SummaryBackground Although some features of dermatomyositis (DM) and polymyositis (PM) have been reported as possible prognostic indicators for cancer development, previous studies were small in size and were unable to establish a definitive relationship between neoplasms and DM and PM. Objectives To evaluate risk factors for developing malignancies in patients with DM and PM. Methods Meta-analysis of the studies reported in the literature was performed to unveil risk factors for developing cancer among patients with DM and PM. The included studies were either cohort or retrospective case-control studies with information on cancer status. Risk for malignancy was determined as the odds ratio (OR) or weighted mean difference (WMD) with a 95% confidence interval (CI), determined by fixed and random effects models. Stata 10.0 software was used to identify possible publication bias. Results Twenty studies with 380 patients and 1575 controls were included in the analysis. The factors that may increase the risk of cancer in patients with DM and PM were older age (WMD 11Á41, 95% CI 9Á84-12Á98), male sex (OR 1Á92, 95% CI 1Á49-2Á48), cutaneous necrosis (OR 5Á52, 95% CI 3Á49-8Á74) and dysphagia (OR 2Á41, 95% CI 1Á50-3Á86), whereas those that may provide protection against cancer included arthritis (OR 0Á38, 95% CI 0Á24-0Á61) and interstitial lung disease (OR 0Á32, 95% CI 0Á20-0Á51). Conclusions Our data suggest that age, sex, cutaneous necrosis, dysphagia, arthritis and lung complications may influence susceptibility to cancer in patients with DM and PM.

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Background/Aims: Acute myocardial infarction (AMI) occurs when blood supply to the heart is diminished (ischemia) for long time; ischemia is primarily caused due to hypoxia. The present study evaluated the effects of long non-coding RNA H19 on hypoxic rat H9c2 cells and mouse HL-1 cells. Methods: Hypoxic injury was confirmed by measuring cell viability, migration and invasion, and apoptosis using MTT, Transwell and flow cytometry assays, respectively. H19 expression after hypoxia was estimated by qRT-PCR. We then measured the effects of non-physiologically expressed H19, knockdown of miR-139 with or without H19 silence, and abnormally expressed Sox8 on hypoxia-induced H9c2 cells. Moreover, the interacted miRNA for H19 and downstream target gene were virtually screened and verified. The involved signaling pathways and the effects of abnormally expressed H19 on contractility of HL-1 cells were explored via Western blot analysis. Results: Hypoxia induced decreases of cell viability, migration and invasion, increase of cell apoptosis and up-regulation of H19. Knockdown of H19 increased hypoxia-induced injury in H9c2 cells. H19 acted as a sponge for miR-139 and H19 knockdown aggravated hypoxia-induced injury by up-regulating miR-139. Sox8 was identified as a target of miR-139, and its expression was negatively regulated by miR-139. The mechanistic studies revealed that overexpression of Sox8 might decrease hypoxia-induced cell injury by activating the PI3K/AKT/mTOR pathway and MAPK. Besides, H19 promoted contractility of HL-1 cells. Conclusion: These findings suggest that H19 alleviates hypoxia-induced myocardial cell injury by miR-139-mediated up-regulation of Sox8, along with activation of the PI3K/AKT/mTOR pathway and MAPK.

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