Hepatocellular carcinoma (HCC) is prevalent throughout the world. The aim of this study is to explore new long non-coding RNAs (lncRNAs) associated with hepatocellular carcinoma and detect their expression levels in hepatocellular carcinoma cell lines and tissues. These results will provide new clues on further function and biomarker studies of HCC-related lncRNAs. All patients were diagnosed as HCC between 30th, March, 2015 and 30th, July, 2018. LncRNA human gene expression microarray was applied to the profiling of lncRNAs in four cancerous tissues and the paired paracancerous tissues. We retrospectively reviewed 63 patients with primary HCC who underwent a curative liver resection at the Department of Hepatology, Qingdao Sixth People's Hospital. The expression level of lncRNA NRAD1 and LINC00152 was detected by real-time PCR. Prognostic factors were evaluated using Kaplan-Meier curves and Cox proportional hazards models. By microarray profiling of lncRNAs, 256 lncRNAs were found to be differentially A NRAD1 and LINC00152 expressed significantly higher in HCC tissues compared with non-tumorous tissues. Overexpression of lncRNA NRAD1 and LINC00152 were independent risk factors associated with the prognosis of patients with HCC. We found lncRNA NRAD1 and LINC00152 expressed significantly higher in HCC tissues compared with non-tumorous tissues. Overexpression of lncRNA NRAD1 and LINC00152 were independent risk factors associated with the prognosis of patients with HCC. This study aims to systematically analyze multi-omics data to explore new prognosis biomarkers in colon adenocarcinoma (COAD). Multi-omics data of COAD and clinical information were obtained from The Cancer Genome Atlas (TCGA). Univariate Cox analysis was used to select genes which significantly related to the overall survival. GISTIC 2.0 software was used to identify significant amplification or deletion. Mutsig 2.0 software was used to identify significant mutation genes. The 9-gene signature was screened by random forest algorithm and Cox regression analysis. GSE17538 dataset was used as an external dataset to verify the predictive ability of 9-gene signature. qPCR was used to detect the expression of 9 genes in clinical specimens. A total of 71 candidate genes are obtained by integrating genomic variation, mutation and prognostic data. Then, 9-gene signature was established, which includes HOXD12, RNF25, CBLN3, DOCK3, DNAJB13, PYGO2, CTNNA1, PTPRK, and NAT1. The 9-gene signature is an independent prognostic risk factor for COAD patients. In addition, the signature shows good predicting performance and clinical practicality in training set, testing set and external verification set. The results of qPCR based on clinical samples showed that the expression of HOXD12, RNF25, CBLN3, DOCK3, DNAJB13, and PYGO2 was increased in colon cancer tissues and the expression of CTNNA1, PTPRK, NAT1 was decreased in colon cancer tissues. In this study, 9-gene signature is constructed as a new prognostic marker to predict the survival of COAD patients. In this study, 9-gene signature is constructed as a new prognostic marker to predict the survival of COAD patients. ROS1 fusions have been identified in 1-2% of non-small-cell lung cancer (NSCLC) patients; they are validated as a driver of carcinogenesis and could be subjected to inhibition by crizotinib. However, previous studies suggested a variable progression-free survival (PFS) ranging from 9.1 to 20.0 months for crizotinib treatment in ROS1-rearranged NSCLC. Here, we reported a 45-year-old female diagnosed with stage IVB lung adenocarcinoma with multiple lymph nodes and bone metastasis carrying a novel MPRIP-ROS1 fusion, which was identified by RNA-based NGS (next-generation sequencing) and was sensitive to crizotinib treatment. A targeted NGS panel was used to analyze genomic DNA and total RNA isolated from formalin-fixed paraffin-embedded (FFPE) tissue block of the patient. An RNA fusion panel based on amplicon sequencing was designed for detection fusion variation. Fusion results were validated using reverse transcriptase polymerase chain reaction and Sanger sequencing. We reported a novel MPRIP-ROS1 fusion er of lung adenocarcinoma and potential therapeutic target for crizotinib. It also expanded NSCLC treatment of ROS1 rearrangement and highlighted the importance of genetic testing for precise treatment decision-making. Cervical cancer (CC) is the fourth most common cancer with high death rate in females. The study aims to detect the mechanism of long non-coding RNA (LncRNA) PCAT1 on radiosensitivity of CC. The expression of PCAT1, miR-128 and GOLM1 in CC tissues and cells was measured by qRT-PCR. Different doses of X-ray were used for radiation treatment of CC cells and 6 Gy was chosen to perform the following experiments. The proliferation, migration and invasion of CC cells were measured by MTT assay, wound healing assay and transwell assay, respectively. The target relationships among PCAT1, miR-128 and GOLM1 were predicted by StarBase and TargetScan and verified by luciferase reporter assay. https://www.selleckchem.com/products/ipi-549.html The protein level of GOLM1 was determined by Western blot. The xenograft tumor model was constructed in nude mice to verify the effect of PCAT1 on radiosensitivity of CC in vivo. The PCAT1 expression was upregulated in CC tissues and cells. PCAT1 silencing enhances radiosensitivity of CC cells on proliferation, migration and invasion. MiR-128 was the target of PCAT1 and was negatively regulated by PCAT1. Upregulation of miR-128 enhances radiosensitivity of CC cells on proliferation, migration and invasion. GOLM1 was a target of miR-128 and was negatively regulated by miR-128. Upregulation of GOLM1 and downregulation of miR-128 both reversed the enhanced effect of PCAT1 knockdown on radiosensitivity of CC cells, which partly promoted the proliferation, migration and invasion of CC cells. Silencing of PCAT1 enhanced radiosensitivity of CC via targeting miR-128/GOLM1, which provided a new idea for treating CC. Silencing of PCAT1 enhanced radiosensitivity of CC via targeting miR-128/GOLM1, which provided a new idea for treating CC.