The inhibitory effect of vitamin E on K-ras mutation at an early stage of lung carcinogenesis in mice

Yano, Tomohiro; Uchida, Mikako; Yuasa, Mutsuko; Murakami, Ayumi; Hagiwara, Kiyokazu; Ichikawa, Tomio

doi:10.1016/s0014-2999(97)00094-0

Cited by 9 publications

(6 citation statements)

References 12 publications

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“…More specifically, if we further dissect these results by analysing both genes separately, we saw that while p16 INK4A inactivation was more frequently recognised at an advanced tumor stage, K-ras did not, as it was more frequently detected in tumors at an early stage. These findings are in keeping with studies of Ng et al [38] showing a correlation between p16 INK4A methylation and an advanced tumor stage and with the studies of Mao et al [10], Graziano et al [39], Ichikawa et al [40] and Yano et al [41] showing K-ras mutations at an early stage of lung carcinogenesis.…”

Section: Discussionsupporting

confidence: 92%

K-ras and p16INK4Aalterations in sputum of NSCLC patients and in heavy asymptomatic chronic smokers

et al. 2004

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Section: Discussionsupporting

confidence: 92%

K-ras and p16INK4Aalterations in sputum of NSCLC patients and in heavy asymptomatic chronic smokers

et al. 2004

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“…This finding agrees with previous experimental studies in animal models of carcinogenesis, which reported a protective effect of vitamin E against K-ras mutations. 27 The proposed mechanisms for the anti-carcinogenic effect of vitamin E include the inhibition of lipid peroxidation and formation of its reactive products. It has been shown that the pancreas suffers DNA damage from oxidative stress and lipid peroxidation.…”

Section: Discussionmentioning

confidence: 99%

“…1 A lung carcinogenesis study in mice showed that a diet supplemented with vitamin E decreased the frequency of Kras mutations. 27 Despite the firmly established importance of K-ras mutations in the aetiopathogenesis of EPC, and the potential role of dietary components in modifying risk, the relation between diet and K-ras mutations has so far not been studied in this disease, and seldom in other neoplasms. The objective of the present study was therefore to analyse the relation between food and nutrient intakes and the prevalence at diagnosis of mutations in codon 12 of the K-ras oncogene in patients with EPC.…”

mentioning

confidence: 99%

Food and nutrient intakes and K-ras mutations in exocrine pancreatic cancer

Morales

Porta

Vioque

et al. 2007

Journal of Epidemiology & Community Health

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Background: No studies have investigated the relation between K-ras mutations and dietary factors in exocrine pancreatic cancer (EPC), and fewer than 10 studies have done so in other neoplasms. Patients and Methods: Incident cases of EPC were prospectively identified, and interviewed face-to-face during hospital admission. Food and nutrient intakes were measured with a food frequency questionnaire. Logistic regression was used to compare EPC cases (n = 107) with and without K-ras mutations (case-case study). Results: K-ras mutations were more common among daily consumers of milk and other dairy products than among non-daily consumers: the odds ratio adjusted by total energy, age, sex, smoking, alcohol and coffee consumption (ORa) was 5.1 (95% CI 1.1 to 24.5, p = 0.040). For all dairy products, including butter, the ORa for the medium and upper tertiles of intake were 5.4 and 11.6, respectively (p for trend = 0.023). The ORa for regular coffee drinkers further adjusted by dairy consumption was 4.7 (95% CI 1.1 to 20.7, p = 0.043). K-ras mutated cases reported a lower intake of vitamin E (ORa = 0.2, p for trend = 0.036), polyunsaturated fats and omega 3 fatty acids (ORa = 0.2; p for trend ,0.03). Conclusions: Results support the hypothesis that in EPC exposure to specific dietary components or contaminants may influence the occurrence or persistence of K-ras mutations.

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“…Epidemiological surveys and animal studies have illustrated that smoking tobacco is the main cause of lung cancer (4)(5)(6). Chemoprevention, particularly antioxidant intervention, may prove an effective approach to reducing the incidence of lung cancer; however, epidemiological surveys have demonstrated that antioxidant intervention in the prevention of lung cancer has significally different, even counterproductive, outcomes (7)(8)(9)(10)(11). By means of an animal study, we validated that vitamin E (VE) can significantly reduce the incidence and number of tumors in lung cancer (12).…”

Section: Introductionmentioning

confidence: 81%

Angiopoietin-3 overexpression in tobacco smoke-induced mouse lung tumors and its relation to vitamin E intervention

Zhang¹

2008

Mol Med Rep

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Abstract. Animal studies have shown that tobacco smoke can induce lung cancer in mice,and that the intake of Vitamin E (VE) has a protective effect against its risk. However, the mechanisms of action of VE remain unclear. In this study, DNA microarrays for gene expression profiles of the mouse genome were applied in order to screen for the upregulated genes associated with VE intervention in smoke-induced lung cancer. Real-time PCR was used to validate the screened upregulated angiopoietin-3 gene (Ang-3), and Western blotting was used to investigate the expression of the Ang-3 protein.Our results demonstrate that smoking and VE intervention involve 621 upregulated genes, including oncogenes, nononcogenes with clear function and genes with unclear function. Of these, Ang-3 presented high expression in both the smoking and tumor groups. Real-time PCR and Western blotting further indicated that smoking could upregulate the expression of Ang-3; moreover, Ang-3 was overexpressed in lung cancer tissue. VE intervention decreased its expression to some extent. This illustrates that Ang-3 may play an important role in the carcinogenesis and development of smoke-induced lung cancer, and could also be a target in lung cancer treatment.

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The inhibitory effect of vitamin E on K-ras mutation at an early stage of lung carcinogenesis in mice

Cited by 9 publications

References 12 publications

K-ras and p16INK4Aalterations in sputum of NSCLC patients and in heavy asymptomatic chronic smokers

K-ras and p16INK4Aalterations in sputum of NSCLC patients and in heavy asymptomatic chronic smokers

Food and nutrient intakes and K-ras mutations in exocrine pancreatic cancer

Angiopoietin-3 overexpression in tobacco smoke-induced mouse lung tumors and its relation to vitamin E intervention

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