scholarly journals Association of ZNF331 and WIF1 methylation in peripheral blood leukocytes with the risk and prognosis of gastric cancer

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Chuang Nie ◽  
Xu Han ◽  
Rongrong Wei ◽  
Anastasiia Leonteva ◽  
Jia Hong ◽  
...  

Abstract Background Peripheral blood leukocyte (PBL) DNA methylation may serve as a surrogate marker to evaluate the susceptibility to and prognosis of gastric cancer (GC). In this study, blood-derived DNA methylation levels of two tumour-related genes, namely, ZNF331 and WIF1, and their impacts on the risk and prognosis of GC were evaluated. Methods In total, 398 GC cases and 397 controls were recruited for the study. Then, all cases were followed up for 5 years. ZNF331 and WIF1 promoter methylation status in PBLs was measured using a methylation-sensitive high-resolution melting method. Logistic and Cox regression models were used to analyse the correlation between gene methylation and the risk and prognosis of GC. Confounders were balanced through propensity score (PS) matching. Results High ZNF331 methylation significantly decreased GC risk after PS adjustment (OR = 0.580, 95% CI: 0.375–0.898, P = 0.015), which also presented in males (OR = 0.577, 95% CI: 0.343–0.970, P = 0.038). However, WIF1 methylation was not associated with GC risk. Additionally, significant combined effects between ZNF331 methylation and the intake of green vegetables and garlic were observed (OR = 0.073, 95% CI: 0.027–0.196, P < 0.001 and OR = 0.138, 95% CI: 0.080–0.238, P < 0.001, respectively). Furthermore, ZNF331 and WIF1 methylation had no impact on the prognosis of GC. Conclusion ZNF331 methylation in PBLs may affect GC risk in combination with the consumption of green vegetables and garlic and may act as a potential biomarker of GC.

2013 ◽  
Vol 23 (2) ◽  
pp. 66-70
Author(s):  
Albertas Daukša ◽  
Antanas Gulbinas ◽  
Aurelija Kazlauskaitė ◽  
Johannes Oldenburg ◽  
Osman El-Maarri

Gastric cancers are usually diagnosed at an advanced stage in the progression of the disease, thus reducing the survival chances of the patients. Non-invasive early detection would greatly enhance therapy and survival rates. For this aim, we investigated tumor suppressor genes CDKN2A/p16, RARBeta, TNFRSF10C, APC, ACIN1, DAPK1, 3OST2, BCL2 and CD44 for methylation changes in peripheral blood leukocytes of gastric cancer patients. This study shows that methylation changes in peripheral blood leukocyte DNA could provide a promising method for the early detection of gastric cancer. However, larger studies are essential to explore the clinical usefulness of a peripheral blood leukocyte DNA methylation based tests for non-invasive early detection of gastric cancer.


2012 ◽  
Vol 18 (12) ◽  
pp. 2334-2341 ◽  
Author(s):  
Alan R. Harris ◽  
Dorottya Nagy-Szakal ◽  
Natalia Pedersen ◽  
Antone Opekun ◽  
Jiri Bronsky ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
pp. 53-63 ◽  
Author(s):  
Edward J. Fox ◽  
Guy J. Buckle ◽  
Barry Singer ◽  
Vibhuti Singh ◽  
Aaron Boster

Purpose of reviewTo provide neurologists with an update on the proposed mechanisms of action (MOAs) of disease-modifying therapies (DMTs) for the treatment of relapsing MS, and their effect on peripheral blood leukocytes, in order to inform treatment decisions.Recent findingsDMTs have vastly differing MOAs, including effects on peripheral blood leukocyte counts, particularly lymphocytes. The clinical implications of changes in lymphocyte counts need to be understood in the context of the underlying MOAs of each respective DMT, with treatment tailored to individual patient needs.SummaryDMTs can alter lymphocyte counts, subsets, activation, and distribution, and thus can influence immune surveillance. Serial monitoring of total leukocytes and absolute lymphocyte counts (ALCs) is advisable in patients receiving DMTs. ALCs should be interpreted regarding expected immunologic changes and individual patient characteristics. Any decision to switch DMTs should consider these factors, along with drug efficacy, safety, and effect on quality of life.


Endocrine ◽  
2009 ◽  
Vol 35 (2) ◽  
pp. 204-210 ◽  
Author(s):  
Sofia Movérare-Skrtic ◽  
Dan Mellström ◽  
Liesbeth Vandenput ◽  
Mathias Ehrich ◽  
Claes Ohlsson

Author(s):  
Bing Cui ◽  
Xiao Xiao ◽  
Jin’e Wang ◽  
Hongrui Wang ◽  
Cunjin Wu ◽  
...  

Abnormal thyroid hormone (TH) function has been observed in all components of metabolic syndrome (MetS), but the mechanisms remain unclear. Altered genomic methylation status is closely related to MetS. Our aim was to determine whether methylation regulation in TH function–related genes is involved in MetS. In a small strictly selected cohort, low TH function was observed in MetS group, as well as lower THRB promoter methylation levels in peripheral blood leukocytes in a genome-wide methylation screening by Illumina 450K beadchip. The results of beadchip assay were then confirmed by Sequenom MassARRAY. Low THRB promoter methylation levels and low TH function in MetS were confirmed in another big-size validation cohort. Lower methylation levels were associated with higher THRB expression in peripheral blood leukocytes, and altered THRB promoter methylation status influenced its promoter activity and expression. In the MetS rat models constructed by high fat and high fructose diet, lower TH function was also observed, as well as lower Thrb promoter methylation levels. Furthermore, systematic inflammation observed in MetS was found to induce decreased THRB promoter methylation levels as well as corresponding THRB expression. Additionally, oral treatment with a physiological T3 dose mitigated hypertension and insulin resistance and partially alleviated hepatic steatosis and adipocyte hypertrophy in MetS rats. Low methylation levels of THRB promoter in peripheral blood leukocytes induced by systematic inflammation were involved in low TH function in MetS, whereas low TH function deteriorates MetS. This might serve as a novel therapeutic target of MetS.


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