Analysis of total meat intake and exposure to individual heterocyclic amines in a case-control study of colorectal cancer: contribution of metabolic variation to risk

Nowell, Susan; Coles, Brian; Sinha, Rashmi; MacLeod, Stewart L.; Ratnasinghe, Duminda; Stotts, Craig; Kadlubar, Fred F.; Ambrosone, Christine B.; Lang, Nicholas P.

doi:10.1016/s0027-5107(02)00164-1

Cited by 135 publications

(120 citation statements)

References 29 publications

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“…From the Medline search using the search terms described earlier, we identified 34 case -control studies for SULT1A1 Arg 213 His polymorphism (Seth et al, 2000;Steiner et al, 2000;Bamber et al, 2001;Zheng et al, 2001Zheng et al, , 2003Ozawa et al, 2002;Wang et al, 2002;Nowell et al, 2002aNowell et al, , 2004Tang et al, 2003;Wu et al, 2003;Chacko et al, 2004;Hung et al, 2004;Langsenlehner et al, 2004;Liang et al, 2004;Tiemersma et al, 2004;Tsukino et al, 2004;Boccia et al, 2005Boccia et al, , 2006 with different types of cancers including UADT TRC, which is biologically more plausible, the studies included in meta-analysis were categorised according to the site of primary cancer as UADT TRC, genitourinary, breast, colorectal and other cancer sites. All the studies were further analysed with respect to genotypes, source of controls, ethnicity and carcinogen exposure.…”

Section: Resultsmentioning

confidence: 99%

Case–control study and meta-analysis of SULT1A1 Arg213His polymorphism for gene, ethnicity and environment interaction for cancer risk

et al. 2008

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Cytosolic sulphotransferase SULT1A1 plays a dual role in the activation of some carcinogens and inactivation of others. A functional polymorphism leading to Arg 213 His substitution (SULT1A1*2) affects its catalytic activity and thermostability. To study the association of SULT1A1*2 polymorphism with tobacco-related cancers (TRCs), a case -control study comprising 132 patients with multiple primary neoplasm (MPN) involving TRC and 198 cancer-free controls was carried out. One hundred and thirteen MPN patients had at least one cancer in upper aerodigestive tract including lung (UADT-MPN). SULT1A1*2 showed significant risk association with UADT-MPN (odds ratio (OR) ¼ 5.50, 95% confidence interval (CI): 1.09, 27.7). Meta-analysis was conducted combining the data with 34 published studies that included 11 962 cancer cases and 14 673 controls in diverse cancers. The SULT1A1*2 revealed contrasting risk association for UADT cancers (OR ¼ 1.62, 95% CI: 1.12, 2.34) and genitourinary cancers (OR ¼ 0.73, 95% CI: 0.58, 0.92). Furthermore, although SULT1A1*2 conferred significant increased risk of breast cancer to Asian women (OR ¼ 1.91, 95% CI: 1.08, 3.40), it did not confer increased risk to Caucasian women (OR ¼ 0.92, 95% CI: 0.71, 1.18). Thus risk for different cancers in distinct ethnic groups could be modulated by interaction between genetic variants and different endogenous and exogenous carcinogens.

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Section: Resultsmentioning

confidence: 99%

Case–control study and meta-analysis of SULT1A1 Arg213His polymorphism for gene, ethnicity and environment interaction for cancer risk

et al. 2008

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“…In vivo and in vitro studies have suggested that meats cooked at a high temperature generate heterocyclic amines (HCAs) and other potent mutagens and carcinogens, which can induce tumours in multiple tissue sites in many animal species (Spingarn et al, 1980;Wakabayashi et al, 1992;Okochi et al, 1999;Nagao et al, 2002). Although a number of epidemiologic studies suggest a possible link between dietary intake of HCAs and risk of colorectal and breast cancers (Zheng et al, 1998;Nowell et al, 2002;Sinha et al, 2005), no studies have been conducted on endometrial cancer.…”

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confidence: 99%

Animal food intake and cooking methods in relation to endometrial cancer risk in Shanghai

et al. 2006

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We evaluated animal food intake and cooking methods in relation to endometrial cancer risk in a population-based case -control study in Shanghai, China. A validated food frequency questionnaire was used to collect the usual dietary habits of 1204 cases and 1212 controls aged 30 -69 years between 1997 and 2003. Statistical analyses were based on an unconditional logistic regression model adjusting for potential confounders. High intake of meat and fish was associated with an increased risk of endometrial cancer, with adjusted odds ratios for the highest vs the lowest quartile groups being 1.7 (95% confidence interval: 1.3 -2.2) and 2.4 (1.8 -3.1), respectively. The elevated risk was observed for all types of meat and fish intake. Intake of eggs and milk was not related to risk. Cooking methods and doneness levels for meat and fish were not associated with risk, nor did they modify the association with meat and fish consumption. Our study suggests that animal food consumption may play an important role in the aetiology of endometrial cancer, but cooking methods have minimal influence on risk among Chinese women.

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“…20 Many researchers have pointed to relationships between intake of a high fat diet or red meat and colon cancer risks. [21][22][23] PhIP itself could be a candidate risk factor for human colon cancer, 21 with other factors (fruit, vegetables, fiber and fecal weight) implicated as modulating influences. [22][23][24] In the animal experimental fields, however, no colon tumors were induced in rats treated with 25 ppm PhIP for 104 weeks.…”

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Lack of large intestinal carcinogenicity of 2‐amino‐1‐methyl‐6‐phenylimidazo[4,5‐b]pyridine at low doses in rats initiated with azoxymethane

Doi

Wanibuchi

Salim

et al. 2005

Intl Journal of Cancer

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2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine (PhIP), an abundant food-derived heterocyclic amine (HCA), has attracted particular attention as a human colon carcinogen. Humans are in fact exposed to continuous low doses of HCAs during lifetime. Therefore, we focused on rat large intestinal carcinogenicity of PhIP at levels that mimic practical human exposure. A total of 192 6-weekold male F344 rats were subcutaneously injected twice with 15 mg/ kg body weight azoxymethane (AOM), then continuously fed various doses (0, 0.001, 0.01, 0.1, 1, 10, 50 and 200 ppm) of PhIP in the diet. At week 16, aberrant crypt foci (ACF) were quantitatively analyzed. At week 36, tumor occurrence was pathologically analyzed. Then immunohistochemical examinations were performed. PhIP was found to enhance strongly AOM-initiated rat large intestinal tumorigenesis at high doses (50 and 200 ppm), while lower doses (0.001-10 ppm) had no apparent effects. High doses also caused variation in tumor histologic types and their distribution throughout the large intestinal segments. Frequencies of ACF/cm 2 did not meaningfully vary between the groups. Cellular proliferation activity in normal-appearing colonic mucosa was significantly increased at high doses. These novel findings may provide evidence of a low-dose potential for PhIP, with a no-observed effect level speculated to be 10 ppm in the present initiation-promotion experimental model. ' 2005 Wiley-Liss, Inc.Key words: rat; large intestine; carcinogenesis; PhIP; azoxymethane; no-observed effect level Carcinogenesis is widely accepted to be a multistep process caused by a series of genetic and/or subsequent epigenetic alterations that are indispensable to the different stages from initiation to promotion and progression of cancer development. 1,2 Humans are consistently exposed to very many naturally occurring or synthetic chemical carcinogens at quite low-dose levels in the environment, 3 although concomitantly they may consume mixtures of naturally occurring anticarcinogenic compounds in their daily diets. 4 One focus of attention has been food-derived heterocyclic amines (HCAs) generated in cooking processes that have proved to be carcinogenic in rodent species. 5,6 HCAs are highly mutagenic 6 and genotoxic carcinogens that are generally thought to have no threshold in exerting their carcinogenic potential, which was postulated to exhibit dose dependence in vivo. 3 However, in practice, low-dose administration has not necessarily led to cancer development in the rat liver. 7 Thereby, in our laboratory, the nonthreshold theory for hepatocarcinogenesis of one HCA, 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), has been challenged, since in vivo dose-response curves do not show linearity at low-dose levels. 8,9 Moreover, thresholds for chemical carcinogenesis were concluded in a recent article. 10 In practice, the many factors active in vivo, from intake of carcinogens through to lesion development, mean that the processes are highly complicated, so that if the DNA-damaging pote...

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Analysis of total meat intake and exposure to individual heterocyclic amines in a case-control study of colorectal cancer: contribution of metabolic variation to risk

Cited by 135 publications

References 29 publications

Case–control study and meta-analysis of SULT1A1 Arg213His polymorphism for gene, ethnicity and environment interaction for cancer risk

Case–control study and meta-analysis of SULT1A1 Arg213His polymorphism for gene, ethnicity and environment interaction for cancer risk

Animal food intake and cooking methods in relation to endometrial cancer risk in Shanghai

Lack of large intestinal carcinogenicity of 2‐amino‐1‐methyl‐6‐phenylimidazo[4,5‐b]pyridine at low doses in rats initiated with azoxymethane

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