The cooked meat-derived mammary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine promotes invasive behaviour of breast cancer cells

Lauber, Sandra N.; Gooderham, Nigel J.

doi:10.1016/j.tox.2010.10.004

Cited by 29 publications

(17 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Interestingly, BCL-2 expression has been shown to be repressed in MCF-7 cells by miR-21 (Wickramasinghe et al, 2009), miR-16 (Yu et al, 2012, and miR-24 (Srivastava et al, 2011), all of which were downregulated by PhIP in this study. PhIP has also been shown to affect metastatic potential in vitro (Lauber and Gooderham, 2011). In this study PhIP repressed miR200c/141, miRNA that are master regulators of invasiveness and metastasis (Burk et al, 2008).…”

Section: Discussionmentioning

confidence: 55%

The cooked meat-derived mammary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) elicits estrogenic-like microRNA responses in breast cancer cells

2014

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 55%

The cooked meat-derived mammary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) elicits estrogenic-like microRNA responses in breast cancer cells

2014

View full text Add to dashboard Cite

“…A key example is the glucuronidation of PhIP, an amine formed in cooked meat and fish and metabolized by phase I biotransformation cytochrome P450 enzymes (37). Heterocyclic amines are associated with colorectal carcinoma, breast cancer and bladder carcinoma (38)(39)(40). Another essential group of carcinogens found in red meat and tobacco smoke, are the N-nitroso compounds (NOC), also eliminated by the UGT1A8 isozyme (41), which could further explain the role of the low activity UGT1A8 * 3 allele in esophageal SCC risk.…”

Section: Discussionmentioning

confidence: 99%

High enzyme activity UGT1A1 or low activity UGT1A8 and UGT2B4 genotypes increase esophageal cancer risk

et al. 2012

View full text Add to dashboard Cite

Abstract. Esophageal cancer (EC) has a globally increasing incidence with poor curative treatment options and survival rates. Environmental and dietary factors have crucial roles in esophageal carcinogenesis. Polymorphisms in the UGT genes, a superfamily of enzymes essential for the detoxification of carcinogens, may alter enzyme activity and subsequently may play a role in EC etiology. Rather than solely establishing differences in genotype distribution, we investigated whether functional polymorphisms in UGT genes that can predict enzyme activity in vivo, may influence EC risk. A case-control study including 351 Caucasian EC patients and 592 Caucasian controls was conducted and polymorphisms in seven UGT genes were determined, using the polymerase chain reaction. On the basis of allelic in vitro enzyme activity measurements, genotypes were categorized according to their predicted in vivo enzyme activity into high, medium and low categories. Predicted enzyme activity groups were combined and compared between patients and controls. The UGT1A1 and UGT1A8 predicted high enzyme activity genotypes were significantly more (OR=1.62; 95% CI, 1.02-2.56) and less frequent (OR=0.36; 95% CI, 0.15-0.84) among patients with esophageal squamous cell carcinoma (ESCC), respectively. High (OR=0.42; 95% CI, 0.22-0.84) and medium (OR=0.25; 95% CI, 0.12-0.52) activity UGT2B4 genotypes were significantly less often present in ESCC patients. No association was detected between UGT genotypes and esophageal adenocarcinoma (EAC) risk. Polymorphisms in UGT genes, resulting in altered enzyme activity genotypes, do not seem modifiers of EAC risk. However, the predicted high activity UGT1A1 genotype, associated with low serum levels of the antioxidant bilirubin, was associated with an increased ESCC risk. The UGT1A8 and UGT2B4 genotypes associated with decreased predicted enzyme activities, were significantly associated with an increased risk of ESCC, probably by a decreased detoxification of carcinogens.

show abstract

“…Diets low in fruits and vegetables and high in red meat have been linked to increased risk of weight gain and/or obesity [68, 69]. Additionally, diets high in fruits and vegetables may exert a protective effect against breast cancer-specific mortality [70], and some components of cooked meat may increase invasiveness of breast cancer cells [71, 72]. Alcohol consumption has been linked to increases in tumor progression, serum estrogen levels, and expression of growth factors that promote tumor angiogenesis [73–76].…”

Section: Discussionmentioning

confidence: 99%

Healthy lifestyle impact on breast cancer-specific and all-cause mortality

Heitz

Baumgartner

et al. 2017

Breast Cancer Res Treat

View full text Add to dashboard Cite

Purpose While several studies have evaluated the association of combined lifestyle factors on breast cancer-specific mortality, few have included Hispanic women. We constructed a “healthy behavior index” (HBI) and evaluated its associations with mortality in non-Hispanic White (NHW) and Hispanic women diagnosed with breast cancer from the southwestern U.S. Methods Diet and lifestyle questionnaires were analyzed for 837 women diagnosed with invasive breast cancer (1999–2004) in New Mexico as part of the 4-Corners Women’s Health Study. An HBI score ranging from 0 to 12 was based on dietary pattern, physical activity, smoking, alcohol consumption, and body size and shape, with increasing scores representing less healthy characteristics. Hazard ratios for mortality over 14 years of follow-up were estimated for HBI quartiles using Cox proportional hazards models adjusting for education and stratified by ethnicity and stage at diagnosis. Results A significant increasing trend was observed across HBI quartiles among all women, NHW women, and those diagnosed with localized or regional/distant stage of disease for all-cause (AC) mortality (p-trend = 0.006, 0.002, 0.03, respectively). AC mortality was increased >2-fold for all women and NHW women in HBI Q4 versus Q1 (HR = 2.18, 2.65, respectively). The association was stronger in women with regional/distant than localized stage of disease (HR = 2.62, 1.94, respectively). Associations for Hispanics or breast cancer-specific mortality were not significant. Conclusions These findings indicate the associations between the HBI and AC mortality, which appear to differ by ethnicity and stage at diagnosis. Interventions for breast cancer survivors should address the combination of lifestyle factors on prognosis.

show abstract

The cooked meat-derived mammary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine promotes invasive behaviour of breast cancer cells

Cited by 29 publications

References 52 publications

The cooked meat-derived mammary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) elicits estrogenic-like microRNA responses in breast cancer cells

The cooked meat-derived mammary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) elicits estrogenic-like microRNA responses in breast cancer cells

High enzyme activity UGT1A1 or low activity UGT1A8 and UGT2B4 genotypes increase esophageal cancer risk

Healthy lifestyle impact on breast cancer-specific and all-cause mortality

Contact Info

Product

Resources

About