Bratisl Med J
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Gastric cancer is common and can be found throughout the world. Notoriously like other cancers, gastric cancer is a consequence of cellular regulation disorder. Epigenetics, including many oncogenes or tumour suppressor genes, can provide some clues for this kind of disorder. DNA methylation, especially promoter methylation, which causes the silence/decrease of tumour related genes, has become a focus in various tumour types. The aim of this study was to investigate promoter methylation of certain genes: p16, survivin, retinoblastoma (Rb), all of which have been regarded as genes related to gastric cancer. ⋯ In this study, promoter methylation was observed for the p16 gene, which was considered an early potential marker in gastric cancer. This data supports that further investigations should study Rb and survivin as candidate markers for gastric cancer (Tab. 2, Fig. 1, Ref. 35).
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To identify possible association between the selected HLA-G gene polymorphisms and risk of pre-eclampsia. ⋯ Genetic predisposition of HLA-G to pre-eclampsia in Slovak women was examined for the first time. No association between analysed HLA-G gene polymorphisms and susceptibility to pre-eclampsia was observed. Further investigations are needed to determine the role of immunosuppressive molecule HLA-G in pre-eclampsia development (Tab. 5, Fig. 2, Ref. 37).
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The aim of the present study was to reveal the possible effect of sulforaphane on oxidative stress and inflammation in rats liver with toxic hepatitis induced by acetaminophene. ⋯ Sulforaphane is a protective agent against acetaminophen-induced liver damage and it can be added in the treatment protocol (Tab. 1, Fig. 5, Ref. 51).
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To explore the role of the MAPK signaling pathway in the cardiomyocyte apoptosis of mice with post-infarction heart failure (HF). ⋯ MI was accompanied by ERS, probably involving the MAPK signaling pathway. SB203580, a specific inhibitor of this pathway, can relieve cardiomyocyte apoptosis and protect the myocardium by suppressing such stress (Tab. 3, Fig. 7, Ref. 20).