Article

Well-done meat intake, heterocyclic amine exposure, and cancer risk.

Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37203-1738, USA.
Nutrition and Cancer (Impact Factor: 2.7). 07/2009; 61(4):437-46. DOI: 10.1080/01635580802710741
Source: PubMed

ABSTRACT High intake of meat, particularly red and processed meat, has been associated with an increased risk of a number of common cancers such as breast, colorectum, and prostate in many epidemiological studies. Heterocyclic amines (HCAs) are a group of mutagenic compounds found in cooked meats, particularly well-done meats. HCAs are some of most potent mutagens detected using the Ames/salmonella tests and have been clearly shown to induce tumors in experimental animal models. Over the past 10 years, an increasing number of epidemiological studies have evaluated the association of well-done meat intake and meat carcinogen exposure with cancer risk. The results from these epidemiologic studies were evaluated and summarized in this review. The majority of these studies have shown that high intake of well-done meat and high exposure to meat carcinogens, particularly HCAs, may increase the risk of human cancer.

1 Bookmark
 · 
94 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Breast cancer is the most common type of cancer affecting women in North America and Europe. More than 85% of breast cancers are sporadic and attributable to long-term exposure to small quantities of multiple carcinogens. To understand how multiple carcinogens act together to induce cellular carcinogenesis, we studied the activity of environmental carcinogens 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and benzo[a]pyrene (B[a]P), and dietary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) using our breast cell carcinogenesis model. Our study revealed, for the first time, that combined NNK and B[a]P enhanced breast cell carcinogenesis chronically induced by PhIP in both non-cancerous and cancerous breast cells. Co-exposure was more potent than sequential exposure to combined NNK and B[a]P followed by PhIP in inducing carcinogenesis. Initiation of carcinogenesis was measured by transient endpoints induced in a single exposure, while progression of carcinogenesis was measured by acquisition of constitutive endpoints in cumulative exposures. Transient endpoints included DNA damage, Ras-Erk-Nox pathway activation, reactive oxygen species elevation, and increased cellular proliferation. Constitutive endpoints included various cancer-associated properties and signaling modulators, as well as enrichment of cancer stem-like cell population and activation of the epithelial-to-mesenchymal transition program. Using transient and constitutive endpoints as targets, we detected that a combination of the green tea catechins ECG and EGCG, at non-cytotoxic levels, was more effective than individual agents in intervention of cellular carcinogenesis induced by combined NNK, B[a]P, and PhIP. Thus, use of combined ECG and EGCG should be seriously considered for early intervention of breast cell carcinogenesis associated with long-term exposure to environmental and dietary carcinogens.
    PLoS ONE 11/2014; 9(11):e108698. · 3.53 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Polyaromatic hydrocarbons, heterocyclic aromatic amines and dioxin-like compounds are environmental carcinogens shown to initiate cancer in a number of tissue types including prostate and breast. These environmental carcinogens elicit their effects through interacting with the aryl hydrocarbon receptor (AhR), a ligand activated transcription factor. Naturally occurring compounds found in fruits and vegetables shown to have anti-carcinogenic effects also interact with the AhR. This review explores dietary and environmental exposure to chemical carcinogens and beneficial natural compounds whose effects are elicited by the AhR.
    Biochemistry & pharmacology : open access. 03/2014; 3(1).
  • [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND: The level of evidence regarding the association between red and processed meat intakes and breast cancer risk is still low, due to insufficient prospective studies. Moreover, mechanistic data suggest that some antioxidants may modulate this relationship but epidemiological evidence is lacking. Our objectives were to investigate relationships between red and processed meat intakes and breast cancer risk, and to study whether an antioxidant supplementation modulates these associations, which, to our knowledge, has never been investigated before. METHODS: The SU.VI.MAX study was a randomized, double-blind, placebo-controlled trial in which participants received a combination of low-dose antioxidants or a placebo from 1994 to 2002. This observational prospective analysis included 4684 women among whom 190 developed a first incident breast cancer between 1994 and 2007 [mean (range) follow-up = 11.3 (0-13)years]. Baseline dietary data were assessed by repeated dietary records in 1994-1995. Associations between quartiles of red and processed meat intakes and breast cancer risk were characterized by multivariate Cox proportional hazards models. RESULTS: Breast cancer risk was directly associated with processed meat intake [hazard ratio (HR)Q4vsQ1 = 1.45 (0.92-2.27), Ptrend = 0.03] and this association was stronger when excluding cooked ham [HRQ4vsQ1 = 1.90 (1.18-3.05), Ptrend = 0.005]. In stratified analyses, processed meat intake was directly associated with breast cancer risk in the placebo group only [HRQ4vsQ1 = 2.46 (1.28-4.72), Ptrend = 0.001], but not in the supplemented group [HRQ4vsQ1 = 0.86 (0.45-1.63), Ptrend = 0.7]. CONCLUSION: Processed meat intake was prospectively associated with increased breast cancer risk. This study also suggests that antioxidants may modulate this association by counteracting the potential pro-carcinogenic effects of processed meat on breast cancer.
    International Journal of Epidemiology 07/2014; · 9.20 Impact Factor

Preview

Download
1 Download
Available from