BACKGROUND & AIMS:We performed a systematic review and meta-analysis to comprehensively estimate adenoma miss rate (AMR) and advanced AMR (AAMR) and explore associated factors. METHODS: We searched the PubMed, Web of Science, and Ovid EMBASE databases for studies published through April 2018 on tandem colonoscopies, with AMR and AAMR as the primary outcomes. We performed meta-regression analyses to identify risk factors and factors associated with outcome. Primary outcomes were AMR and AAMR and secondary outcomes were AMR and AAMR for different locations, sizes, pathologies, morphologies, and populations. RESULTS: In a meta-analysis of 43 publications and more than 15,000 tandem colonoscopies, we calculated miss rates of 26% for adenomas (95% confidence interval [CI] 23%-30%), 9% for advanced adenomas (95% CI 4%-16%), and 27% for serrated polyps (95% CI 16%-40%). Miss rates were high for proximal advanced adenomas (14%; 95% CI 5%-26%), serrated polyps (27%; 95% CI 16%-40%), flat adenomas (34%; 95% CI 24%-45%), and in patients at high risk for colorectal cancer (33%; 95% CI 26%-41%). Miss rates could be decreased by adequate bowel preparation and auxiliary techniques (P ¼ .06; P ¼ .04, and P ¼ .01, respectively). The adenoma detection rate (ADR), adenomas per index colonoscopy, and adenomas per positive index colonoscopy (APPC) were independently associated with AMR (P ¼ .02, P ¼ .01, and P ¼ .008, respectively), whereas APPC was the only factor independently associated with AAMR (P ¼ .006). An APPC value greater than 1.8 was more effective in monitoring AMR (31% vs 15% for AMR P < .0001) than an ADR value of at least 34% (27% vs 17% for AMR; P ¼ .008). The AAMR of colonoscopies with an APPC value below 1.7 was 35%, vs 2% for colonoscopies with an APPC value of at least 1.7 (P ¼ .0005). CONCLUSIONS: In a systematic review and meta-analysis, we found that adenomas and advanced adenomas are missed (based on AMR and AAMR) more frequently than previously believed. In addition to ADR,

Angiogenesis is recognized as an important hallmark of cancer. Although telomerase is thought to be involved in tumor angiogenesis, the evidence and underlying mechanism remain elusive. Here, we demonstrate that human telomerase reverse transcriptase (hTERT) activates vascular epithelial growth factor (VEGF) gene expression through interactions with the VEGF promoter and the transcription factor Sp1. hTERT binds to Sp1 in vitro and in vivo and stimulates angiogenesis in a manner dependent on Sp1. Deletion of the mTert gene in the first generation of Tert null mice compromised tumor growth, with reduced VEGF expression. In addition, we show that hTERT expression levels are positively correlated with those of VEGF in human gastric tumor samples. Together, our results demonstrate that hTERT facilitates tumor angiogenesis by up-regulating VEGF expression through direct interactions with the VEGF gene and the Sp1 transcription factor. These results provide novel insights into hTERT function in tumor progression in addition to its role in telomere maintenance.

Background Accumulating data have suggested seizures occur frequently in patients with neuronal surface antibody‐mediated autoimmune encephalitis. We aimed to evaluate seizure outcomes and potential factors associated with the development of epilepsy in patients with anti‐N‐methyl‐D‐aspartate receptor (NMDAR), anti‐leucine‐rich glioma‐inactivated 1 (LGI1), and anti‐gamma‐aminobutyric‐acid B receptor (GABABR) encephalitis. Methods Patients with anti‐NMDAR, anti‐LGI1, and anti‐GABABR encephalitis were prospectively recruited from 2014 to June 2019, with a median follow‐up period of 30.5 months (range 8–67 months). Seizure outcomes were assessed and risk factors of epilepsy were analyzed. Results A total of 119 patients with anti‐NMDAR, anti‐LGI1, and anti‐GABABR encephalitis were included, and 83 (69.7%) of them developed new‐onset seizures. By the end of follow‐up, 17 (21.3%) of 80 patients had seizure relapses after intermittent seizure remission or exhibited uncontrolled seizure episodes, contributing to epilepsy. Immunotherapy delay and interictal epileptic discharges (IEDs) were identified to be associated with the development of epilepsy in patients with anti‐NMDAR, anti‐LGI1, and anti‐GABABR encephalitis, particularly anti‐NMDAR encephalitis. Furthermore, multivariate logistic regression analysis demonstrated that immunotherapy delay was an independent predictor for epilepsy. Conclusion Our study suggested that immunotherapy delay and IEDs were associated with the development of epilepsy in patients with anti‐NMDAR, anti‐LGI1, and anti‐GABABR encephalitis. Early diagnosis and treatment were required, and particular consideration should be given to patients with these risk factors.

Pyroptosis is a form of caspase-1-dependent programmed cell death with anti-tumor properties, but the underlying molecular mechanisms are not fully understood. The results of our study showed that the antihyperlipidemic drug simvastatin induced pyroptosis in non-small cell lung cancer (NSCLC) cell lines and a xenograft mouse model. Inhibition of pyroptosis attenuated the effects of simvastatin on tumor cell viability and migration. These data suggest that simvastatin may induce pyroptosis, thereby potentially serving as a novel therapeutic agent for NSCLC.

respectively. The disease stage and tumor differentiation subgroups showed significantly different detection sensitivities; the sensitivity was 10% in early-stage patients and 56% in advanced-stage patients (p = 0.0014). For patients with poorly differentiated tumors, the sensitivity was 77.8%, which was significantly different from those with highly differentiated (20%; p = 0.0230) and moderately differentiated tumors (19%; p = 0.0042). Conclusion: Blood analyses for EGFR mutations may be effectively used in advanced-stage patients or patients with poorly differentiated tumors.

Introduction: Disparities in the incidence, mortality, and survival of cancer types between urban and rural areas in China reflect the effects of different risk factor exposure, education, and different medical availability. We aimed to characterize the disparities in the incidence, mortality, and survivals of cancer types between urban and rural areas in Shanghai, China, 2002-2015.Materials and Methods: The incidence and mortality were standardized by Segi's world standard population. Trends in the incidence and mortality of cancers were compared using annual percent change. The 5-year observed and relative survivals were calculated with life table and Ederer II methods.Results: Age-standardized incidences and mortalities were 212.55/105 and 109.45/105 in urban areas and 210.14/105 and 103.99/105 in rural areas, respectively. Female breast cancer and colorectal cancer occurred more frequently in urban than in rural areas, quite in contrast to liver cancer and cervical cancer. Cancers of lung and bronchus, liver, stomach, and colon and rectum were the leading causes of cancer death in both areas. Age-standardized incidence of female breast cancer and colorectal cancer in urban areas increased while gastric cancer and liver cancer decreased in both areas. Age-standardized mortalities of cancers of breast, esophagus, stomach, colon and rectum, liver, and lung and bronchus decreased in both areas. For all cancers combined, the 5-year observed and relative survivals of cancer patients were higher in urban than in rural areas. The 5-year observed and relative survivals of cancers of liver, pancreas, stomach, brain and central nervous system (CNS), and prostate were higher in urban than in rural areas. The 5-year observed and relative survivals of cervical cancer were higher in rural than in urban areas.Conclusions: Factors promoting female breast cancer and colorectal cancer in urban areas and liver cancer and cervical cancer in rural areas should be specifically intervened in cancer prophylaxis. Improved medical services can greatly prolong the survival of major cancers in rural areas.

Background and aims: The contribution of hepatitis B virus (HBV) infection to the aggressiveness of primary liver cancer (PLC) remains controversial. We aimed to characterize this in eastern China. Methods: We enrolled 8,515 PLC patients whose specimens were reserved at the BioBank of the hepatobiliary hospital (Shanghai, China) during 2007–2016. Of those, 3,124 who received primary radical resection were involved in survival analysis. A nomogram was constructed to predict the survivals using preoperative parameters. Results: Hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (ICC), and combined hepatocellular cholangiocarcinoma (CHC) accounted for 94.6, 3.7, and 1.7%, respectively. The rates of HBV infection were 87.5, 49.2, and 80.6%, respectively. HBV infection was significantly associated with 10-year earlier onset, more cirrhosis, higher α-fetoprotein, higher carbohydrate antigen 19-9 (CA19-9), more microvascular invasion (MVI), lower neutrophil-to-lymphocyte ratio (NLR), and lower platelet-to-lymphocyte ratio (PLR) in HCC. HBV infection was also associated with 7-year earlier onset, more cirrhosis, higher α-fetoprotein, more MVI, and lower PLR in ICC. In the multivariate Cox analysis, high circulating HBV DNA, α-fetoprotein, CA19-9, NLR, tumor size, number, encapsulation, Barcelona Clinic Liver Cancer (BCLC) stage, and MVI predicted an unfavorable prognosis in HCC; only CA19-9 and BCLC stage, rather than HBV-related parameters, had prognostic values in ICC. A nomogram constructed with preoperative HBV-related parameters including HBV load, ultrasonic cirrhosis, and α-fetoprotein perform better than the current staging systems in predicting postoperative survival in HCC. Conclusion: HBV promotes the aggressiveness of HCC in Chinese population. The contributions of HBV to ICC and other etiological factors to HCC might be indirect via arousing non-resolving inflammation.

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