Notes

A good Intracellular Feeling and Sign Transduction System In which Manages the Metabolism regarding Polycyclic Perfumed Hydrocarbons in Germs.
LINC00963 was obviously up-regulated in bladder cancer cells. Knockdown of LINC00963 significantly reduced bladder cancer cells viability, colony formation, migration and invasion. Luciferase reporter experiment and RNA pulldown experiment revealed that LINC00963 promoted MTA1 expression via directly inhibiting miR-766-3p. MTA1 was up-regulated in bladder cancer patients. MTA1 up-regulation reversed the inhibitory effect of LINC00963 knockdown on bladder cancer cell viability, migration and invasion. Conclusion LINC00963 functions as an oncogene in bladder cancer by regulating the miR-766-3p/MTA1 axis.Background Epithelial-mesenchymal Transition (EMT) is involved in various cancers including glioblastoma. Our previous study has shown that miR-340 negatively correlated with EMT process in glioblastoma. Purpose In the present study, we aim to explore the underlying molecular mechanisms of miR-340 in EMT process of glioblastomas. Materials and methods Using RT-qPCR assay, we analyzed the expression of miR-340 in glioma cell lines and normal human glia (NHA) cell line. Using CCK8, Colony formation assays, transwell and Western blot assays, we investigated tumor growth and EMT process. Using luciferase reporter assay, we confirmed a target of miR-340. Results Our results showed that miR-340 was down-regulated in glioma cell lines (U87, U251 and LN229) compared to NHA cells. MiR-340 overexpression remarkably inhibited cell proliferation and invasion as well as up-regulated E-cadherin expression and down-regulated N-cadherin, Vimentin, ZEB1, Slug and Snail expressions in U251 and LN229 cells. Further studies have confirmed c-MET as a target gene of miR-340. The EMT-inhibitory effect of miR-340 was lost after c-MET expression was restored. We also identified the antitumorigenic activity of miR-340 in vivo. Conclusion These results demonstrated that miR-340 functioned as a tumor suppressor via targeting EMT process and could be a potential therapeutic candidate for treating glioblastomas.Objective To investigate the clinical safety, efficacy, therapeutic outcomes and risk factors of computed tomography-guided percutaneous cryoablation (CT-PCRA) for subcardiac hepatocellular carcinoma (HCC). Patients and methods In this study, patients with single HCC nodules located on the left lobe who subsequently underwent CT-PCRA were reviewed from July 2012 to August 2016. According to the definition of subcardiac HCC, the patients were grouped into the subcardiac HCC group (n=33) and the non-subcardiac HCC group (n=40). The technical success rates, tumour response rates, oncological outcomes including overall survival (OS) and recurrence-free survival (RFS) and complications were compared. Multivariate analysis was performed on clinicopathological variables to identify factors affecting long-term outcomes. Results Seventy-three patients with subcardiac HCC were included in this study. After a median follow-up time of 37.8 months, 27.4% (20/73) of the patients died. The technical success and complete response rates were not significantly different between the two groups (p = 1.000; p = 0.590). The cumulative OS and RFS of the subcardiac HCC group were comparable to those of the non-subcardiac HCC group (p =0.820, p =0.922). Two major complications, intra-abdominal bleeding and right pleural effusion, were found at 2.2 and 3.1 months in the subcardiac HCC group, which were comparable with those in the non-subcardiac HCC group (p = 0.683). The multivariate analysis results showed that older age (hazard ratio [HR] 2.382, 95% confidence interval [CI] 1.884-7.823; p = 0.038) and ALBI grade 2-3 (HR 3.398, 95% CI 1.950-6.058; p = 0.021) may be predictors of poor OS and that tumour size ≥3 cm in diameter (HR 3.302, 95% CI 2.232-8.293; p = 0.012) may be a predictor of poor RFS. Conclusion CT-PCRA for subcardiac HCC can be performed safely and efficiently and contribute to improving survival prognosis.[This corrects the article DOI 10.2147/CMAR.S250171.].Objective To investigate the curative and adverse effects (AEs) of additional use of nimotuzumab combined with induction chemotherapy and concurrent chemoradiotherapy in unresectable locoregionally advanced hypopharyngeal carcinoma. Patients and methods We retrospectively evaluated 36 patients with stage III or IVA hypopharyngeal carcinoma who received induction chemotherapy followed by concurrent chemoradiotherapy with or without nimotuzumab. The induction chemotherapy included two or three cycles of TPF regimen. The intensity-modulated radiation therapy (IMRT) dose was 70 Gy to the planning target volume. Concurrent with radiotherapy, patients received chemotherapy consisting of cisplatin q3w. Adjuvant chemotherapy consisting of TPF regimen was administered 1 month later after concurrent chemoradiotherapy. Nimotuzumab (200 mg day 1, q3w) was given to patients concurrently with induction chemotherapy and was administered concurrently with IMRT at a weekly dose of 200 mg. Results After induction chemotherapy,ents without using nimotuzumab. Caerulein mouse The toxicity was tolerable.Purpose Molecular characteristics using gene-expression profiling can undoubtedly improve the prediction of treatment responses, and ultimately, the clinical outcome of cancer patients. We aimed at developing a genetic signature to improve the prediction of chemosensitivity and prognosis of patients with colorectal cancer (CRC). Patients and methods We analyzed microarray data of 32 CRC patients to explore the potential functions and pathways involved in the disease relapse in CRC. Gene expression profiles and clinical follow-up information of GSE39582, GSE17536, and GSE103479 were downloaded from the Gene Expression Omnibus database (GEO) to identify prognostic genes. Eventually, a model of 15-mRNA signature was established, in which its efficacy for predicting chemosensitivity and prognosis was examined. Results Based on the proposed model of 15-mRNA signature, the test series patients could be classified into high-risk or low-risk subgroup with significantly different overall survival (OS) rate (hazard ratio [HR]=1.48, 95% confidence interval [CI]=1.30-1.70, P≤0.001). The prognostic value of this 15-mRNA signature was confirmed in another validation series. Further analysis revealed that the prognostic value of this signature was independent of the TNM stage and can predict adjuvant chemosensitivity of patients with early-stage CRC. Conclusion We identified a novel 15-mRNA signature in patients with CRC, which could be clinically helpful in the prognosis evaluation and the process of selection of patients with early-stage CRC for undergoing adjuvant chemotherapy.Purpose Hepatic injury is a common side effect following tyrosine kinase inhibitor (TKI) therapy and our understanding usually comes from clinical trials. In this retrospective study, we aimed to investigate the characteristics, risk factors and regimen-related differences of epidermal growth factor receptor (EGFR)-TKI-related hepatic toxicity in patients with advanced lung adenocarcinoma (LAD). Patients and methods Liver function tests were documented in 424 patients admitted into the Shanghai Chest Hospital between January 2014 and December 2016 with advanced (IIIB/IV) LAD who received first-line gefitinib, erlotinib or icotinib. Hepatotoxicity was graded according to the Common Terminology Criteria for Adverse Events (CTCAE), version 4.0. The clinical spectrum and onset time of hepatic injury were evaluated. The risk factors of hepatic dysfunction were determined using a logistic regression analysis. Results A total of 87 (20.5%) patients experienced hepatotoxicity and 5.7% were of grade 3/4 liver dysfunction. The median onset time of hepatotoxicity was 7 weeks. Presence of hepatitis virus (HR 2.593, 95% CI 1.090-6.170, P=0.031) and pretreatment liver impairment (HR 3.460, 95% CI 1.746-6.855, P less then 0.001) were risk factors associated with increased risk of hepatotoxicity. Gefitinib (HR 1.872, 95% CI 1.028-3.412, P=0.040) and erlotinib (HR 3.578, 95% CI 1.683-7.609, P=0.001) had increased risk of hepatotoxicity compared to icotinib. Conclusion The different toxic profile of EGFR-TKIs should be taken into account in the choice of treatment based on the patients' comorbidity.Background The role of circular RNA (circRNA) in papillary thyroid cancer (PTC) is largely unknown. This study aims to determine the function and mechanism of circPRMT5 in the regulation of PTC development. Methods PTC tissues and cell lines were used to determine circPRMT5 expression via quantitative real-time polymerase chain reaction. Small interfering RNA (siRNA) was utilized to knock down circPRMT5. Proliferation was analyzed through CCK8 and colony formation assays. Transwell assay was performed to determine cell migration and invasion. Luciferase assay and RIP assay were carried out to analyze the interaction between circPRMT5 and miR-30c. Results CircPRMT5 expression was upregulated in PTC tissues and cell lines. And circPRMT5 level was positively linked with advanced stage and lymph node metastasis. CircPRMT5 knockdown inhibited proliferation, migration and invasion while inducing apoptosis. CircPRMT5 worked as a competing endogenous RNA for miR-30c. By inhibiting miR-30c, circPRMT5 promoted the expression of E2F3. Conclusion Our findings demonstrate that circPRMT5 acts as an oncogenic circRNA to promote PTC progression via regulating miR-30c/E2F3 axis.Background This study was designed to investigate the prognostic value of the lymphocyte to monocyte ratio (LMR) in patients with gallbladder carcinoma (GBC). Patients and methods We retrospectively enrolled 154 consecutive GBC patients from 2005 to 2017 in this study. The LMR of preoperative blood samples was calculated by dividing the lymphocyte count by the monocyte count. A receiver operating characteristic (ROC) curve was employed to identify the optimal cut-off value of the LMR in the determination of overall survival (OS). The Kaplan-Meier method was utilized to assess OS, and the Log rank test was employed to compare survival differences. Univariate and multivariate Cox regression analyses were conducted to detect independent prognostic indicators. Results The optimal cut-off point for the LMR was 4.76 according to the ROC curve. Patients ≤60 years old with an LMR ≤4.76 experienced significantly worse OS than those with an LMR >4.76 (hazard ratio (HR) 0.399, 95% confidence interval (CI) 0.265-0.602, P4.21 (HR 1.830, 95% CI 1.129-2.967, P=0.014). Multivariate Cox regression analysis indicated that both the high and low LMR cut-off values were independent risk factors for OS (HR 0.272, 95% CI 0.105-0.704, P=0.007; HR 0.544, 95% CI 0.330-0.895, P=0.017). Conclusion The LMR is an independent prognostic indicator for GBC patients, the cut-off value of which is age dependent.Purpose Adenocarcinoma of the esophagogastric junction (AEG) patient immune characteristics were analyzed in this study, and these features were compared with patient clinical pathology and prognosis. Patients and methods The clinicopathological data and prognostic information of 96 AEG patients who were admitted to Ren Ji Hospital between December 2008 and December 2015 were collected. PD-1/PD-L1, Tim-3/Gal-9, and CD3/CD8/Foxp3 expression in these patients, as well as the correlation of the expression of these molecules with clinicopathological data and survival time, were analyzed. Comparisons of count data were performed using the chi-square test or Fisher's exact test. The survival rate and survival curves were calculated and drawn, respectively, with the Kaplan-Meier method, and the Log rank test was used for survival analysis. Results The positive rate for PD-L1 and Gal-9 in these AEG patients was 30.21% and 31.25%, respectively. Tim-3 positivity had a close relationship with patient Siewert type. CD8+ T cell infiltration and patient TNM stage, as well as CD3+CD8+ T cell infiltration and patient Lauren type, had a close relationship based on analysis of the correlation between immune factor expression and clinicopathological data.
Homepage: https://www.selleckchem.com/products/caerulein.html