Folate intake, serum folate levels and esophageal cancer risk: an overall and dose-response meta-analysis

Zhao, Yan; Guo, Cheng; Hu, Hongtao; Lin, Zheng; Ma, Junli; Jiang, Li; Zhao, Erjiang; Li, Hailiang

doi:10.18632/oncotarget.14432

Cited by 31 publications

(33 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… NS Tio [ 52 ] 36 studies. Breast Dietary folate NS: once adjusted 608,265 sample size, 34,602 cases Total folate intake NS Menopausal status NS once adjusted Hormone status NS Study design S: retrospective study design showed decreased risk of postmenopausal breast cancer Fan C [ 18 ] 4,090/10,902 9 case-control studies: 7 dietary folate with FFQ; 2 studies serum folate concentration; 4 studies dose-response analysis Head and neck Folate intake S: decreased risk comparing highest to lowest folate intake Dose-response S: every 100 mcg/day increase in folate intake associated with 4.3% decreased risk Galeone C [ 19 ] 5,127/13,249 Pooled analysis of individual-level data from 10 case-control studies Oral cavity and pharyngeal (OPC) Total folate intake S: Reduced risk for highest compared lowest quintile total folate intake and overall OPC risk S: decreased risk for oral cavity Alcohol S: increased risk for heavy drinkers with low folate intake compared to low alcohol intake with higher folate intake Smoking S: increased risk for smoking Zhao Y [ 20 ] 19 studies Esophageal Dietary folate intake S: decreased risk with highest folate intake compared to lowest intake 14 case-control 1 cohort dietary folate intake 6 case-control 1 cohort for dose-response Dose-response S: 100 mcg/day increment in dietary folate intake reduced risk by 12% Tio M [ 21 ] 9 case-control 2574/9254 for any histological type of esophageal cancer. Esophageal, gastric, pancreatic Dietary folate S: dietary folate associated with decreased risk of esophageal and pancreatic cancer NS: gastric cancer 8 studies (5 prospective, 3 retrospective) 2209/295,526 for pancreatic cancer.…”

Section: Methodsmentioning

confidence: 99%

Folate and Its Impact on Cancer Risk

Paver²,

et al. 2018

View full text Add to dashboard Cite

Purpose of ReviewResearch has evaluated the potential impact of folate on cancer risk with conflicting findings. Studies have demonstrated increased risk, no effect, and decreased risk. This review summarizes findings of mixed results between folate intake, serum levels, gene polymorphisms, and cancer risk based on meta-analyses from the past five years.Recent FindingLow or deficient folate status is associated with increased risk of many cancers. Folic acid supplementation and higher serum levels are associated with increased risk of prostate cancer. Gene polymorphisms may impact risk in certain ethnic groups.SummaryFolate has been studied extensively due to its role in methylation and nucleotide synthesis. Further prospective studies are needed to clarify optimal levels for nutrient remediation and risk reduction in those at risk, as well as elucidate the association between high intake, high serum levels, and prostate cancer risk. Future considerations for cancer risk may include gene interactions with nutrients and environmental factors.

show abstract

Section: Methodsmentioning

confidence: 99%

Folate and Its Impact on Cancer Risk

Paver²,

et al. 2018

View full text Add to dashboard Cite

show abstract

“…In mammals, the vitamin folate is a key source of the one carbon group used to methylate DNA, DNA methylation is an epigenetic modification critical to normal genome regulation and development (11). So the biological function of folate and FHIT suggest that influence of folate to cervical carcinogenesis may be associated with the activity and function of FHIT gene, poor folate status may contribute to CC risk through effects on one-carbon metabolism and DNA methylation (38) there is enormous interest in assessing the potential for changes in folate intake to modulate DNA methylation as a mechanistic link to cancer. Research in rat liver showed a significant 20% decrease in genomic DNA methylation associated with a severe degree of dietary folate deficiency of 4 weeks' duration (39).…”

Section: Discussionmentioning

confidence: 99%

Folate deficiency and aberrant DNA methylation and expression of FHIT gene were associated with cervical pathogenesis

Ding

Nan

et al. 2017

Oncol Lett

View full text Add to dashboard Cite

Abstract. Aberrant DNA methylation is a recognized feature in various types of human cancer, and folate has a vital role in the epigenetics of mammalian cells by supplying methyl groups for DNA methylation reactions. Fragile histidine triad (FHIT) is a tumor suppressor gene that is frequently silenced in cervical cancer (CC) and preneoplastic lesions. Promoter hypermethylation was previously observed in CC, and its epigenetic silencing has been observed at mRNA or protein levels. Changes in folate intake to modulate DNA methylation may be a mechanistic link to cancer, but this remains to be elucidated. The aim of the present study was to evaluate the influences of folate on FHIT gene methylation and expression in the progression of cervical cancerization. In the present study, red blood cell (RBC) folate levels, FHIT gene methylation status, and mRNA and protein expression levels were detected in 254 women, including normal cervix (NC, n=80), cervical intraepithelial neoplasm grade 1 (CIN1, n=55; CIN2/3, n=55) and cervical squamous cell carcinoma (SCC, n=64) samples. The methylation status of FHIT gene and its mRNA and protein expression levels were measured in CaSki (HPV16 positive) and C33A (HPV16 negative) CC cells treated with different concentrations of folate. The results indicated that FHIT gene methylation rate increased with the severity of cervix lesions, however, RBC folate levels, FHIT mRNA and protein expression levels were reduced. The proliferation inhibition rate, apoptosis rate, and FHIT protein and mRNA expression levels increased along with rising concentrations of folate, whereas the degree of FHIT gene methylation gradually weakened in CaSki or C33A cell lines. The present findings indicated that folate deficiency, FHIT gene promoter hypermethylation and reduced expression were significantly associated with cervical carcinogenesis. The results indicated that folate was able to enhance apoptosis and inhibit the cervical cell proliferation while regulating FHIT gene methylation and expression. Adequate intake of folate to maintain normal DNA methylation status is an effective way for cervical lesions prevention, and demethylation treatment may offer a new strategy for therapy of CC.

show abstract

“…Furthermore, dietary factors [7] may affect the risk of esophageal cancer. Previous studies suggested that vitamins intake [8,9], fiber intake [10], folate intake [11,12], could decrease the development of esophageal cancer. Intakes of bioactive compounds from various plant sources also reduced the risk of cancer [13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

The association between dietary protein intake and esophageal cancer risk: a meta-analysis

et al. 2020

View full text Add to dashboard Cite

Correspondence: Hua Wang (wang hua@yeah.net) Several papers studied dietary protein intake as a potential influence factor for esophageal cancer, but their findings were inconsistent. Thus, this meta-analysis was performed to identify the effect of protein intake on esophageal cancer risk. Potential case-control studies or cohort studies from the databases of Embase, Web of Science and PubMed were searched. The strength of association was quantified by pooling odds ratio (OR) and 95% confidence interval (CI). In total, 11 articles involving 2537 cases and 11432 participants were included in this meta-analysis. As a result, dietary protein intake had non-significant association on esophageal cancer risk overall (pooled OR = 1.11, 95% CI = 0.88-1.40). Meanwhile, we obtained consistent results in the subgroups analyses by study design, protein type, geographic locations and number of cases. Interestingly, dietary protein intake could significantly increase the risk of esophageal squamous cell carcinoma (pooled OR = 1.29, 95% CI = 1.02-1.62), instead of other disease type. To sum up, dietary protein intake had no significant association with esophageal cancer risk in the overall analysis; but, protein intake may be associated with the risk of esophageal squamous cell carcinoma. While some limitations existed in the present paper, more studies with large sample size are warranted to further confirm this result.Statistical analysis was conducted by Stata 12.0 (StataCorp, College Station, U.S.A.). Pooled ORs with their 95% CIs was calculated using the independent OR and its 95% CI in each individual study [21]. Stratified analyses were

show abstract

Folate intake, serum folate levels and esophageal cancer risk: an overall and dose-response meta-analysis

Cited by 31 publications

References 43 publications

Folate and Its Impact on Cancer Risk

Folate and Its Impact on Cancer Risk

Folate deficiency and aberrant DNA methylation and expression of FHIT gene were associated with cervical pathogenesis

The association between dietary protein intake and esophageal cancer risk: a meta-analysis

Contact Info

Product

Resources

About