Translational research : the journal of laboratory and clinical medicine
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The clinical efficacy of organ protection interventions are limited by the redundancy of cellular activation mechanisms. Interventions that target epigenetic mechanisms overcome this by eliciting genome wide changes in transcription and signaling. We aimed to review preclinical studies evaluating the organ protection effects of histone deacetylase inhibitors (HDACi) with a view to informing the design of early phase clinical trials. ⋯ HDACi administration resulted in myocardial, brain and kidney protection across diverse species and injuries that was attributable to increases in prosurvival cell signaling, and reductions in inflammation and programmed cell death. Heterogeneity in the analyses of secondary outcomes was explained by differences in species, type of injury, HDACi class (Class I better), drug (trichostatin better), and time of administration (at least 6 hours prior to injury better). These findings highlight a potential novel application for HDACi in clinical settings characterized by acute organ injury.
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Metadherin (MTDH) was found to be highly expressed in various squamous cell carcinomas (SCCs); however, meta-analysis evaluating the association of MTDH in SCC has not been performed. The purpose of this study was to explore the biological functions of MTDH in esophageal squamous cell carcinoma (ESCC) and to meta-analyze the association between MTDH and SCC. Immunohistochemistry was performed to examine MTDH expression using an ESCC tissue array consisting of 86 ESCC and 78 paired normal adjacent tissues (NATs). ⋯ Knockdown of MTDH using an MTDH-short hairpin RNA plasmid caused cell cycle arrest at the G0/G1 phase and induced apoptosis of EC9706 cells. Knockdown of MTDH suppressed the proliferation, invasion, and migration of ESCC cells. Furthermore, meta-analysis revealed that overexpression of MTDH was significantly associated with the lymph node metastasis, advanced clinical stage, and T classification of tissues in SCC, suggesting that MTDH might be used as a potential therapeutic target in the lymph node metastasis of ESCC.
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The diagnostic value of tumor markers, carcinoembryonic antigen (CEA), cancer antigen (CA) 15-3, CA 19-9, CA 125, cytokeratin fragment (CYFRA), and neuron-specific enolase (NSE) in pleural fluid to differentiate between benign and malignant pleural effusion (MPE) has not yet been clearly established. A review of English language studies using human subjects was performed. Sensitivity and specificity values of the chosen tumor markers were pooled using a random effects model to generate hierarchical summary receiver operator curves to determine the diagnostic performance of each tumor marker. ⋯ Although these tumor markers exhibit high specificity, the low sensitivity of each marker limits the diagnostic value. We conclude that tumor markers used individually are of insufficient diagnostic accuracy for clinical use. Tumor markers used in various combinations or from serum may have some potential worth further investigation.