Narrow band imaging (NBI) is a real-time imaging technique. The aim of this meta-analysis was to estimate the sensitivity, specificity, and diagnostic accuracy on the role of NBI in the detection and characterization of specialized intestinal metaplasia (SIM), high-grade dysplasia (HGD) in the Barrett's esophagus. We identified studies by performing a literature search of Medline, EMBASE, and the Cochrane Library databases up to May 2013. We performed data analysis using Meta-DiSc (version 1.4) software. To assess study quality and potential for bias, we used the Quality Assessment of Diagnostic Accuracy Studies-2 tool (QUADAS-2). Overall, seven eligible studies including over 3988 lesions of 502 patients were retrieved. The results showed that endoscopic diagnosis of dysplasia performed using NBI has a high diagnostic performance, with an area under the summary receiver operating characteristic (SROC) curve near 0.90 both in HGD lesions and SIM lesions. We also found that NBI has a sensitive and specificity of 0.91 (95% confidence interval [CI] = 0.86-0.94) and 0.85 (95% CI = 0.76-0.92) on a per-patient element, and 0.97 (95% CI = 0.95-0.98) and 0.64 (95% CI = 0.59-0.68) on a per-lesion element for SIM diagnosis, respectively. The pooled per-patient sensitivity and specificity for identifying HGD are 0.91 (95% CI = 0.75-0.98) and 0.95 (95% CI = 0.91-0.97). The pooled per-lesion sensitivity and specificity for identifying HGD are 0.69 (95% CI = 0.63-0.74) and 0.90 (95% CI = 0.88-0.91). In conclusion, we found that endoscopic diagnosis with NBI is an accurate test to diagnosis dysplasia of Barrett's esophagus.
The tumor microenvironment significantly affects tumor progression, and tumor cells can also remodel the tumor microenvironment through complex interaction. Inflammasomes are innate immune system receptors/sensors that regulate an inflammatory response mainly mediated by the nucleotide-binding oligomerization domain-like receptors in macrophages, which can also influence the formation, progression and therapeutic response of cancer. However, the effects of tumorderived factors in the microenvironment on inflammasomes have rarely been reported. In this study, we found that lactate, as the main metabolite of tumor cells could specifically activate the nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain-containing protein 3 inflammasome through increasing the level of reactive oxygen species (ROS) in THP-1-derived macrophages. Fur
DDX39B (also called UAP56 or BAT1) which is a kind of DEAD-box family helicase plays pivotal roles in mRNA binding, splicing, and export. It has been found upregulated in many kinds of tumors as an oncogene. Nevertheless, the underlying molecular mechanisms of DDX39B in the proliferation of human colorectal cancer (CRC) remain fairly elusive. In our study, function experiments including the CCK8 and colony formation assay revealed that DDX39B facilitates CRC proliferation in vitro. DDX39B knockdown cells were administered for the orthotopic CRC tumor xenograft mouse model, after which tumor growth was monitored and immunohistochemistry (IHC) was performed to prove that DDX39B can also facilitates CRC proliferation in vivo. Flow cytometry demonstrated that DDX39B promotes the proliferation of CRC cells by driving the cell cycle from G0/G1 phase to the S phase. Mechanistically, RNA-binding protein immunoprecipitation-sequencing (RIP-seq) confirmed that DDX39B binds directly to the first exon of the CDK6/CCND1 pre-mRNA and upregulates their expression. Splicing experiments in vitro using a RT-PCR and gel electrophoresis assay confirmed that DDX39B promotes CDK6/CCND1 pre-mRNA splicing. Rescue experiments indicated that CDK6/CCND1 is a downstream effector of DDX39B-mediated CRC cell proliferation. Collectively, our results demonstrated that DDX39B and CDK6/CCND1 direct interactions serve as a CRC proliferation promoter, which can accelerate the G1/S phase transition to enhance CRC proliferation, and can offer novel and emerging treatment strategies targeting this cell proliferation-promoting gene.
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