DNA adducts as markers of exposure to carcinogens and risk of cancer

Víneis, Paolo; Perera, Frederica P.

doi:10.1002/1097-0215(20001101)88:3<325::aid-ijc1>3.0.co;2-k

Cited by 73 publications

(26 citation statements)

References 11 publications

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“…Quantification of 8-oxo-2¢-deoxyguanosine (8-oxodG) in blood or urine is the most commonly utilized biomarker of in vivo oxidative DNA damage [36,58,66,67]. Elevated levels of 8-oxodG are believed to reflect deficient DNA repair capacity and an increased risk of cancer [68][69][70]. However, no studies have evaluated the role of oxidative stress or oxidative DNA damage in mutation carriers.…”

Section: Brca Mutation Carriers Of Todaymentioning

confidence: 99%

Brief Report: Towards a dietary prevention of hereditary breast cancer

Kotsopoulos

Narod

2005

Cancer Causes Control

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Inheritance of a deleterious mutation in BRCA1 or BRCA2 confers a high lifetime risk of developing breast cancer. Variation in penetrance between individuals suggests that factors other than the gene mutation itself may influence the risk of cancer in susceptible women. Several risk factors have been identified which implicate estrogen-induced growth stimulation as a probable contributor to breast cancer pre-disposition. The protein products of both of these genes appear to help preserve genomic integrity via their participation in the DNA damage response and repair pathways. To date, the evidence for a cancer-protective role of dietary nutrients, for the most part those with antioxidant properties, has been based on women without any known genetic pre-disposition and it is important to identify and evaluate dietary factors which may modify the risk of cancer in BRCA carriers. Here we propose that diet modification may modulate the risk of hereditary breast cancer by decreasing DNA damage (possibly linked to estrogen exposure) or by enhancing DNA repair. The prevention of hereditary breast cancer through diet is an attractive complement to current management strategies and deserves exploration.

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Section: Brca Mutation Carriers Of Todaymentioning

confidence: 99%

Brief Report: Towards a dietary prevention of hereditary breast cancer

Kotsopoulos

Narod

2005

Cancer Causes Control

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“…Biomarkers are used to identify molecular and cellular alterations in target tissues during toxicological processes that occur within crucial pathways following exposure to toxic chemicals such as carcinogens (Vineis and Perera, 2000;Lee et al, 2002;Bartsch et al, 2011;Aylward et al, 2014) (Figure 1). In some cases, biomarker alterations may be determined in blood, body fluids, cells, and tissues to evaluate exposure levels in animals and humans (Perera et al, 1988;DeCaprio, 1997;Pedersen et al, 2012;Roh et al, 2012;DeMarini, 2013).…”

Section: In Order To Investigate the Potential Application Of Blood Bmentioning

confidence: 99%

Potential Application of Benzo(a)Pyrene-Associated Adducts (Globin or Lipid) as Blood Biomarkers for Target Organ Exposure and Human Risk Assessment

Kwack

Kim

et al. 2014

Journal of Toxicology and Environmental Health, Part A

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In order to investigate the potential application of blood biomarkers as surrogate indicators of carcinogen-adduct formation in target-specific tissues, temporal formation of benzo[a]pyrene (BaP)-associated DNA adducts, protein adducts, or lipid damage in target tissues such as lung, liver, and kidney was compared with globin adduct formation or plasma lipid damage in blood after continuous intraperitoneal (ip) injection of [(3)H]BaP into female ICR mice for 7 d. Following treatment with [(3)H]BaP, formation of [(3)H]BaP-DNA or -protein adducts in lung, liver, and kidney increased linearly, and persisted thereafter. This finding was similar to the observed effects on globin adduct formation and plasma lipid damage in blood. The lungs contained a higher level of DNA adducts than liver or kidneys during the treatment period. Further, the rate of cumulative adduct formation in lung was markedly greater than that in liver. Treatment with a single dose of [(3)H]BaP indicated that BaP-globin adduct formation and BaP-lipid damage in blood reached a peak 48 h after treatment. Overall, globin adduct formation and lipid damage in blood were significantly correlated with DNA adduct formation in the target tissues. These data suggest that peripheral blood biomarkers, such as BaP-globin adduct formation or BaP-lipid damage, may be useful for prediction of target tissue-specific DNA adduct formation, and for risk assessment after exposure.

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“…Conceptually, DNA adducts are de®ned as biologically e ective dose markers of exposure to carcinogens; they not only re¯ect prior exposure to carcinogens but also imply a tangible risk for cancer (Poirier et al 2000, Vineis and Perera 2000, Hemminki et al 2001). The latter aspect should be interpreted quite cautiously since DNA adduct formation is only one step in the multi-stage process of carcinogenesis, and many other in¯uential factors such as cellular proliferation are also involved in this process (Poirier et al 2000, Vineis and Perera 2000, Hemminki et al 2001. Therefore, it is premature to rely solely on dosimetry of DNA adducts for cancer risk estimation.…”

Section: Tobacco Smoke Carcinogensmentioning

confidence: 99%

Biomonitoring of tobacco smoke carcinogenicity by dosimetry of DNA adducts and genotyping and phenotyping of biotransformational enzymes: a review on polycyclic aromatic hydrocarbons

2002

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In this review article, we summarize the data on tobacco smoke carcinogenicity in relation to DNA adduct dosimetry and genotyping and phenotyping of biotransformational enzymes. A major class of carcinogens, polycyclic aromatic hydrocarbons, present in substantial quantities in tobacco smoke, is discussed. The historical background and an overview of the metabolic pathways are given. The epidemiological and biological data in particular on dosimetry of the representative DNA adducts and genotyping and phenotyping of the respective activating and detoxifying enzymes are presented. The salient findings are highlighted, the uncertainties are underlined and, finally, recommendations for future research are made.

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DNA adducts as markers of exposure to carcinogens and risk of cancer

Cited by 73 publications

References 11 publications

Brief Report: Towards a dietary prevention of hereditary breast cancer

Brief Report: Towards a dietary prevention of hereditary breast cancer

Potential Application of Benzo(a)Pyrene-Associated Adducts (Globin or Lipid) as Blood Biomarkers for Target Organ Exposure and Human Risk Assessment

Biomonitoring of tobacco smoke carcinogenicity by dosimetry of DNA adducts and genotyping and phenotyping of biotransformational enzymes: a review on polycyclic aromatic hydrocarbons

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