORTS ; STRATIFICATION
    Abstract: BACKGROUND: Prevalence of advanced colorectal neoplasms increases with age and is higher among men than women. Cross-sectional analyses estimated that men reach an equivalent prevalence at a much younger age than women. However, cross-sectional estimates may be confounded by birth cohort effects. OBJECTIVE: To estimate age and cohort effects in advanced colorectal neoplasms and to adjust risk-advancement periods for men compared with women for birth cohort effects. DESIGN: Age-cohort analyses. SETTING: German screening colonoscopy program, 2003 to 2007. PARTICIPANTS: 2 185 153 participants aged 55 to 75 years. MEASUREMENTS: Sex- and age-specific prevalence of colorectal cancer (CRC) and advanced neoplasms (CRC or advanced adenoma) were plotted with and without stratification by birth cohort. Risk-advancement periods with 95% CI for men compared with women were estimated from log-binomial regression models with and without cross-sectional analysis adjustment for birth cohort effects. RESULTS: Overall, 17 196 participants (0.8%) had CRC and 152 429 (7.0%) had any advanced neoplasm. Age-specific prevalence was higher in men than in women and in later birth cohorts. The apparent modest increase in prevalence by age in cross-sectional analysis was much steeper after birth cohort effects were controlled for. In cross-sectional analysis, risk-advancement periods (95% CI) for men compared with women were 8.4 years (CI, 7.7 to 9.0 years) and 16.1 years (CI, 15.8 to 16.5 years) for CRC and any advanced neoplasm, respectively, and 3.4 years (CI, 2.6 to 4.3 years) and 6.9 years (CI, 6.4 to 7.4 years) after controlling for birth cohort effects. LIMITATION: Information on covariates that could explain cohort effects was lacking. CONCLUSION: In this population, strong cohort effects reduced age gradients in advanced colorectal neoplasms and inflated risk-advancement periods for men compared with women, but major risk advancement persisted, even after birth cohort effects were controlled for. Primary Funding Source: None.
    Type of Publication: Journal article published
    PubMed ID: 20513827
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  • 7
    Keywords: TUMOR-CELLS ; MARKER ; resistance ; COLORECTAL-CANCER ; STEM-CELLS ; POOR SURVIVAL
    Abstract: BACKGROUND: Aldehyde dehydrogenase 1A1 (ALDH1A1) has been described as a cancer stem cell marker and as a regulator of cellular chemoresistance. Therefore, ALDH1A1 has been suggested as potential biomarker to stratify patients into different risk categories for a "personalized" therapy approach. We have investigated the prognostic role of ALDH1A1 in primary colorectal cancer and its value in predicting response to chemotherapy in metastatic colorectal cancer. METHODS: Immunostaining against ALDH1A1 was performed on a paraffin-embedded tissue microarray including 659 primary colon cancer samples and 338 rectal cancer samples. Likewise, tissue of 44 palliatively resected colorectal liver metastases on whole-mount tissue slides was immunostained against ALDH1A1. Cytoplasmic, nuclear, and stromal expression of ALDH1A1 was assessed and merged with histopathological and clinical data. RESULTS: Univariate and multivariate analysis revealed that cytoplasmic and stromal expression of ALDH1A1 is not significantly associated with prognosis either in colon or in rectal cancer. Furthermore, cytoplasmic expression of ALDH1A1 does not predict response to palliative chemotherapy in patients with metastatic diseases. Intriguingly, as a novel finding, nuclear expression of ALDH1A1 was observed in a small subgroup of patients with colon cancer and rectal cancer. In colon cancer, nuclear expression was significantly associated with shortened overall survival by univariate and multivariate analysis. CONCLUSIONS: Immunohistochemical expression analysis of ALDH1A1 in colon cancer is useful for the detection of nuclear expression in a small subpopulation of patients and is associated with shorter survival. Cytoplasmic expression fails to be of clinical relevance as prognostic or predictive marker in colorectal cancer.
    Type of Publication: Journal article published
    PubMed ID: 22878609
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  • 8
    Keywords: POPULATION ; RISK-FACTORS ; score ; COLORECTAL-CANCER ; COMPLICATIONS ; RANDOMIZED CONTROLLED-TRIAL ; POLYPECTOMY ; sigmoidoscopy ; THERAPEUTIC COLONOSCOPY ; PERFORATION
    Abstract: BACKGROUND: The incidence of adverse events (AEs) is a crucial factor when colonoscopy is considered for mass screening, but few studies have addressed delayed and non-GI AEs. OBJECTIVES: To investigate the risk of AEs requiring hospitalization after screening and nonscreening colonoscopies compared with control subjects who did not undergo colonoscopy. DESIGN: Retrospective matched cohort. SETTING: Statutory health insurance fund in Germany. PATIENTS: A total of 33,086 individuals who underwent colonoscopy as an outpatient (8658 screening, 24,428 nonscreening) and 33,086 matched controls who did not undergo colonoscopy. INTERVENTIONS: Outpatient screening and nonscreening colonoscopies. MAIN OUTCOMES MEASUREMENTS: Risk of AEs (perforation, bleeding, myocardial infarction, stroke, splenic injury, and others) requiring hospitalization within 30 days after colonoscopy/index date and risk differences between the group that underwent colonoscopy and the group that did not. RESULTS: The incidence of perforation was 0.8 (95% confidence interval [CI], 0.3-1.7) and 0.7 (95% CI, 0.4-1.1) per 1000 screening and nonscreening colonoscopies, respectively. Hospitalizations because of bleeding occurred in 0.5 (95% CI, 0.1-1.2) and 1.1 (95% CI, 0.8-1.7) per 1000 screening and nonscreening colonoscopies, respectively. The incidence of myocardial infarction, stroke, and other non-GI AEs was similar in colonoscopy and control groups. No splenic injury was observed. Those with AEs generally had a higher mean age and comorbidity rate than the overall study population. LIMITATIONS: The analysis relies on health insurance claims data. CONCLUSIONS: This study provides further evidence of the safety of colonoscopy in routine practice with regard to delayed and non-GI AEs. Hospitalizations because of the investigated AEs were uncommon or rare for both screening and nonscreening colonoscopies.
    Type of Publication: Journal article published
    PubMed ID: 23410698
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  • 9
    Keywords: RISK ; COLORECTAL-CANCER
    Type of Publication: Journal article published
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  • 10
    Keywords: FOLLOW-UP ; POPULATION ; COLORECTAL-CANCER ; sensitivity ; EUROPE ; PROGRAM ; colonoscopy ; METAANALYSIS ; AVERAGE-RISK ; IMMUNOCHEMICAL TESTS
    Abstract: OBJECTIVES: Randomized trials have shown that annual or biannual screening by guaiac-based fecal occult blood tests (gFOBTs) reduces colorectal cancer (CRC) mortality. Few clinical studies have evaluated diagnostic performance of gFOBT through validation by colonoscopy in all participants. We aimed for a comprehensive evaluation of diagnostic performance of gFOBT by age and sex under routine screening conditions. METHODS: Our analysis is based on 20,884 colonoscopies following up a positive gFOBT and 182,956 primary screening colonoscopies documented in a state-wide quality assurance program in Bavaria, Germany, in 2007-2009. Positive likelihood ratios (LR+), which represent an integrative measure of diagnostic performance, were derived, by age groups (55-59, 60-64, 65-69, 70-74 years) and sex, from a joint and comparative analysis of prevalences of colorectal neoplasms in both groups. RESULTS: Overall LR+ (95% confidence intervals) were 1.11 (1.06-1.15), 1.80 (1.72-1.88), and 5.04 (4.64-5.47) for non-advanced adenoma, advanced adenoma, and cancer, respectively. Assuming a specificity of gFOBT of 95.2%, as recently observed in a German study among 2,235 participants of screening colonoscopy, these LR+ would translate to sensitivities of 5.3%, 8.6%, and 24.2% for the three outcomes, respectively. Diagnostic performance was similarly poor among women and men and across age groups. CONCLUSIONS: The performance of gFOBT under routine screening conditions is even worse than previously estimated from clinical studies. In routine screening application, gFOBTs are expected to miss more than 9 out of 10 advanced adenomas and 3 out of 4 cancers. These results underline the need and the potential for better noninvasive CRC screening tests.
    Type of Publication: Journal article published
    PubMed ID: 24343548
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