Vitamin E Intake and Pancreatic Cancer Risk: A Meta-Analysis of Observational Studies

Lujian, Peng; Liu, Xiangde; Lü, Qian; Tang, Tengqian; Yang, Zhanyu

doi:10.12659/msm.893792

Cited by 36 publications

(30 citation statements)

References 26 publications

(34 reference statements)

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“…conducted a meta-analysis to assess the relationship between dietary vitamin C and pancreatic cancer risk and found that a higher vitamin C intake was inversely correlated with pancreatic cancer risk7. Similarly, dietary vitamin E was found to be a protective factor against pancreatic cancer8. However, a recent pooled analysis suggested that higher levels of vitamin D might increase pancreatic cancer risk30.…”

Section: Discussionmentioning

confidence: 99%

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Association between vitamin A, retinol and carotenoid intake and pancreatic cancer risk: Evidence from epidemiologic studies

Huang

Yuan-fu

Zhi

et al. 2016

Sci Rep

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Pancreatic cancer is a devastating disease with poor prognosis. The association between vitamin A, retinol and carotenoid intake and the risk of pancreatic cancer occurrence remains controversial, and therefore it is necessary to make a meta-analysis to clarify the association between vitamin A, retinol and carotenoid intake and pancreatic cancer risk. In the present study, PubMed and EMBASE databases were used to identify qualified studies. The association between dietary vitamin A, retinol and carotenoids was estimated by pooled odds ratios (ORs) and corresponding 95% confidence intervals (CIs). It was found that there was an inverse correlation between vitamin A, beta-carotene and lycopene intake and the risk of pancreatic cancer (for vitamin A, pooled OR = 0.85, 95%CI = 0.74–0.97, P = 0.015; for beta-carotene, pooled OR = 0.78, 95%CI = 0.66–0.92, P = 0.003; for lycopene, pooled OR = 0.84, 95%CI = 0.73–0.97, P = 0.020), which was more prominent in case-control study subgroup. In conclusion, dietary vitamin A, beta-carotene and lycopene might inversely correlate with pancreatic cancer.

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Section: Discussionmentioning

confidence: 99%

“…A number of epidemiologic studies have been published in an attempt to explore the relationship between nutrient intake and the risk of pancreatic cancer occurrence. Various vitamins including vitamin B6, vitamin C7 and vitamin E8 have been implicated in the risk of pancreatic cancer occurrence according to previous studies.…”

mentioning

confidence: 97%

Association between vitamin A, retinol and carotenoid intake and pancreatic cancer risk: Evidence from epidemiologic studies

Huang

Yuan-fu

Zhi

et al. 2016

Sci Rep

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“…Several epidemiological studies investigating the effects of AA against breast cancer link many inconsistent results, but, reports indicate that it can also reduce the risk of this type of cancer due to its antioxidant action for protection of DNA damage by neutralizing the free radicals and initiation of carcinogenesis [48].…”

Section: Discussionmentioning

confidence: 99%

Ascorbic acid modulates doxorubicin and cyclophosphamide-induced cytogenetic damages in Sarcoma 180 cells

Alencar¹,

Islam²,

Rocha³

et al. 2016

Int Arch Med

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Cancer is a public health global problem. Cyclophosphamide (CPA) and Doxorubicin (DOX) are used in chemotherapy, especially by generating reactive oxygen species. The clinical use of ascorbic acid during chemotherapy also raises several controversies due to its antagonistic effects on antineoplastic agent. In this sense, this study aims to evaluate the effects of ascorbic acid (2 µg/mL) on the modulation of cytogenetic damage induced by CPA (20 µg/mL) and DOX (2 µg/ mL), as well as their interaction (AC protocol) on Sarcoma 180 tumor cells. Cytogenetic damage classified as apoptosis, necrosis, micronuclei, buds and nucleoplasmic bridges were linked to the CytokinesisBlock Micronucleus Assay application. CPA and DOX induce significant (p<0.05) increases in apoptosis, necrosis and micronuclei in the cell types tested. The damage on Sarcoma 180 cells was modulated by ascorbic acid with percentage modulation in more than 70% of CPA relative to apoptosis and micronuclei, and 32% to necrosis. The damage of DOX has been modulated by 70% to apoptosis, 40% to necrosis, rather than micronuclei, whereas, in AC protocol, modulations were observed by 52% to apoptosis and 32% and 40% to necrosis and micronuclei, respectively. There was no significance in relation to the nuclear buds and nucleoplasmic bridges. In addition, ascorbic acid did not show any effect. These results are other studies, which indicate hazards to chemotherapy effectiveness due to the antioxidant effects

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“…A number of studies have revealed that tobacco smoke (TS), the environment and diet are primary risk factors for BC, in addition to drinking water contaminants, including chlorinated byproducts and arsenic, the use of pioglitazone, obesity, hypertension and diabetes (2,6,7). A previous study reported that 23% of female and 50% of male BC cases have been attributed to TS (8).…”

Section: Introductionmentioning

confidence: 99%

ERK5 regulates tobacco smoke-induced urocystic epithelial-mesenchymal transition in BALB/c mice

Min

Geng

Liu

et al. 2017

Molecular Medicine Reports

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Abstract. Tobacco smoke (TS) is an important risk factor of bladder cancer. Epithelial-mesenchymal transition (EMT) is involved in the initiation and development of cancer. The role of extracellular signal-regulated kinase (ERK) 5 in regulating TS-induced EMT remains to be elucidated. The aim of the present study was to investigate the regulatory role of ERK5 in TS-triggered EMT in the bladder of mice. BALB/c mice were used for an in vivo TS exposure model. Mice were treated for 6 h a day for 12 weeks. The results demonstrated that mice exposed to TS had decreased mRNA and protein expression levels of the epithelial markers E-cadherin and zonula occludens-1, whereas expression levels of the mesenchymal markers Vimentin and N-cadherin were increased. Treatment with XMD8-92, a highly specific ERK5 inhibitor, effectively abrogated TS-triggered activation of ERK5, activator protein-1 and EMT alterations in the bladder of BALB/c mice. The data suggested that ERK5 regulates TS-mediated urocystic EMT. These findings provide insight into the molecular mechanisms of TS-associated bladder tumorigenesis. IntroductionBladder cancer (BC) is the fifth most common type of malignant tumor worldwide (1) and one of the most frequently occurring in the urinary system. It is predominantly present in Europe, North America and Australia, with approximately 420,000 newly diagnosed cases each year and a leading cause of cancer-associated mortality (2,3). Of all urinary malignancies, BC is the primary cause of mortality in China (4,5).A number of studies have revealed that tobacco smoke (TS), the environment and diet are primary risk factors for BC, in addition to drinking water contaminants, including chlorinated byproducts and arsenic, the use of pioglitazone, obesity, hypertension and diabetes (2,6,7). A previous study reported that 23% of female and 50% of male BC cases have been attributed to TS (8). It has been reported that current tobacco smokers have a fourfold greater risk of developing BC, compared with non-smokers (9). Progress in the understanding of the molecular mechanisms underlying the initiation and progression of BC has been made; however, the molecular pathogenesis remains to be fully elucidated.Epithelial-mesenchymal transition (EMT) is an important mechanism in embryonic progression and cancer development (10). Cells progressively lose their epithelial characteristics and acquire mesenchymal features during the process of EMT (11). In addition to facilitating tumor invasion and metastasis, EMT is also involved in the initiation of tumorigenesis by promoting cell malignant transformation. TS has been previously demonstrated to promote the initial progression of . TS-triggered EMT has been revealed to regulate early events in carcinogenesis, including downregulation of E-cadherin, loss of cell-cell adhesion and increased mobility of cells. However, the underlying molecular mechanisms by which TS induces EMT remain to be fully elucidated.Extracellular signal-regulated kinase (ERK) 5 is the least studied member of the ...

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Vitamin E Intake and Pancreatic Cancer Risk: A Meta-Analysis of Observational Studies

Cited by 36 publications

References 26 publications

Association between vitamin A, retinol and carotenoid intake and pancreatic cancer risk: Evidence from epidemiologic studies

Association between vitamin A, retinol and carotenoid intake and pancreatic cancer risk: Evidence from epidemiologic studies

Ascorbic acid modulates doxorubicin and cyclophosphamide-induced cytogenetic damages in Sarcoma 180 cells

ERK5 regulates tobacco smoke-induced urocystic epithelial-mesenchymal transition in BALB/c mice

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