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  • 1
    Keywords: CANCER ; LUNG ; PHASE-I ; lung cancer ; LUNG-CANCER ; EPIDEMIOLOGY ; CARCINOGENESIS ; ASSOCIATION ; polymorphism ; SUSCEPTIBILITY ; METABOLITES ; PROMOTER ; AGE ; genetics ; REDUCED RISK ; smoking ; DATABASE ; REGION ; heredity ; DEFICIENCY ; VARIANT ; CARCINOGEN ; METAANALYSIS ; INTERVAL ; ENZYME ; analysis ; PHASE ; MISSENSE MUTATION ; GENOTYPE ; USA ; female ; Male ; odds ratio ; E ; Phase I ; MPO ; cooperative studies ; metabolic gene polymorphisms ; ACID RESPONSE ELEMENT ; DNA ADDUCT LEVELS ; HUMAN SKIN FIBROBLASTS ; HYPOCHLOROUS ACID
    Abstract: Myeloperoxidase is a phase I metabolic enzyme that converts the metabolites of benzo[a]pyrene from tobacco smoke into highly reactive epoxides. A polymorphism in the promoter region of myeloperoxidase (463G -〉 A) has been found to be inversely associated with lung cancer; differences in the association with age and gender have been suggested. We conducted a pooled analysis of individual data from 10 studies (3688 cases and 3874 controls) from the Genetic Susceptibility to Environmental Carcinogens database. The odds ratio for lung cancer was 0.88 (95% confidence interval: 0.80-0.97) for the AG variant of myeloperoxidase G-463A polymorphism, and 0.71 (95% confidence interval: 0.57-0.88) for the AA variant after adjusting for smoking, age, gender, and ethnicity. The inverse association between lung cancer and myeloperoxidase G-463A polymorphism was equally found in males and females (odds ratio for the AA genotype 0.73 [95% confidence interval: 0.56-0.96] and 0.67 [95% confidence interval: 0.46-0.98], respectively), without differences in the association according to age in the two genders. The myeloperoxicase G-463A polymorphism was significantly protective in "ever" smokers but not in "never" smokers. Myeloperoxidase is a key enzyme in tobacco-induced carcinogenesis
    Type of Publication: Journal article published
    PubMed ID: 17304047
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  • 2
    Keywords: GENETIC POLYMORPHISMS ; POLYCYCLIC AROMATIC-HYDROCARBONS ; CATALYTIC ACTIVITY ; WHITE BLOOD-CELLS ; ARYL-HYDROCARBON HYDROXYLASE ; CANCER MUTATIONAL HOTSPOTS ; TRANSFERASE M1 ; FLUOROMETRIC ASSAY ; CYTOCHROME P4501A1 ; FRENCH POPULATION
    Abstract: Benzo[a]pyrene diol epoxide (BPDE)-DNA adducts are involved in the induction of p53 mutations and probably in the causation of human lung cancer associated with cigarette smoking. The ratio between CYP1A1 and GST enzyme activities is a critical determinant of the target dose of carcinogenic BPDE and other DNA-reactive PAH metabolites. In this review, we summarize the published data on modulation of (+)-anti-BPDE-DNA adduct levels in smokers' lungs by CYP1A1*2 genotypes alone or in combination with GSTM1 polymorphism and compare these results with those reported for aromatic/hydrophobic (bulky) DNA adducts. The data published so far show only a trend for a non-significant increase in bulky DNA adduct levels in subjects with GSTM1*0 or the CYP1A1*2-GSTM1*0 genotype combination. In contrast, a clear dependence of (+)-anti-BPDE-DNA adduct levels was found as a function of the CYP1A1 and GSTM1 genotypes: In lung parenchyma, this adduct was more pronounced in persons with the GSTM1*0 genotype, and CYP1A1*2-GSTM1*0 carriers had higher (+)-anti-BPDE-DNA adduct levels than those with CYP1A1*1/*1-GSTM1*0. The homozygous CYP1A1*2/*2 carriers in the GSTM1*0 group had the highest (+)-anti-BPDE-DNA adduct levels. Our analysis leads to the conclusion that the risk-modifying effects of metabolic genotypes and of gene interactions might be more easily identifiable if specific markers of structurally defined adducts were used, such as the (+)-anti-BPDE-DNA adduct. These results are also consistent with the hypothesis that BP (PAH) induce G:C to T:A transversion mutations in the hotspot codons of the p53 tumor suppressor gene and are thus involved in malignant transformation of the lung tissue of smokers.
    Type of Publication: Journal article published
    PubMed ID: 12507920
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  • 3
    Abstract: OBJECTIVE: There is an overwhelming abundance of genetic association studies available in the literature, which can often be collectively difficult to interpret. To address this issue, the Venice interim guidelines were established for determining the credibility of the cumulative evidence. The objective of this report is to evaluate the literature on the association of common glutathione S-transferase (GST) variants (GSTM1 null, GSTT1 null and GSTP1 Ile105Val polymorphism) and lung cancer, and to assess the credibility of the associations using the newly proposed cumulative evidence guidelines. METHODS: Information from the literature was enriched with an updated meta-analysis and a pooled analysis using data from the Genetic Susceptibility to Environmental Carcinogens database. RESULTS: There was a significant association between GSTM1 null and lung cancer for the meta-analysis (meta odds ratio=1.17, 95% confidence interval: 1.10-1.25) and pooled analysis (adjusted odds ratio=1.10, 95% confidence interval: 1.04-1.16), although substantial heterogeneity was present. No overall association between lung cancer and GSTT1 null or GSTP1 Ile105Val was found. When the Venice criteria was applied, cumulative evidence for all associations were considered 'weak', with the exception of East Asian carriers of the G allele of GSTP1 Ile105Val, which was graded as 'moderate' evidence. CONCLUSION: Despite the large amounts of studies, and several statistically significant summary estimates produced by meta-analyses, the application of the Venice criteria suggests extensive heterogeneity and susceptibility to bias for the studies on association of common genetic polymorphisms, such as with GST variants and lung cancer.
    Type of Publication: Journal article published
    PubMed ID: 20729793
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  • 4
    Keywords: CANCER ; INFORMATION ; EXPOSURE ; NEW-YORK ; RISK ; ENZYMES ; GENE ; GENES ; SAMPLE ; METABOLISM ; GENETIC POLYMORPHISMS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; DIFFERENCE ; smoking ; DATABASE ; case-control studies ; TOBACCO ; INDIVIDUALS ; BEHAVIOR ; CONSUMPTION ; SMOKERS ; SUBSET ; NICOTINE METABOLISM ; pooled analysis,molecular epidemiology,smoking ; SMOKING-BEHAVIOR
    Abstract: Polymorphisms in genes that encode for metabolic enzymes have been associated with variations in enzyme activity between individuals. Such variations could be associated with differences in individual exposure to carcinogens that are metabolized by these genes. In this study, we examine the association between polymorphisms in several metabolic genes and the consumption of tobacco in a large sample of healthy individuals. The database of the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens was used. All the individuals who were controls from the case-control studies included in the data set with information on smoking habits and on genetic polymorphisms were selected (n = 20,938). Sufficient information was available on the following genes that are involved in the metabolism of tobacco smoke constituents: CYPIAI, GSTMI, GSTTI, NAT2 and GSTPI. None of the tested genes was clearly associated with smoking behavior. Information on smoking dose, available for a subset of subjects, showed no effect of metabolic gene polymorphisms on the amount of smoking. No association between polymorphisms in the genes studied and tobacco consumption was observed; therefore, no effect of these genes on smoking behavior should be expected. (C) 2004 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 15069692
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  • 5
    ISSN: 1432-1041
    Keywords: Key words Trimethoprim ; Sulfamethoxazole ; Combination therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1433-0563
    Keywords: Schlüsselwörter Harnblasenkarzinom ; Aromatische Amine ; N-Acetyltransferase-2 ; Histopathologischer Befund ; Prognose ; Key words Bladder cancer ; N-Acetyltransferase 2 ; Histopathological grading ; Invasiveness ; Prognosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary A total of 196 patients with urothelial tumours were phenotyped for N-acetyltransferase 2 by the molar ratio of two caffeine metabolites excreted in urine. The proportion of “slow” acetylators, who are genetically predisposed to urothelial tumours if they have been exposed to aromatic amines in the past, in the entire group was 55 %, within the range in a normal population. Among 40 patients with assumed former occupational exposure to aromatic amines, 65 % were “slow” acetylators. Invasiveness, histopathological grading of the urothelial tumour at the time of first diagnosis, and course were not related to acetylator phenotype.
    Notes: Zusammenfassung Bei 196 Patienten mit urothelialen Tumoren wurde der Acetyliererphänotyp mittels zweier im Harn ausgeschiedener Koffeinmetabolite bestimmt. Der Anteil der „langsamen“ Acetylierer, die bei Exposition gegen aromatische Amine hinsichtlich der Entstehung eines Harnblasentumors prädisponiert sind, weicht mit 55 % im Gesamtkollektiv nicht von der Verteilung in der normalen Bevölkerung ab. Personen mit anzunehmender beruflicher Exposition gegen aromatische Amine (n = 40) weisen mit 65 % einen höheren Anteil „langsamer“ Acetylierer auf. Die Ausdehnung des Tumors bei Erstdiagnose, das histopathologische Grading und auch der Verlauf der Harnblasentumore der Klassifikation T1G1 und T1G2 waren unabhängig vom Acetyliererstatus. Der Acetyliererstatus erlaubt somit keine Aussage über die Prognose von Urotheltumoren.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1440
    Keywords: Cytochrome P-450 ; CYP1A1 ; Polymorphism ; Lung cancer ; Polymerase chain reaction ; Cancer epidemiology ; Risk factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Genetic differences in the metabolism of carcinogens may codetermine individual predisposition to cancer. Cytochrome P-4501A1 (CYP1A1) metabolically activates precarcinogens in cigarette smoke, such as benzo(a)pyrene, which is also an inducer of CYP1A1. Two point mutations have been reported, m1 in the 3′-flanking region (6235T to C), and m2 within exon 7 (4889A to G), the latter leading to an isoleucine to valine exchange. In the Japanese population ml and m2 are correlated with lung cancer, suggesting an increased susceptibility to cigarette smoking related lung cancer. We studied 142 lung cancer and 171 reference patients in an ethnically homogeneous German group for m1 and m2 mutations by restriction fragment length polymorphism and allele-specific polymerase chain reaction, respectively. No statistically significant difference was found in the distribution of m1 alleles between lung cancer and controls; the frequency was 8.5% and 7.3% of the alleles, respectively (odds ratio = 1.17). A trend to an overrepresentation of ml alleles was observed among 52 squamous cell carcinoma patients (odds ratio = 1.65). In contrast, the frequency of m2 alleles in lung cancer patients was twofold higher (6.7%) than in the reference group (3.2%; odds ratio = 2.16; 95% confidence limits 0.96–5.11, P = 0.033); the odds ratio of m2 alleles in squamous cell carcinoma was 2.51 (95% confidence limits 0.85–7.05, P = 0.05). There was a close genetic linkage of m2 to m1 (10 of 11 reference patients), but a significantly higher number of cancer patients showed no linkage compared to the controls (odds ratio = 8.89, 95% confidence limits 0.83–433, P = 0.04). Thus no association was found between presence of ml alleles and lung cancer, but, in contrast, m2 alleles proved as a hereditary risk factor, especially if not linked with m1 alleles.
    Type of Medium: Electronic Resource
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  • 8
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  Gemeinsame Jahrestagung der Gesellschaft für Medizinische Ausbildung (GMA), des Arbeitskreises zur Weiterentwicklung der Lehre in der Zahnmedizin (AKWLZ) und der Chirurgischen Arbeitsgemeinschaft Lehre (CAL); 20190925-20190928; Frankfurt am Main; DOCV7-05 /20190920/
    Publication Date: 2019-09-21
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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