Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

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Tytuł oryginału: O**6-Alkylguanine-DNA-alkyltransferase activity in peripheral leukocytes, smoking and risk of lung cancer.
Autorzy: Boffetta Paolo, Nyberg Fredrik, Mukeria Anush, Benhamou Simone, Constantinescu Vali, Batura-Gabryel Halina, Brske-Hohlfeld Irene, Schmid Giovanni, Simonato Lorenzo, Pelkonen P„ivi, Hall Janet
Źródło: Cancer Lett. 2002: 180 (1) s.33-39, tab., bibliogr. 25 poz.
Sygnatura GBL: 306,023

Hasła klasyfikacyjne GBL:
  • genetyka
  • pulmonologia
  • onkologia

    Typ dokumentu:
  • praca kliniczna
  • tytuł obcojęzyczny
  • praca opublikowana za granicą

    Wskaźnik treści:
  • ludzie
  • dorośli = 65 r.ż.

    Streszczenie angielskie: The level of activity of O**6-alkalguanine-DNA-alkytransferase (AGT), a DNA repair enzyme, in blood lymphocytes may be a marker of susceptibility to lung cancer. We measured the AGT activity level, expressed as plomes of repaired bases/mg protein, in leukocytes of 153 lung cancer cases (of whom 80 were never smokers) and 106 controls (76 never smokers) enrolled in eight centres from seven countries. Subjects were interviewed with respect to active smoking and exposure to environmental tobacco smoke (ETS). Among never smokers, the odds ratios (ORs) of lung cancer were 1.3 (95 p.c. confidence interval 0.5-3.9), 1.5 (0.6-4.1) and 1.4 (0.5-3.8) in quartiles of decreasing AGT activity level, as compared to the upper quartile (P value of test for linear trend 0.6). Corresponding ORs among smokers were 3.4 (0.9-13), 2.0 (0.5-8.3) and 0.4 (0.1-1.6) (P value of test for linear trend 0.4). No interaction was suggested between AGT activity level and either cumulative smoking or exposure to ETS. Reduced AGT activity was not clearly associated with increased lung cancer risk in either smokers or non-smokers. However, the small size of our study argues for a prudent interpretation of our results.

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    Tytuł oryginału: Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk.
    Autorzy: Benhamou Simone, Lee Won Jin, Alexandrie Anna-Karin, Boffetta Paolo, Bouchardy Christine, Butkiewicz Dorota, Brockm”ller Jurgen, Clapper Margie L., Daly Ann, Dolzan Vita, Ford Jean, Gaspari Laura, Haugen Aage, Hirvonen Ari, Husgafvel-Pursiainen Kirsti, Ingelman-Sundberg Magnus, Kalina Ivan, Kihara Masahiro, Kremers Pierre, Le Marchand Loic, London Stephanie J., Nazar-Stewart Valle, Onon-Kihara Masako, Rannug Agneta, Romkes Marjorie, Ryberg David, Seidegard Janeric, Shields Peter, Strange Richard C., Stcker Isabelle, To-Figueras Jordi, Brennan Paul, Taioli Emanuela
    Źródło: Carcinogenesis 2002: 23 (8) s.1343-1350, il., tab., bibliogr. 54 poz.
    Sygnatura GBL: 312,779

    Hasła klasyfikacyjne GBL:
  • pulmonologia
  • onkologia

    Typ dokumentu:
  • praca kliniczna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie

    Streszczenie angielskie: Susceptibility to lung cancer may in part be attributable to inter-individual variability in metabolic activation or detopxification of tobacco carcinogens. The glutathione S-transferase M1 (GSTM1) genetic polymorphism has been extensively studied in this context; two recent meta-analyses of case-control studies suggested an association between GSTM1 deletion and lung cancer. At least 15 studies have been published after these overviews. We undertook a new meta-analysis to summarize the results of 43 published case-control studies including 18000 individuals. A slight excess of risk of lung cancer for individuals with the GSTM1 null genotype was found (odds ratio (OR) = 1.17, 95 p.c. confidence interval (CI) 1.07 - 1.27). No evidence of publication bias was found (P = 0.4), however, it is not easy to estimate the extent of such bias and we cannot rule out some degree of publications bias in our rsults. A pooled analysis of the original dsata of about 9500 subjects involved in 21 case-control studies from the international Collaborative Study on genetic Dusceptibility to Environmental Carcinogens (GSEC) data set was performed to assess the role of gsTM1 genotype as a modifier of the effect of smoking on lung cancer risk with adequate power. Analyses revealed no evidence of increased risk of lung cancer among carriers of the GSTM1 null genotype (age-, gender- and center-adjusted OR = 1.08, 95 p.c. CI 0.98 - 1.18) and no evidence of interaction between GSTM1 genotype and either smoking status or cumulative tobacco consumption.

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