BackgroundAnti-fibrotic, anti-VEGF (vascular endothelial growth factor) medications, or radiotherapy, as adjuvant for pterygium surgical procedure, has been suggested for reducing recurrence, but difficulties may be experienced in deciding which treatment to use. The purpose of this study was to compare the efficacies of these different adjuvants for preventing recurrence following pterygium surgery.MethodsWe conducted a systematic review to identify randomized controlled trials of patients with primary or recurrent pterygium who received anti-fibrotic, anti-VEGF medication, or radiotherapy as adjuvants in combination with surgical procedure. The surgical procedure contained bare sclera technique or petrygium excision combination with tissue grafting. The primary outcome of this study was recurrence. Direct-comparison and Bayesian network meta-analyses were performed to assess direct and indirect evidence of efficacy.ResultsWe obtained data from 34 randomized controlled trials, representing a total of 2483 patients. Adjuvants included bevacizumab, 5-FU (5-fluorouracil), MMC (mitomycin C), and β-RT (beta-radiotherapy). Compared with placebo, we found distinguishable improvement in recurrence with bevacizumab (odds ratio [OR] 0.38, 95% confidence interval [CI] 0.18–0.80), MMC (0.12, 95% CI 0.06–0.21), and β-RT (0.17, 95% CI 0.04–0.69), but not with 5-FU (0.41, 95% CI 0.12–1.39). MMC significantly reduced recurrence when compared to bevacizumab (0.31, 95% CI 0.13–0.77) and 5-FU (0.28, 95% CI 0.08–0.99). The probability of having the most recurrences after excision was lowest for MMC, followed by bevacizumab and β-RT. Similar results were found in subgroup analyses, including for primary pterygium, and the patients receiving bare sclera technique or conjunctival autograft.ConclusionsAdjuvants such as MMC, bevacizumab, and β-RT could effectively prevent recurrence following pterygium excision. However, their efficacy and acceptability require further clarification in future randomized controlled trials.Electronic supplementary materialThe online version of this article (10.1186/s12886-017-0601-5) contains supplementary material, which is available to authorized users.

The epigenetic silencing of tumor suppressor genes in myelodysplastic syndromes (MDS) can potentially confer a growth advantage to individual cellular clones. Currently, the recommended treatment for patients with high-risk MDS is the methylation agent decitabine (DAC), a drug that can induce the reexpression of silenced tumor suppressor genes. We investigated the effects of DAC treatment on the myeloid MDS cell line SKM-1 and investigated the role of FOXO3A, a potentially tumor-suppressive transcription factor, by silencing its expression prior to DAC treatment. We found that FOXO3A exists in an inactive, hyperphosphorylated form in SKM-1 cells, but that DAC both induces FOXO3A expression and reactivates the protein by reducing its phosphorylation level. Furthermore, we show that this FOXO3A activation is responsible for the DAC-induced differentiation of SKM-1 cells into monocytes, as well as for SKM-1 cell cycle arrest, apoptosis, and autophagy. Collectively, these results suggest that FOXO3A reactivation may contribute to the therapeutic effects of DAC in MDS.

Purpose: Autologous blood has been used exploratively with conjunctival autograft in pterygium surgery. However, it is controversial whether autologous blood performed better than other fixation methods, including fibrin glue and sutures. This meta-analysis was conducted to evaluate the effectiveness of using autologous blood in pterygium surgery with conjunctival autograft. Methods: The study was conducted according to the PRISMA guidelines. The MEDLINE, Cochrane library, and Embase databases were systematically searched from their establishment until April 1, 2018. Randomized controlled trials comparing autologous blood with fibrin glue/suture in pterygium surgery with conjunctival autograft were included. The methodological quality of the included studies was assessed using the Cochrane risk of bias tool. Outcome measurements were recurrence, graft displacement, graft retraction, and surgical duration. Review Manager 5.3 (Cochrane Community, Cochrane Collaboration, London, UK) was used to perform the statistical analysis. When I2 < 50%, statistical heterogeneity was considered acceptable, and a fixed-effects model was adopted; alternatively, the random-effects model was used. Results: Seven randomized controlled trials including 516 patients were finally included in the meta-analysis. Four studies with 379 patients compared autologous blood and fibrin glue. Autologous blood was inferior to fibrin glue with respect to surgical duration, graft retraction, and graft displacement. However, there was no statistical difference between the 2 groups in terms of the recurrence rate. Four studies with 152 patients compared autologous blood and traditional suturing. Autologous blood was superior to sutures in terms of surgical duration and inferior to sutures in terms of graft retraction. No difference was detected in terms of graft displacement and recurrence rate. Conclusions: In conclusion, autologous blood is an appropriate method for graft fixation in pterygium surgery. Current research suggests that autologous blood derivatives may be a promising approach after pterygium excision. However, this requires further confirmation.

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Mesenchymal epithelial transition (C-MET) factor overexpression has been found in many types of cancer and has served as an important molecular target for therapeutic intervention. However, the role of C-MET in retinoblastoma remains largely unclear.The present study aimed to investigate the potential role and mechanism of C-MET in Y79 retinoblastoma cells. We found that C-MET was highly expressed in Y79 retinoblastoma cells, and, in addition, the levels of C-MET were positively correlated with cell proliferation and retinoblastoma growth. Inhibition of C-MET suppressed Y79 retinoblastoma cell proliferation and tumour growth. Mechanistically, we showed that HGF-induced C-MET-dependent signal transduction resulted in ERK 1/2 phosphorylation, which subsequently promoted the nuclear translocation of PKM2. Nuclear PKM2 further interacted with histone H3 and contributed to C-MET-dependent cyclin D1 and c-Myc expression and cell proliferation. These findings highlight the role of C-MET in Y79 retinoblastoma cells and reveal a C-MET-dependent signal transduction mechanism. C-MET may be a potential therapeutic target for retinoblastoma.Significance of the study: We demonstrated a new target of retinoblastoma, C-MET. C-MET-dependent signal transduction promotes Y79 retinoblastoma cell proliferation and tumour growth through ERK 1/2/PKM2/histone H3 signalling pathway. C-MET may be a potential target for retinoblastoma therapy.