Pollution increases the chance of pulmonary embolism a new metaanalysis

Gastric cancer (GC) with lymph node metastasis (LNM) at diagnosis is associated with a unstable prognosis and indefinite survival times. The aim of the present study was to construct and validate a model for the Overall survival (OS) estimation for patients with LNM. The nomogram was constructed to predict the OS for LNM-positive GC using the primary group of 836 patients and validated using an independent cohort of 411 patients. Factors in the nomogram were identified by multivariate Cox hazard analysis. The predictive capability of nomogram was evaluated by calibration analysis and decision curve analysis. Multivariate analysis suggested that eight pre-treatment characteristics were used for developing the nomogram. In the primary cohort, the C-index for OS prediction was 0.788 (95% CI 0.753-0.823), while in validation cohort, the C-index for OS prediction was 0.769 (95% CI 0. 720-0.818). The calibration plot for the probability of OS and decision curve analyses showed an optimal agreement. Based on the nomogram, we could divided patients into three groups low-risk group, middle-risk group and a high-risk group(p less then 0.001).Taken together, we have provided an easy-to-used and accurate tool for predicting OS, furthermore could be used for risk stratification of OS of LNM-positive GC patients. © The author(s).Gastric cancer (GC) is one of the most common malignant tumors worldwide. Peripheral myelin protein 22 (PMP22) is a 22-kDa tetraspan glycoprotein that is predominantly expressed by myelinating Schwann cells. However, recent studies have shown that PMP22 is closely related to cell proliferation and tumorigenesis in different cancers. In this study, we discovered a new miRNA that regulates PMP22 and gastric cancer cell prolifration. Our bioinformatics analysis suggested that there is a conserved miRNA recognition site for miR-139-5p on the 3' UTR of PMP22. Bcl-2 inhibitor Interestingly, our results showed overexpression of miR-139-5p significantly suppressed growth and prolifration in GC cells and inhibited tumor growth in nude mice xenografted with GC cells. MiR-139-5p suppressed the activity of a luciferase reporter containing the PMP22-3' UTR, and the ectopic expression of PMP22 rescued the miR-139-5p-mediated inhibition of cell proliferation in GC cells. Mechanistically, miR-139-5p may negatively regulate PMP22 to repress cell proliferation by targeting the NF-κB signaling pathway in gastric cancer. Finally, overexpression of miR-139-5p significantly inhibited tumor growth in nude mice xenografted with GC cells.and the miR-139-5p levels were inversely correlated with PMP22 expression in nude mice tumor. Taken together, our data suggest an important regulatory role of miR-139-5p in gastric cancer, suggesting that miR-139-5p and PMP22 might be important diagnostic or therapeutic targets for gastric cancer and other human diseases. © The author(s).Intrahepatic cholangiocarcinoma (ICC) is a lethal malignancy with high mortality and lack of effective therapeutic targets. Here, we found that expression of cyclin-dependent kinase 7 (CDK7) was significantly associated with higher tumor grade and worse prognosis in 96 ICC specimens. Depletion of CDK7 significantly inhibited cell growth, induced a G2/M cell cycle arrest, and reduced the migratory and invasive potential in ICC cells. Subsequent experiments demonstrated that ICC cells were highly sensitive to the CDK7 inhibitor THZ1. A low concentration of THZ1 markedly inhibited cell growth, cell cycle, migration, and invasion in ICC cell lines. RNA-sequencing (RNA-seq) analysis revealed that THZ1 treatment decreased the levels of massive oncogene transcripts, particularly those associated with cell cycle and cell migration. Quantitative reverse transcriptase PCR (qRT-PCR) analysis confirmed that transcription of oncogenes involved in cell cycle regulation (AURKA, AURKB, CDC25B, CDK1, CCNA2, and MKI67) and the c-Met pathway (c-Met, AKT1, PTK2, CRK, PDPK1, and ARF6) was selectively repressed by THZ1. In addition, THZ1 exhibited significant anti-tumor activity in a patient-derived xenograft (PDX) model of ICC, without causing detectable side effects. © The author(s).Metabolic reprogramming is a hallmark of cancer. Mammalian genome is characterized by pervasive transcription, generating abundant non-coding RNAs (ncRNAs). Long non-coding RNAs (lncRNAs) are freshly discovered functional ncRNAs exerting extensive regulatory impact through diverse mechanisms. Emerging studies have revealed widespread roles of lncRNAs in the regulation of various cellular activities, including metabolic pathways. In this review, we summarize the latest advances regarding the regulatory roles of lncRNAs in cancer metabolism, particularly their roles in mitochondrial function, glucose, glutamine, and lipid metabolism. Moreover, we discuss the clinical application and challenges of targeting lncRNAs in cancer metabolism. Understanding the complex and special behavior of lncRNAs will allow a better depiction of cancer metabolic networks and permit the development of lncRNA-based clinical therapies by targeting cancer metabolism. © The author(s).This study focused on investigating the relationships of TAF1L expression and clinical features or pathological stages of oral squamous cell carcinoma (OSCC), and its potential roles of TAF1L on OSCC development. Western blot and immunohistochemical staining were used to detect TAF1L expression in OSCC tissues and cells. Effects of TAF1L on OSCC cells in vitro were examined by cell proliferation assay, wound healing assay, transwell chamber assay, flow cytometry analysis and siRNA technique. Cellular key proteins related to cell autophagy and apoptosis were evaluated by Western blot and immunofluorescent staining. Moreover, functions of TAF1L on OSCC process were observed in nude mouse model. Testing results showed that expression of TAF1L protein was higher in OSCC tissues than that in normal oral epithelial or paracancerous tissues. Additionally, the level of TAF1L protein expression was upregulated in OSCC cell lines, compared to that in normal oral epithelial cells. Furthermore, cell proliferation, migration, autophagy and apoptosis were modulated post siRNA-TAF1L treatment in vitro.