034). However, disease free survival rate was not different statistically (

=0.938).

These findings suggest that rs36115365 may contribute to the progression of NSCLC.

These findings suggest that rs36115365 may contribute to the progression of NSCLC.

Tspan8 (tetraspanin 8) plays critical roles in cell adhesion and motility. Recently, Tspan8 overexpression has been found in various tumors. However, its expression status and prognostic significance in clear cell renal cell carcinoma (ccRCC) remains unknown. The objective of the present study was to assess the expression of Tspan8 and its correlation with clinicopathological features in ccRCC.

Tspan8 expression was detected in 150 cases of ccRCC and matched paracancerous tissues by immunohistochemistry (IHC) and its relevance with prognosis was analyzed.

Our data showed that the high-expression rate of Tspan8 in ccRCC tissues was 74.0%, which was significantly higher than those in paracancerous kidney tissues (43.3%,

=0.001). Meanwhile, Tspan8 expression was positively correlated with tumor size and WHO/ISUP grade in ccRCC. Significantly, Kaplan-Meier analysis and log-rank test revealed that Tspan8 higher expression was associated with poorer overall survival (OS) in ccRCC patients (

<0.05). Cox regression analysis further showed that Tspan8 was a significant independent negative prognostic factor for these patients.

Tspan8 is overexpressed in ccRCC and indicates poor prognosis, suggesting potential roles of Tspan8 in prognostication and targeted therapy.

Tspan8 is overexpressed in ccRCC and indicates poor prognosis, suggesting potential roles of Tspan8 in prognostication and targeted therapy.Dravet syndrome, one of the epileptic encephalopathies of childhood, is a genetic epilepsy caused by SCN1A mutation in 70-80% of the cases. Other genetic variants have been revealed in SCN1A-negative patients with Dravet syndrome. check details We investigated the utility of targeted gene panel testing in patients with Dravet syndrome and delineated the genotype-phenotype correlation. Targeted epilepsy gene panel testing including 40 genes was performed in 24 patients clinically diagnosed with Dravet syndrome. Detected variants were classified according to the guidelines of American College of Medical Genetics and Genomics 2015 and validated by Sanger sequencing. We investigated the relationship between clinical characteristics and genetic mutations. Causative variants including 16 SCN1A and two PCDH19 mutations were detected in 18 patients (75.0%). There were 27 variants with uncertain significance related to diverse genes other than SCN1A Analysis of clinical phenotypes of the detected variants did not reveal significant differences in patients with those variants. Dravet syndrome can be caused by various disease-causing variants whose clinical manifestations may differ according to the causative genes. Therefore, targeted epilepsy gene panel testing is efficient for genetic diagnosis of Dravet syndrome and may help in establishing therapeutic plans and forecasting disease course and prognosis.

Patients with epithelial ovarian cancers experience the highest fatality rates among all gynecological malignancies which require development of novel treatment strategies. Tumor cell necrosis was previously reported in a number of cancer cell lines following treatment with a p53-derived anti-cancer peptide called PNC-27. This peptide induces necrosis by transmembrane pore formation with HDM-2 protein that is expressed in the cancer cell membrane. We aimed to extend these studies further by investigating expression of membrane HDM-2 protein in ovarian cancer as it relates to susceptibility to PNC-27.

Herein, we measured HDM-2 membrane expression in two ovarian cancer cell lines (SKOV-3 and OVCAR-3) and a non-transformed control cell line (HUVEC) by flow cytometric and western blot analysis. Immunofluorescence was used to visualize colocalization of PNC-27 with membrane HDM-2. Treatment effects with PNC-27 and control peptide were assessed using a MTT cell proliferation assay while direct cytotoxicity was described in a number of solid tissue and hematologic malignancies.

Our results suggest that HDM-2 is highly expressed in the membranes of these ovarian cancer cell lines and colocalizes with PNC-27. We therefore conclude that the association of PNC-27 with preferentially expressed membrane HDM-2 isoforms results in the proposed model for the formation of transmembrane pores and epithelial ovarian cancer tumor cell necrosis, as previously described in a number of solid tissue and hematologic malignancies.

Tuberculosis (TB) is the most common cause of acquired immune deficiency syndrome (AIDS)-related deaths worldwide. The purpose of this study was to identify genes that are significant for the mechanisms involved in Mycobacterium tuberculosis (MTB) and human immunodeficiency virus (HIV) co-infection.

We selected 113 HIV/TB and 109 HIV/LTBI (latent TB infection) genes from GSE37250 and GSE69581 datasets. The Database for Annotation, Visualization and Integrated Discovery (DAVID) was used for Kyoto Encyclopedia of Gene and Genome (KEGG) pathway and gene ontology (GO) analyses. The protein-protein interaction (PPI) network of common differentially expressed genes (DEGs) were visualized using Cytoscape software with Search Tool for the Retrieval of Interacting Genes (STRING).

A total of 83 DEGs were found to be common to both datasets. These included 64 up-regulated genes and 19 down-regulated genes. The PPI network was analyzed, and 12 up-regulated genes were identified. Re-analysis using DAVID found no significant signaling pathways enriched by these twelve genes (CAMP, CTSG, DEFA1, DEFA1B, DEFA3, DEFA4, ELANE, HP, HPSE, OLFM4, PGLYRP1, TCN1).

Twelve significantly up-regulated DEGs that may be potential therapeutic targets for HIV/TB were identified using a series of bioinformatics analytical methods.

Twelve significantly up-regulated DEGs that may be potential therapeutic targets for HIV/TB were identified using a series of bioinformatics analytical methods.Treatment-free remission (TFR) is emerging as a new therapy goal for chronic myeloid leukemia (CML) patients in the tyrosine kinase inhibitors (TKI) era. Data indicates the unfavorable success rate of TFR. This study aimed to compare and evaluate the clinical value of dd-PCR in predicting relapse in CML patients entering TFR. Using dd-PCR and RT-qPCR technology, dynamic BCR/ABL transcripts were detected in 13 CML patients who discontinued TKI treatment after sustaining undetectable BCR-ABL levels for a median time of 25 months. The results showed that in 13 patients, only 2 cases (22.2%) of 9 patients who executed planned discontinuation achieved TFR within 12 months. In the first 6 months, the detection rate of BCR/ABL transcripts by dd-PCR was higher than that by RT-qPCR and the two methods kept a positive correlation (r=0.9651, P=0.0349). Meanwhile, the time of detectable BCR/ABL by dd-PCR were significantly shorter (P less then 0.05), which was an average of 2.98 months earlier than RT-qPCR. The total TKI therapy and MR4.