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0002). VM was not associated with MVD. TMVD was able to distinguish between patients with high and low MVD in terms of survival, thus TMVD was better compared with MVD alone at distinguishing between patients with different survival prognoses. TCGA data analysis revealed that among the VM-associated genes, nodal growth differentiation factor, caspase-3, matrix metalloproteinase-9 and galectin-3 had a statistically significant impact on the overall/disease-free survival of patients with RCC. In conclusion, the TMVD concept may be more appropriate and sensitive compared with the MVD or VM alone in predicting tumor aggressiveness and patient survival, particularly in RCC, which is a highly vascularized, VM-rich neoplasm, and certain VM formation-associated genes are negatively associated with the survival of patients with RCC.The present study aimed to investigate the expression levels and clinical value of miR-365 and miR-25 in serum of patients with non-small cell lung cancer (NSCLC). Patients (180) diagnosed with NSCLC at the Affiliated Hospital of Guangdong Medical University from July 2011 to December 2013 were used as the experimental group. Volunteers (90) undergoing health examinations were used as the control group. The serum of the patients was collected after fasting in the morning. The expression levels of miR-365 and miR-25 in the serum of patients was assessed by quantitative real-time PCR (qRT-PCR), and the relationship among miR-365, miR-25 and the postoperative survival rate of NSCLC patients was analyzed. The relative expression level of miR-25 of patients with peripheral infiltration was significantly higher than that of patients without peripheral infiltration (P less then 0.05). There were significant differences in the relative expression level of miR-25 in different pathological grades and TNM stages, as wel metastasis. Moreover, it was revealed that miR-25 and miR-365 affected the 5-year survival rate of patients. miR-25 and miR-365 could be used as important tumor markers to evaluate the prognosis of NSCLC patients.Evidence is limited regarding the immunologic profile and immune microenvironment of soft tissue sarcoma subtypes. The aim of the present study was to describe the clinical significance and prognostic implications of PD-L1, PD-L2, and PD-1 in patients with retroperitoneal sarcoma (RSar). In this retrospective, multicenter, collaborative study, medical charts were reviewed and the immunohistochemical staining results of resected tissue specimens from 51 patients with RSar were examined. Immunohistochemical staining was performed with primary antibodies against PD-L1, PD-L2, PD-1, and Ki-67. The correlations between the baseline clinical parameters and expression levels of the four molecules in sarcoma cells were evaluated, and their prognostic values after tumor resection were assessed. Dedifferentiated liposarcoma (41%), leiomyosarcoma (20%), and undifferentiated pleomorphic sarcoma (16%) were the three major types identified. Dedifferentiated liposarcoma and leiomyosarcoma showed higher levels of PD-L1 expretigations are needed to determine the immunologic landscape of RSar and provide a foundation for therapeutic intervention using immune checkpoint inhibitors.The aim of the present study was to elucidate the association between excessive chronic iodine exposure and the risk of developing papillary thyroid carcinoma (PTC). The demographic information and pathological characteristics of patients with thyroid nodules were retrieved from medical records at The Second Hospital of Shandong University. A fasting urine specimen was collected, and creatinine and urinary iodine concentration (UIC) were determined. The water iodine data from the domicile districts of these patients were collated from published reports. The results revealed that almost half of the patients with PTC (44.3%) also exhibited a high UIC (≥300 µg/l). Multivariate analysis revealed that the adjusted odds ratio for high UIC was 3.987 (95% CI 1.355-11.736) and the adjusted area under the receiver operating characteristic curve was 0.776 (95% CI 0.687-0.864), which was associated with PTC risk in patients with thyroid nodules. Integrated ecological assessment of chronic iodine exposures demonstrated that >80% (81.4%) of the patients with PTC who also exhibited a high UIC were from historically non-iodine-deficient regions, and 66.7% of patients with PTC who resided in historically iodine-excessive regions were characterized by high UICs. Importantly, a high UIC was significantly associated with capsular invasion and extrathyroid metastasis (P less then 0.05). Moreover, self-matching results indicated that, in patients with PTC, there were no significant differences in UIC grading between the pre- and postoperative specimens. In conclusion, excessive chronic iodine exposure is significantly associated with the risk of PTC, which contributes to increased capsular invasion and extrathyroid metastases. However, further research is required to validate these findings and to elucidate the potential molecular mechanisms involved.Long non-coding RNAs (lncRNAs) participate in various biological processed involved in tumorigenesis, metastasis and proliferation. The aim of the present study was to identify candidate long non-coding RNAs (lncRNAs) involved in sentinel lymph node (SLN) metastasis in breast cancer. Specimens of SLNs were collected from patients with SLN metastasis via punch biopsy. Total RNA was extracted and RNA sequencing (RNA-seq) was conducted. Differential expression profiles of mRNAs and lncRNAs were obtained via bioinformatics analysis, and Gene Oncology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed on differentially expressed mRNAs. The expression levels of lncRNAs were analyzed via reverse transcription-quantitative PCR (RT-qPCR), and the regulation network of the lncRNAs to downstream microRNAs (miRs) and mRNAs was predicted. Based on RNA-seq results, six differentially expressed candidate lncRNAs were identified in patients with and without SLN metastasis lnc-ANGPTL1-33, lnc-GJA1evels, as well as miR-449a to regulate MAP2K1 expression. The results of the present study suggested that lnc-ANGPTL1-33 and lnc-GJA10-121 may potentially serve a role in SLN metastasis of breast cancer by regulating the PI3K/Akt and MAPK signaling pathways via targeting the miR-302 family, miR-520a-3p, miR-34a-5p and miR-449a. Thus, lnc-ANGPTL1-33 and lnc-GJA10-121 in SLN may serve as potential markers of breast cancer metastasis.Gliomas are the most common type of primary brain tumor in adults with a high mortality rate. Low-grade gliomas progress to glioblastoma multiforme (GBM) in the majority of cases, forming secondary GBM (sGBM), followed by rapid fatal clinical outcomes. Protein tyrosine phosphatase receptor type Z1 (PTPRZ1)-MET proto-oncogene receptor tyrosine kinase (MET) (ZM) fusion has been identified as a biomarker for sGBM that is involved in glioma progression, but the mechanism of gliomagenesis and pathology of ZM-negative sGBM has remained to be fully elucidated. A whole-transcriptome signature is thus required to improve the outcome prediction for patients with sGBM without ZM fusion. In the present study, whole-transcriptome sequencing on 42 sGBM samples with or without ZM fusion from the Chinese Glioma Genome Atlas database identified mRNAs with differential expression between patients with and without ZM fusion and the most significant survival-associated genes were identified. A 6-gene signature was identified as a novel prognostic model reflecting survival probability in patients with ZM-negative sGBM. Clinical characteristics in patients with a high or low risk score value were analyzed with the Kaplan-Meier method and a two-sided log-rank test. In addition, ZM-negative sGBM patients with a high risk score exhibited an increase in immune cells, NF-κB-induced pathway activation and a decrease in endothelial cells compared with those with a low risk score. The present study demonstrated the potential use of a next-generation sequencing-based cancer gene signature in patients with ZM-negative sGBM, indicating possible clinical therapeutic strategies for further treatment of such patients.Colorectal cancer (CRC) is the third most commonly diagnosed cancer worldwide. SAR1 gene homolog B (SAR1B) is a GTPase that has been reported to have a central role in the regulation of lipid homeostasis and is associated with numerous diseases. However, its role in cancer, particularly in CRC, remains unclear. The present study revealed that SAR1B was overexpressed in CRC samples and this was associated with shorter overall survival time in patients with CRC. Colony formation, cell proliferation and flow cytometry assays were conducted to evaluate the functions of SAR1B in CRC. It was reported that SAR1B may be associated with tumorigenesis of CRC. Knockdown of SAR1B suppressed cell proliferation and induced significant apoptosis of RKO cells. Furthermore, microarray analysis was performed to identify the potential targets of SAR1B in CRC. Bioinformatics analysis revealed that SAR1B was significantly involved in regulating 'TGF-β signaling', 'paxillin signaling', 'cell cycle regulation by BTG family proteins' and 'IGF-1 signaling'. These results suggested that SAR1B may be considered a potential prognostic biomarker and therapeutic target for CRC.Y-box binding protein 1 (YB-1) is a regulatory protein associated with oncogenesis and poor prognosis in patients with cancer. In the cell, YB-1 functions as a DNA and RNA binding protein that promotes or suppresses expression of target genes. The cancer-promoting activity of YB-1 is mediated through its activation of oncogenes and repression of tumor suppressor genes. Lipogenic enzyme stearoyl-CoA desaturase (SCD1) drives the production of endogenous monounsaturated fatty acids (MUFAs) in cells and protects against toxic buildup of saturated fatty acids. Clear cell renal cell carcinoma (ccRCC) is often characterized by aberrantly high SCD1 expression and cytosolic accumulation of unsaturated fatty acids. In the present study, a proteomics screen of cells treated with inhibitors of SCD1 supported a potential relationship between YB-1 and SCD1. It was revealed that the presence of MUFAs led to increased protein synthesis and increased expression of high molecular weight forms of YB-1 in ccRCC cells, but not in non-tumorigenic cells. Ectopic expression of YB-1 led to decreased expression levels of SCD1 protein and mRNA in ccRCC cell lines. Conversely, targeted knockdown of YB-1 increased SCD1 mRNA abundance. Analysis of ccRCC patient data from The Cancer Proteome Atlas database showed YB-1 expression was negatively associated with survival, whereas SCD1 was associated with improved survival. These data suggested an antagonistic relationship between YB-1 and SCD1 that may influence survival of patients with ccRCC.The aim of the present study was to investigate the effect and mechanism of action of microRNA (miR)-27b on skin wound healing in rats with deep second-degree scald burns and in BJ human skin fibroblast cells. Rat models with deep second-degree scald burns were constructed and injected with miR-27b mimics and inhibitors at the wound site daily for 21 days. Healing of burned skin tissues was observed at 0, 3, 7, 14 and 21 days following modeling. H&E and Masson staining were used to observe the pathological structure and degree of collagen fibers in the burned skin tissues. The effects of miR-27b on BJ cell proliferation and migration were determined by MTT and scratch assays. Matrix metalloproteinase-1 (MMP-1), α-smooth muscle actin (α-SMA), collagen I and collagen III expression in rat skin tissues and BJ cells were measured via reverse transcription-quantitative PCR and western blot analysis. The results of the in vivo experiments demonstrated that miR-27b inhibition accelerated scalded skin healing and induced fibroblast growth.