Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
Filter
  • BREAST-CANCER  (17)
  • 1
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    Keywords: CANCER ; SURVIVAL ; THERAPY ; BREAST-CANCER ; TRIALS ; colorectal cancer ; chemotherapy ; COLON-CANCER ; QUESTIONNAIRE ; MANAGEMENT ; UPDATE ; quality of life ; SURVIVORS ; ADJUVANT CHEMOTHERAPY ; OLDER ; CANCER SURVIVORS ; Long term
    Abstract: Purpose. To investigate the age-specific pattern of administration of chemotherapy and its association with long-term survival and quality of life (QoL) in stage II and III colorectal cancer patients. Methods. Chemotherapy allocation according to disease and patient characteristics was investigated in a population-based cohort of 562 stage II and III colorectal cancer patients. Five years after diagnosis, survival was determined and QoL was assessed using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire Core 30 Items and a tumor specific module. The association among chemotherapy, survival, and QoL was examined while controlling for potential confounders. Results. Chemotherapy was administered in 71% of patients aged 〈60 years and in only 20% of patients aged 〉/=80 years. A significant association between chemotherapy and longer survival time was found for stage III cancer only. Chemotherapy was associated with higher symptom levels for trouble with taste, anxiety, and hair loss. In age-specific analyses, younger survivors (〈70 years at time of follow-up) with a history of chemotherapy reported significantly lower physical, role, and cognitive functioning and higher pain, appetite loss, hair loss, and trouble with taste symptom levels. In contrast, for older survivors (〉/=70 years), only two (hair loss and dry mouth) out of 38 QoL scores were significantly associated with chemotherapy. Discussion. Chemotherapy is associated with lower long-term QoL, especially in younger survivors. In cases of uncertain survival benefits of chemotherapy, consideration of its long-term effects on QoL should be incorporated into final decisions on treatment.
    Type of Publication: Journal article published
    PubMed ID: 22101506
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    Keywords: CANCER ; Germany ; RISK ; PATIENT ; ASSOCIATION ; polymorphism ; BREAST-CANCER ; AGE ; CIGARETTE-SMOKING ; smoking ; COLORECTAL-CANCER ; BLADDER-CANCER ; METABOLIC-ACTIVATION ; COLON-CANCER ; case-control studies ; TOBACCO ; INDIVIDUALS ; CONSUMPTION ; RECTAL-CANCER ; case-control study ; population-based case-control study ; RE ; case control studies ; INTERVAL ; RISK-FACTOR ; population-based ; PASSIVE SMOKING ; ARYLAMINE N-ACETYLTRANSFERASE ; INCREASES RISK ; RECOMBINANT HUMAN NAT1
    Abstract: N-Acetyltransferases 1 and 2 (NAT1 and NAT2), both being highly polymorphic, are involved in the metabolism of aromatic and heterocyclic aromatic amines present in cigarette smoke and red meat cooked by high-temperature cooking techniques. We investigated the effect of differences in acetylation capacity, determined by NAT1 and NAT2 genotypes, on colorectal cancer risk associated with exposure to tobacco smoke or red meat consumption. In this population-based case-control study in Germany, 505 patients with incident colorectal cancer and 604 age- and sex-matched control individuals with genotyping data and detailed risk factor information were included. Genotyping of NAT1 and NAT2 genetic polymorphisms was done using a fluorescence-based melting curve analysis method. The association between genotypes, environmental exposures, and colorectal cancer risk was estimated using multivariate logistic regression. Colorectal cancer risk associated with active smoking was elevated after accumulation of 30(+) pack-years of smoking [odds ratio (OR), 1.4; 95% confidence interval (95% CI), 0.9-2.2] but not significantly modified by either NAT1 or NAT2 genotype. Exposure to environmental tobacco smoke was associated with an increased risk for colorectal cancer only among NAT2 fast acetylators (OR, 2.6; 95% CI, 1.1-5.9 for exposure in childhood and adulthood). Frequent consumption of red meat significantly increased colorectal cancer risk for the group comprising all NAT2 fast acetylators or carriers of the NAT1*10 allele (OR, 2.6; 95% Cl, 1.1-6.1) but not among those with "slow" NAT1 and NAT2 genotypes. Our findings indicate that NAT1 and NAT2 genotypes may contribute jointly to individual susceptibility and that heterocyclic aromatic amines may play an important role in colorectal cancer associated with red meat and possibly also exposure to environmental tobacco smoke
    Type of Publication: Journal article published
    PubMed ID: 16434594
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    Keywords: CANCER ; FOLLOW-UP ; NEW-YORK ; RISK ; SAMPLE ; ASSOCIATION ; SUSCEPTIBILITY ; VARIANTS ; DISCOVERY ; BREAST-CANCER ; genetics ; meta-analysis ; SNP ; colorectal cancer ; etiology ; COLORECTAL-CANCER ; PROSTATE-CANCER ; REPLICATION ; INDIVIDUALS ; beta-catenin ; SERIES ; germline mutations ; heredity ; RE ; VARIANT ; SNPs ; METAANALYSIS ; POWER ; USA ; ENGLAND ; COMMON VARIANT ; SAMPLE-SIZE ; 8Q24 ; GENOME-WIDE ASSOCIATION ; genetic variants ; CADHERIN GENE CDH1 ; CDH1 ; FAMILIAL GASTRIC-CANCER ; GENOME-WIDE ; JUVENILE POLYPOSIS
    Abstract: Genome-wide association (GWA) studies have identified multiple loci at which common variants modestly influence the risk of developing colorectal cancer (CRC). To enhance power to identify additional loci with similar effect sizes, we conducted a meta-analysis of two GWA studies, comprising 13,315 individuals genotyped for 38,710 common tagging SNPs. We undertook replication testing in up to eight independent case-control series comprising 27,418 subjects. We identified four previously unreported CRC risk loci at 14q22.2 (rs4444235, BMP4; P = 8.1 x 10(-10)), 16q22.1 (rs9929218, CDH1; P = 1.2 x 10(-8)), 19q13.1 (rs10411210, RHPN2; P = 4.6 x 10(-9)) and 20p12.3 (rs961253; P = 2.0 x 10(-10)). These findings underscore the value of large sample series for discovery and follow-up of genetic variants contributing to the etiology of CRC
    Type of Publication: Journal article published
    PubMed ID: 19011631
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    Keywords: CELLS ; SURVIVAL ; THERAPY ; COHORT ; BREAST-CANCER ; MELANOMA ; QUALITY-OF-LIFE ; NOREPINEPHRINE
    Abstract: Recent observational studies have suggested that the use of beta blockers might be associated with better prognosis after cancer. Because evidence is limited for colorectal cancer (CRC), the association of beta blocker use and prognosis was investigated in a large population-based cohort of patients with CRC. METHODS Between 2003 and 2007, information on beta blocker use at diagnosis and potential confounders was collected by personal interviews for 1975 patients with CRC. Vital status, cause of death, and recurrence status were assessed during a median follow-up time of 5.0 years. The associations of beta blocker use and overall, CRC-specific, and recurrence-free survival were estimated by Cox proportional hazard regression. In addition, beta blocker subgroup, site, and stage-specific analyses were performed. RESULTS After adjustment for covariates including sociodemographic, cancer-related, and lifestyle factors and comorbidity and medications, no significant association between beta blocker use at diagnosis and prognosis was observed for all stages combined. However, in stage-specific analyses, beta blocker use was associated with longer overall survival (hazard ratio = 0.50; 95% confidence interval = 0.33-0.78) and CRC-specific survival (hazard ratio = 0.47; 95% confidence interval = 0.30-0.75) in stage IV patients. For these patients, median overall survival was 18 months longer and CRC-specific survival was 17 months longer for beta blocker users than for nonusers (38 versus 20 months and 37 versus 20 months, respectively). CONCLUSIONS These results suggest that beta blocker use might be associated with longer survival in patients with stage IV CRC.
    Type of Publication: Journal article published
    PubMed ID: 24415516
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    Keywords: EXPRESSION ; VARIANTS ; BREAST-CANCER ; COLON-CANCER ; MUTATIONS ; CELL-GROWTH ; METAANALYSIS ; susceptibility loci ; GENOME-WIDE ASSOCIATION ; LYMPHOTOXIN-BETA-RECEPTOR
    Abstract: Known genetic loci explain only a small proportion of the familial relative risk of colorectal cancer (CRC). We conducted a genome-wide association study of CRC in East Asians with 14,963 cases and 31,945 controls and identified 6 new loci associated with CRC risk (P = 3.42 x 10(-8) to 9.22 x 10(-21)) at 10q22.3, 10q25.2, 11q12.2, 12p13.31, 17p13.3 and 19q13.2. Two of these loci map to genes (TCF7L2 and TGFB1) with established roles in colorectal tumorigenesis. Four other loci are located in or near genes involved in transcriptional regulation (ZMIZ1), genome maintenance (FEN1), fatty acid metabolism (FADS1 and FADS2), cancer cell motility and metastasis (CD9), and cell growth and differentiation (NXN). We also found suggestive evidence for three additional loci associated with CRC risk near genome-wide significance at 8q24.11, 10q21.1 and 10q24.2. Furthermore, we replicated 22 previously reported CRC-associated loci. Our study provides insights into the genetic basis of CRC and suggests the involvement of new biological pathways.
    Type of Publication: Journal article published
    PubMed ID: 24836286
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
    Keywords: RECEPTOR ; SIMULATIONS ; APOPTOSIS ; CANCER ; EXPRESSION ; proliferation ; tumor ; CELL ; CELL-PROLIFERATION ; Germany ; LUNG-CANCER ; screening ; DEATH ; POPULATION ; RISK ; GENE ; TIME ; LIGAND ; SIMULATION ; BINDING ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; VARIANTS ; BREAST-CANCER ; STAGE ; AGE ; colorectal cancer ; COLORECTAL-CANCER ; cancer risk ; PREVALENCE ; RECEPTORS ; APOPTOSIS-INDUCING LIGAND ; RECTAL-CANCER ; RE ; TUMOR-SUPPRESSOR ; VARIANT ; SUPPRESSOR GENE ; INCREASE ; cell proliferation ; INTERVAL ; tumor suppressor gene ; TESTS ; death receptor ; LINKAGE PHASE ; CANDIDATE ; population-based ; general population ; CANCER-RISK ; RARE ; NECROSIS ; APO2L/TRAIL
    Abstract: The tumor necrosis factor-related apoptosis-inducing ligand receptor modulates apoptotic response by binding to the proapoptotic death receptor 4 (DR4). Perturbed apoptosis due to missense alterations in the candidate tumor suppressor gene DR4 leads to deregulated cell proliferation and cancer predisposition. Recent studies have discussed the association of DR4 variants with cancer risk. We evaluated, for the first time, the role of the Thr(209)Arg (626C 〉 G) and Glu(228)AIa (683A 〉 C) polymorphisms on colorectal cancer risk by genotyping 659 incident cases and 607 healthy controls drawn from the German population-based Darmkrebs: Chancen der Verhutung durch Screening (DACHS) study. Whereas DR4 Glu(228)Ala was not associated with colorectal cancer, Thr(209)Arg heterozygotes were at a significantly decreased colorectal cancer risk [odds ratio (OR), 0.73; 95% confidence interval (95% CI), 0.54-0.97]. Stratification according to sex and age exhibited a significant association of Thr(209)Arg with a decreased risk for male heterozygotes (OR, 0.68; 95% CI, 0.46-0.99) and for Arg(209) carriers 〉= 65 years of age (OR, 0.65; 95% CI, 0.46-0.92) as well as an enhanced risk for female Ala(228) carriers in a allele dose-dependent manner (P-trend = 0.01). Subsite analysis revealed a protective effect of Thr(209)Arg for rectal cancer risk (OR, 0.67; 95% CI, 0.48-0.95) and a significant risk increase for Ala 228 carriers with advanced colorectal cancer stages (P-trend = 0.04). Haplotype analysis revealed a 2.4-fold risk for carriers of the rare 626C-683C haplotype (1% prevalence in the general population; OR, 2.37; 95% CI, 0.98-5.76). The score statistic yielded an empirical P of 0.03 of the haplotype-specific test for 626C-683C based on 20,000 simulations, suggesting that DR4 626C-683C may affect colorectal cancer predisposition
    Type of Publication: Journal article published
    PubMed ID: 17035413
    Signatur Availability
    BibTip Others were also interested in ...
  • 9
    Keywords: CANCER ; COMBINATION ; Germany ; THERAPY ; COHORT ; RISK ; validation ; FAMILY ; REDUCTION ; BREAST-CANCER ; hormone ; AGE ; WOMEN ; colorectal cancer ; COLORECTAL-CANCER ; cancer risk ; COLON-CANCER ; case-control studies ; POSTMENOPAUSAL WOMEN ; case control study ; case-control study ; population-based case-control study ; FAMILIES ; THERAPIES ; METAANALYSIS ; ESTROGEN ; pharmacology ; USA ; REPLACEMENT THERAPY ; population-based ; CANCER-RISK ; REPLACEMENT ; colorectal ; ESTROGEN REPLACEMENT THERAPY ; hormone therapy ; HORMONE-THERAPY ; CONFIDENCE ; CRC ; LARGE-BOWEL CANCER ; PLUS PROGESTIN
    Abstract: Little is known about the effects of various types, modes, and routes of hormone replacement therapy (HRT) on the risk of colorectal cancer (CRC) among postmenopausal women. We conducted a population-based case-control study with validation of self-reported hormone use and no upper age limit. In 1,456 postmenopausal women aged 45-94 years (546 cases, 910 controls), the use of HRT was associated with reduction in CRC risk among ever users (adjusted odds ratio (OR) 0.65, 95% confidence interval 0.50-0.84), current users, and recent users. There was no evidence that risk reduction among current users varies by age. Risk reduction was seen both in estrogen-only therapy (0.42, 0.23-0.78) and in combination therapy (0.60, 0.41-0.87), the latter regardless of the mode of therapy, whether with hormone patches (0.40, 0.17-0.90) or with oral tablets (0.59, 0.39-0.90). In combination with estrogen, progestagens of the norethisterone and levonorgestrel families were associated with strong reduction in CRC risk
    Type of Publication: Journal article published
    PubMed ID: 19606090
    Signatur Availability
    BibTip Others were also interested in ...
  • 10
    Keywords: ENRICHMENT ; BREAST-CANCER ; COLON-CANCER ; VARIANT ; LOCUS ; COMPLEX TRAITS ; GENETIC-VARIATION ; SCAN ; MISSING HERITABILITY ; CHROMOSOME 8Q24
    Abstract: Genetic susceptibility accounts for approximately 35% of all colorectal cancer (CRC). Ten common low risk variants contributing to CRC risk have been identified through genome-wide association studies (GWASs). In our GWAS, 610.664 genotyped SNPs passed the quality control filtering in 371 German familial CRC patients and 1263 controls, and replication studies were conducted in four additional case-control sets (4915 cases and 5607 controls). Known risk loci at 8q24.21 and 11q23 were confirmed, and a previously unreported association, rs12701937, located between the genes GLI3 (GLI family zinc finger 3) and INHBA (inhibin, beta A) (P = 1.1x10P(-3)P, OR 1.14, 95% CI 1.05-1.23, dominant model in the combined cohort), was identified. The association was stronger in familial compared to unselected cases (P = 2.0x10P(-4)P, OR 1.36, 95% CI 1.16-1.60, dominant model). Two other unreported SNPs, rs6038071, 40kb upstream of CSNK2A1 (casein kinase 2, alpha 1 polypeptide), and an intronic marker in MYO3A (myosin IIIA), rs11014993, associated with CRC only in the familial CRC cases (P = 2.5x10P(-3)P, recessive model, and P = 2.7x10P(-4)P, dominant model). Three software tools successfully pointed to the overrepresentation of genes related to the mitogen-activated protein kinase (MAPK) signalling pathways among the 1340 most strongly associated markers from the GWAS (allelic P value 〈 10(-3)). The risk of CRC increased significantly with an increasing number of risk alleles in seven genes involved in MAPK signalling events (PR(trend) R= 2.2x10P(-16)P, ORR(per allele) = 1.34, 95% CI 1.11-1.61).
    Type of Publication: Journal article published
    PubMed ID: 20610541
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...