DNA repair gene expression level in peripheral blood and tumour tissue from non-small cell lung cancer and head and neck squamous cell cancer patients.
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AbstractThe existence of a significant correlation between blood and tumour tissue expression of some genes of clinical interest, such as ERCC1 in NSCLC and HNSCC, could allow the introduction in clinical practice of a simple test that would measure mRNA levels of DNA repair genes in peripheral blood samples instead of tissue samples to determine prognostic and predictive factors in NSCLC and HNSCC patients.
CitationDNA Repair (Amst.) 2012, 11 (4):374-380
SponsorsThis work was supported by a grant of the Associazione Italiana per la Ricerca sul Cancro (Italy; G.M.), of the Progetto Integrato Oncologia, Regione Toscana – Ministero della Salute “Identification of population risk profiles as an approach to cancer prevention” and of the Environmental Cancer Risk Nutrition and Individual Susceptibility project (G.M.), a network of excellence operating within the European Union Sixth Framework Program, Priority 5: ‘Food Quality and Safety’ (Contract No. 513943). A partial funding for this project has also been received from the Compagnia di San Paolo (Turin, Italy; G.M.) and by Progetto Ricerca Sanitaria Finalizzata Regione Piemonte (G.M., M.S.).
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- Issue date: 2006 Mar
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ECNIS-sponsored workshop on biomarkers of exposure and cancer risk: DNA damage and DNA adduct detection and 6th GUM-32P-postlabelling workshop, German Cancer Research Center, Heidelberg, Germany, 29-30 September 2006.Arlt, Volker M.; Frei, Eva; Schmeiser, Heinz H. (Oxford University Press, 2007-01)Of all the chemicals classified as carcinogenic to humans by the International Agency for Research on Cancer (IARC), 90% exert their biological effects through binding of their metabolically activated intermediates to DNA forming covalent DNA adducts. As a consequence DNA adducts are generally considered to be causative and directly related to tumour formation. DNA adduct analyses reflect tissue-specific rates of adduct formation and removal, which depend on carcinogen uptake, metabolic activation, DNA repair, adduct instability and tissue turnover and are thus useful markers of carcinogen exposure. The measurement of carcinogen-DNA adduct levels is central to the understanding of chemical carcinogenesis both in animals and humans to determine molecular mechanisms and exposure. Sensitive methods for DNA adduct analysis used to date are based on (32)P-post-labelling, immunoassay, mass spectrometry and laser-induced fluorescence. The aim of this workshop held over 2 days (29-30 September 2006) at the German Cancer Research Center (DKFZ) in Heidelberg, Germany, was to discuss methodological improvements of DNA adduct detection with emphasis on the (32)P-post-labelling procedure as well as new findings achieved by applying the methods to studies on understanding human cancer mechanisms and to elucidate the relationship between adduct formation and human cancer risk.
Dietary intake of vitamin K and risk of prostate cancer in the Heidelberg cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC-Heidelberg).Nimptsch, Katharina; Rohrmann, Sabine; Linseisen, Jakob (2008-04)BACKGROUND: Anticarcinogenic activities of vitamin K have been observed in various cancer cell lines, including prostate cancer cells. Epidemiologic studies linking dietary intake of vitamin K with the development of prostate cancer have not yet been conducted. OBJECTIVE: We evaluated the association between dietary intake of phylloquinone (vitamin K1) and menaquinones (vitamin K2) and total and advanced prostate cancer in the Heidelberg cohort of the European Prospective Investigation into Cancer and Nutrition. DESIGN: At baseline, habitual dietary intake was assessed by means of a food-frequency questionnaire. Dietary intake of phylloquinone and menaquinones (MK-4-14) was estimated by using previously published HPLC-based food-content data. Multivariate-adjusted relative risks of total and advanced prostate cancer in relation to intakes of phylloquinone and menaquinones were calculated in 11 319 men by means of Cox proportional hazards regression. RESULTS: During a mean follow-up time of 8.6 y, 268 incident cases of prostate cancer, including 113 advanced cases, were identified. We observed a nonsignificant inverse association between total prostate cancer and total menaquinone intake [multivariate relative risk (highest compared with lowest quartile): 0.65; 95% CI: 0.39, 1.06]. The association was stronger for advanced prostate cancer (0.37; 0.16, 0.88; P for trend = 0.03). Menaquinones from dairy products had a stronger inverse association with advanced prostate cancer than did menaquinones from meat. Phylloquinone intake was unrelated to prostate cancer incidence (1.02; 0.70, 1.48). CONCLUSIONS: Our results suggest an inverse association between the intake of menaquinones, but not that of phylloquinone, and prostate cancer. Further studies of dietary vitamin K and prostate cancer are warranted.
The association of gastric cancer risk with plasma folate, cobalamin, and methylenetetrahydrofolate reductase polymorphisms in the European Prospective Investigation into Cancer and Nutrition.Vollset, Stein Emil; Igland, Jannicke; Jenab, Mazda; Fredriksen, Ase; Meyer, Klaus; Eussen, Simone; Gjessing, Hakon K.; Ueland, Per Magne; Pera, Guillem; Sala, Nuria; Agudo, Antonio; Capella, Gabriel; Del Giudice, Giuseppe; Palli, Domenico; Boeing, Heiner; Weikert, Cornelia; Bueno-de-Mesquita, H. Bas; Carneiro, Fatima; Pala, Valeria; Vineis, Paolo; Tumino, Rosario; Panico, Salvatore; Berglund, Goran; Manjer, Jonas; Stenling, Roger; Hallmans, Goran; Martínez, Carmen; Dorronsoro, Miren; Barricarte, Aurelio; Navarro, Carmen; Quirós, Jose R.; Allen, Naomi; Key, Timothy J.; Bingham, Sheila; Linseisen, Jakob; Kaaks, Rudolf; Overvad, Kim; Tjonneland, Anne; Buchner, Frederike L.; Peeters, Petra H.M.; Numans, Mattijs E.; Clavel-Chapelon, Francoise; Boutron-Ruault, Marie-Christine; Trichopoulou, Antonia; Lund, Eiliv; Slimani, Nadia; Ferrari, Pietro; Riboli, Elio; Gonzalez, Carlos A. (2007-11)Previous studies have shown inconsistent associations of folate intake and polymorphisms of the methylenetetrahydrofolate reductase (MTHFR) gene with gastric cancer risk. Our nested case-control study within the European Prospective Investigation into Cancer and Nutrition cohort is the first prospective study of blood folate levels and gastric cancer. Gastric cancer cases (n=247) and controls (n=631) were matched for study center, age, sex, and time of blood donation. Two common single nucleotide polymorphisms of the MTHFR gene were determined, as were plasma concentrations of folate, cobalamin (vitamin B12), total homocysteine, and methylmalonic acid (cobalamin deficiency marker) in prediagnostic plasma. Risk measures were calculated with conditional logistic regression. Although no relations were observed between plasma folate or total homocysteine concentrations and gastric cancer, we observed a trend toward lower risk of gastric cancer with increasing cobalamin concentrations (odds ratio, 0.79 per SD increase in cobalamin; P=0.01). Further analyses showed that the inverse association between cobalamin and gastric cancer was confined to cancer cases with low pepsinogen A levels (marker of severe chronic atrophic gastritis) at the time of blood sampling. The 677 C-->T MTHFR polymorphism was not associated with gastric cancer, but we observed an increased risk with the variant genotype of the 1298 A-->C polymorphism (odds ratio, 1.47 for CC versus AA; P=0.04). In conclusion, we found no evidence of a role of folate in gastric cancer etiology. However, we observed increased gastric cancer risk at low cobalamin levels that was most likely due to compromised cobalamin status in atrophic gastritis preceding gastric cancer.