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  • 1
    Keywords: CANCER DIAGNOSIS ; THERAPIES ; DNA repair ; methods ; NEW-YORK ; GENE ; GENES ; PATIENT ; CANCER ; CELL ; carcinoma ; radiotherapy ; DIAGNOSIS ; THERAPY ; cell cycle ; CELL-CYCLE ; prognosis ; BREAST ; breast cancer ; BREAST-CANCER ; CANCER-PATIENTS ; side effects ; CANCER PATIENTS
    Type of Publication: Book chapter
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  • 2
    Keywords: CANCER ; IRRADIATION ; radiotherapy ; Germany ; TOXICITY ; LUNG-CANCER ; RISK ; RISKS ; GENE ; GENES ; HYBRIDIZATION ; SURGERY ; radiation ; PATIENT ; DNA ; GENETIC POLYMORPHISMS ; SKIN ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; VARIANTS ; BREAST ; breast cancer ; BREAST-CANCER ; DESIGN ; DNA-REPAIR ; REPAIR ; DAMAGE ; PROBES ; CARRIERS ; CANCER PATIENTS ; body mass index ; NUCLEOTIDE EXCISION-REPAIR ; DNA repair ; radiation sensitivity ; ACID SUBSTITUTION VARIANTS ; radiosensitivity ; MASSES ; RE ; VARIANT ; CAPACITY ; CANCER SUSCEPTIBILITY ; XPD ; ALLELES ; INTERVAL ; DNA repair gene ; DNA repair genes ; GENETIC-POLYMORPHISM ; CARRIER ; GENOTYPE ; HAPLOTYPE
    Abstract: Purpose: Several DNA repair gene polymorphisms have been described, which affect DNA repair capacity and modulate cancer susceptibility. We evaluated the association of six polymorphisms in the DNA repair genes: XRCC1 (Arg(194) Trp, Arg(280)His, and Arg(399)GIn), APE1 (Asp(148)Glu), and XPD (Lys(751)Gln and Asp(312)Asn), with the risk of acute skin reactions following radiotherapy. Design: We conducted a prospective study of 446 female patients with breast cancer who received radiotherapy after breast-conserving surgery. Individual genetic polymorphisms were determined using melting point analysis of sequence-specific hybridization probes. The development of acute skin reactions (moist desquamation) associated with DNA repair gene polymorphisms was modeled using Cox proportional hazards, accounting for cumulative biologically effective radiation dose. Results: Overall, the development of acute toxicity, which presented in 77 patients, was not associated with the genetic variants studied, although the hazard ratios (HR) were generally below 1. Risks were however differential by body mass index. Among normal-weight patients only, both carriers of theAPE1 (148)Glu and the XRCC1 (399)Gln alleles had decreased risk of acute skin reactions after radiotherapy (HR, 0.49 and 0.51, respectively). The results for XRCC1 were confirmed by haplotype analysis. When considering joint effects, we observed that compared with homozygote carriers of the wild-type allele in both genes, the risk was most strongly reduced in carriers of both APE1 (148)Glu and XRCC1 (399)GIn alleles with normal weight [HR, 0.19; 95% confidence interval (95% CI), 0.06-0.56] but not in those with overweight (HR, 1.39; 95% CI, 0.56-3.45; P-interaction = 0-009). Conclusion: The XRCC1 (399)Gln or APE1 (148)Glu alleles may be protective against the development of acute side effects after radiotherapy in patients with normal weight
    Type of Publication: Journal article published
    PubMed ID: 16000577
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  • 3
    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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  • 4
    Keywords: APOPTOSIS ; CANCER ; IONIZING-RADIATION ; radiotherapy ; Germany ; IN-VIVO ; TOXICITY ; RISK ; RISKS ; GENE ; GENES ; HYBRIDIZATION ; SURGERY ; radiation ; PATIENT ; GENETIC POLYMORPHISMS ; SKIN ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; VARIANTS ; BREAST ; breast cancer ; BREAST-CANCER ; AGE ; WOMEN ; REPAIR ; p53 ; PCR ; DNA-DAMAGE ; Jun ; CANCER-PATIENTS ; BODY ; p21 ; CANCER PATIENTS ; TP53 ; MASS INDEX ; RE ; VARIANT ; WEIGHT ; OVERWEIGHT ; prospective ; prospective study ; INCREASED RISK ; acute toxicity ; female breast cancer ; CODON-31 ; REPOPULATION
    Abstract: p53 and p21 play an important role in G1/S checkpoint control in response to ionizing radiation. Yet the genetic polymorphisms in these genes have not been investigated with respect to radiation toxicity in patients. We therefore assessed the association between TP53 Arg72Pro, p53PIN3 and p21 Ser31Arg polymorphisms and the risk of acute skin toxicity after radiotherapy in a prospective study of 446 female breast cancer patients (average age 60.3 +/- 9.0 years) receiving radiotherapy after breast conserving surgery. The p53PIN3 polymorphism was determined by standard PCR, and TP53 Arg72Pro and p21 Ser31Arg polymorphisms using melting point analysis of sequence-specific hybridization probes. The development of acute skin toxicity (moist desquamation) was modelled using Cox proportional hazards, accounting for cumulative biologically effective radiation dose. Overall, the development of acute skin toxicity, which presented in 77 patients, was not significantly associated with the polymorphisms studied. Risks were however differential by body mass index. Compared to non-carriers, TP53 72Pro carriers had a non-significantly decreased risk of acute skin toxicity in normal weight women (hazard ratio 0.46, 95% CI, 0.18-1.18) but not in overweight patients (hazard ratio 1.07, 95% CI, 0.61-1.89) (p(interaction) =0.14). Haplotype analysis for the TP53 polymorphisms suggested that effect modification by TP53 72Pro may differ according to the p53PIN3 allele (p(interaction)=0.06). Furthermore, in TP53 72Pro carriers with p21 Ser/Ser genotype, the occurrence of acute toxicity was reduced in normal weight but not overweight patients. In conclusion, the TP53 72Pro variant may be associated with the development of acute skin toxicity after radiotherapy in patients with normal weight. Large clinical studies are needed to clearly confirm this association
    Type of Publication: Journal article published
    PubMed ID: 16331344
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  • 5
  • 6
    Keywords: CANCER ; CELLS ; tumor ; human ; PATHWAY ; THERAPY ; EXPOSURE ; NEW-YORK ; POPULATION ; RISK ; GENE ; GENES ; CARCINOGENESIS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; BREAST-CANCER ; WOMEN ; colorectal cancer ; HORMONE REPLACEMENT THERAPY ; COLORECTAL-CANCER ; PROSTATE-CANCER ; BLADDER-CANCER ; genetic polymorphism ; case-control studies ; POSTMENOPAUSAL WOMEN ; CYCLIN D1 ; insulin ; E-cadherin ; ONCOLOGY ; case-control study ; REGRESSION ; VARIANT ; THERAPIES ; GENE PROMOTER ; METAANALYSIS ; analysis ; single-nucleotide polymorphism ; USA ; REPLACEMENT THERAPY ; GENETIC SUSCEPTIBILITY ; population-based ; postmenopausal ; A870G POLYMORPHISM ; genetic variants ; CCND1
    Abstract: Cyclin D1 (CCND1) and E-cadherin (CDH1) have been shown to be important genes of the beta-catenin/LEF pathway that is involved in colorectal carcinogenesis. However, epidemiological studies on relationship between genetic variants of these two genes and colorectal cancer (CRC) have shown inconsistent results. In a population-based case-control study (498 cases and 600 controls), we assessed the association of CCND1 G870A and CDH1 C-160A polymorphisms with CRC risk. Multivariable logistic regression analysis was used to estimate the association between genotypes, environmental exposures and CRC risk, adjusting for potential confounders. Compared to common homozygotes, the OR for heterozygous and homozygote variant genotype was 1.08 (95% CI, 0.80-1.46) in CCND1 and 0.97 (95% CI, 0.75-1.25) in CDH1. Neither tumor stage nor location showed an association with genetic susceptibility. However, a significant interaction between hormone replacement therapy (HRT) and CCND1 genotypes in CRC risk was found among postmenopausal women (P-interaction = 0.02). The risk reduction associated with HRT was substantial (OR, 0.09; 95% CI, 0.02-0.35) in women who were GG homozygous. A meta-analyses including 11 published studies on CCND1 G870A in addition to our study showed a slightly increased risk of CRC for carriers of the A allele (OR, 1.19; 95% CI, 1.06-1.34); however, there was some indication of publication bias. We conclude that the CCND1 G870A and CDH1 C-160A polymorphisms are not associated with the risk of CRC in the German population. However, the CCND1 G870A polymorphism may modify the protective effect of postmenopausal hormone use on the development of CRC. (C) 2008 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 18196581
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  • 7
    ISSN: 1432-0630
    Keywords: PACS: 78.55.Ap, 61.46.+w
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Notes: + -implanted SiO2 films is studied as a function of different fabricating conditions (implantation dose, annealing temperature and time). The SiO2 films containing Ge nanocrystals exhibit two photoluminescence (PL) bands peaked at 600 nm and 780 nm. There are two excitation bands in the PL excitation (PLE) spectra. With variation in Ge nanocrystal size, the PL and PLE peak energies show no appreciable shift. The PL and PLE spectral analyses suggest that during the PL process, electron–hole pairs are generated by the E(l) and E(2) direct transitions inside Ge nanocrystals, which then radiatively recombine via luminescent centers in the matrix or at the interface between the nanocrystal/matrix.
    Type of Medium: Electronic Resource
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