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s, such as age and education, were not associated with the scores of any of the WHOQOL-BREF domains. Conclusion Patient trust in healthcare providers is positively associated with different domains of HRQoL. Therefore, building and maintaining trust with patients is important to achieve favorable treatment outcomes. © 2020 AlRuthia et al.Background and Purpose Even though new cancer therapies have improved the overall survival, in some cases they have been associated with adverse effects, including increased cardiotoxicity. The purpose of the present study was to assess the cardiovascular effects of adjuvant chemotherapy for colorectal cancer and mainly the impact on arterial stiffness indices. Material and Methods A total of 70 patients with non-metastatic colorectal cancer who were treated either with FOLFOX (n=16) or with XELOX (n=54) adjuvant chemotherapy were included in the study. All patients were subjected to full cardiovascular evaluation at the beginning and the end of chemotherapy. Arterial stiffness was assessed by means of pulse wave velocity (PWV) and augmentation index (Aix) and full laboratory examinations were conducted prior to, and soon after, the termination of chemotherapy. Results Patients exhibited significantly higher levels of carotid-radial PWV, carotid femoral RWV and Aix post-chemotherapy (p less then 0.001); these findings remained significant when examined separately in each treatment subgroup (FOLFOX, XELOX). The observed changes were independent of treatment regimen and baseline patient characteristics. Univariate regression analyses showed that baseline PWVc-r and PWVc-f were the only factors associated with PWVc-r and PWVc-f change, while Aix change was independent of its baseline value. Conclusion There is a clear burden in arterial stiffness indices post-adjuvant chemotherapy for colorectal cancer in both chemotherapy groups. This is a finding of important clinical significance, however more prospective studies are required in order to encode the possible mechanisms involved. © 2020 Visvikis et al.Background Blood-based biomarkers (liquid biopsy) are increasingly used in precision oncology. Yet, little is known about cancer patients' perspectives in clinical practice. We explored patients' depth of preferences for liquid vs tissue biopsies and knowledge regarding the role of blood biomarkers on their cancer. Methods Three interviewer-administered trade-off scenarios and a 54-item self-administered questionnaire were completed by cancer outpatients across all disease sites at the Princess Margaret Cancer Centre. Results Of 413 patients, 54% were female; median age was 61 (range 18-101) years. In trade-off scenario preference testing, 90% (n=372) preferred liquid over tissue biopsy at baseline; when wait times for their preferred test were increased from 2 weeks, patients tolerated an additional mean of 1.8 weeks (SD 2.1) for liquid biopsy before switching to tissue biopsy (with wait time 2 weeks). Patients also tolerated a 6.2% decrease (SD 8.8) in the chance that their preferred test would conclusively determine optimal treatment before switching from the baseline of 80%. 216 patients (58%) preferred liquid biopsy even with no chance of adverse events from tissue biopsy. Patients' knowledge of blood-based biomarkers related to their cancer was low (mean 23%); however, the majority viewed development of blood biomarkers as important. Conclusion Patients had limited understanding of cancer-specific blood-based biomarkers, but 90% preferred liquid over tissue biopsies to assess biomarkers. There was little tolerance to wait longer for results, or for decreased test-conclusiveness. Developing accurate, low-risk tests for cancer diagnosis and management for blood biomarkers is therefore desirable to patients. © 2020 Lee et al.Introduction Numerous studies have demonstrated that long noncoding RNAs (lncRNAs) are deregulated in many cancers and exert their functions through multiple cancer-related biological processes. Glioma is the most common primary malignant central nervous system tumor and has a high fatality rate in adults. In current study, we aimed to determine the role and functional mechanism of the lncRNA BCYRN1 in glioma. Methods Gain-of-function and loss-of function approaches were used to investigate the function of BCYRN1. The effects of BCYRN1 on glioma cell proliferation, migration and invasion were evaluated using MTS, Transwell and wound-healing assays. The correlation between the expression of BCYRN1 and miR-125a-5p was verified by quantitative real-time PCR. Results The upregulation of BCYRN1 promoted the proliferation, migration and invasion of glioma cells. Meanwhile, the knockdown of BCYRN1 had the opposite effects. BCYRN1 was negatively correlated with miR-125a-5p. Additionally, TAZ, the endogenous target of miR-125a-5p, could be regulated by BCYRN1 in RNA and protein levels. A miR-125a-5p inhibitor restored BCYRN1 siRNA function in glioma. Conclusion The present study indicates that BCYRN1 promotes glioma cell proliferation, invasion and migration in vitro. Mechanistically, upregulated expression of BCYRN1 in glioma acts as a sponge to sequester the endogenous tumor suppressor miR-125a-5p and to further increase the expression TAZ. Our findings suggest that BCYRN1 is a novel oncogene and a new therapeutic target for glioma. © 2020 Yu et al.Background Prostate cancer (PCa) is a common malignant tumor in men. lncRNA ZFAS1 plays a carcinogenic role in many types of cancer; however, its potential role in PCa remains unclear. The current study aimed to determine the expression and function of ZFAS1 in PC. Methods The ZFAS1 expression in PC tissues and cells was determined by quantitative polymerase chain reaction (qPCR). SiZFAS1, miR-135a-5p mimic and miR-135a-5p inhibitor were transfected into PCa cells. The direct target of ZFAS1 was predicted by Starbase and verified by dual-luciferase reporter. Cell viability, proliferation, apoptosis, migration and invasion of the PCa cells were determined by cell counting kit-8, clone formation assay, flow cytometer, scratch and Transwell assay, respectively. The expression levels of related proteins and mRNAs were determined by Western blotting and qPCR. Results ZFAS1 expression was up-regulated in PCa cells and tissues. ZFAS1 could competitively bind to miR-135a-5p in PCa cells, and down-regulation of ZFAS1 inhibited cell viability, proliferation, migration, invasion of PCa cells and the occurrence of epithelial-mesenchymal transformation (EMT) and promoted apoptosis of PCa cells and increased the miR-135a-5p expression. Moreover, the function of miR-135a-5p mimic in PCa cells was consistent with ZFAS1 knockdown, while the function of miR-135a-5p inhibitor was opposite to that of miR-135a-5p mimic in PCa cells. The results showed that knocking down ZFAS1 could attenuate the effects of miR-135a-5p inhibitor on cell proliferation, invasion and EMT of PCa cells. Conclusion Knocking down ZFAS1 could inhibit the proliferation, invasion and metastasis of PCa cells through regulating miR-135a-5p expression. © 2020 Pan et al.Introduction We explored the roles of lncRNA HCP5 in non-small cell lung cancer (NSCLC). [https://www.selleckchem.com/products/canagliflozin.html read more] Methods Levels of HCP5 were measured by performing qPCR and data were compared between non-tumor and NSCLC tissue samples by performing a paired t-test. Expression levels of miR-320 and survivin mRNA in NSCLC tissues were also measured by performing qPCR. The effects of HCP5, miR-320 and survivin overexpression on the proliferation of H23 cells were analyzed by cell proliferation assay. Results We found that HCP5 was up-regulated in NSCLC and predicted the poor survival of NSCLC patients. HCP5 was negatively correlated with miR-320 but positively correlated with survivin in NSCLC tissues. In NSCLC cells, HCP5 overexpression led to the up-regulated survivin and down-regulated miR-320. Moreover, miR-320 overexpression failed to affect HCP5 but down-regulated survivin. Cell proliferation assay showed that HCP5 and survivin overexpression led to increased, while miR-320 overexpression led to decreased cell proliferation rate. In addition, miR-320 overexpression reduced the effects of HCP5 overexpression. Conclusion Therefore, HCP5 may stimulate the proliferation of NSCLC cells by up-regulating survivin through the down-regulation of miR-320. © 2020 Li et al.Background The aim of this study was to compare the histopathological quality and physical features of the specimen of a full-core end-cut biopsy system with that of the standard side-notch system for liver biopsies. Methods A full-core end-cut 16G biopsy device and a standard side-notch 16G needle were used to take biopsies of unclear liver lesions. Patients were randomized in two groups of 16 patients each. The primary endpoint of this prospective study was the core length measured using a dedicated microscope imaging software. Secondary endpoints were the quality of the specimen rated by an independent pathologist unaware of the device (scale from 1 to 5; with 1 as best and 5 as worst), the core diameter (determined by the microscopic imaging software) and presence of fragmentation (evaluated by the pathologist). Results For the full-core (FC) and side-notch (SN) groups, the mean core length was similar with 13,599 μm and 11,570 μm (p=0.131), respectively. The quality of the specimen was significantly better in the FC-group with an average rating of 1.68 vs 2.50 (p=0.009). The fragmentation rate in the FC-group was statistically significantly lower at 2/27 (7%) than in the SN-group at 13/33 (39%) (p=0.021). The diameter in the FC-group was 1042 μm vs 930 μm in SN-group (p=0.018). © 2020 Schaible et al.Background RP11-334E6.12 is a dysregulated long noncoding RNA (lncRNA) that has never been studied in breast cancer. The biological function and potential mechanism of RNA RP11-334E6.12 in tumorigenesis are still unknown. Methods We scanned the Cancer Genome Atlas (TCGA) database and identified RP11-334E6.12 as one of the most dysregulated lncRNAs. The level of RP11-334E6.12 was assessed in breast cancer (BC) tissue samples and BC cell lines. The survival and RP11-334E6.12 expression of patients were analysed. The biological influence of RP11-334E6.12 on BC cell lines was studied using proliferation, Transwell migration, and invasion assays. Results RP11-334E6.12 was upregulated in both the TCGA database and our own database. Moreover, survival analyses indicated that RP11-334E6.12 was related to poor overall survival. Moreover, RP11-334E6.12 promoted the proliferation, migration and invasion of BC cells. RP11-334E6.12 promotes the epithelial mesenchymal transition of BC by activating the STAT3 pathway. Conclusion Taken together, our results demonstrate that RP11-334E6.12 is associated with the progression of breast cancer. Our findings indicate that long noncoding RNA RP11-334E6.12 promotes the proliferation, migration and invasion of breast cancer cells by activating the STAT3 pathway. © 2020 Sun et al.Objective This study describes the epidemiological pattern of liver cancer in all regions of Saudi Arabia. It explores the frequency of cases diagnosed, the age-specific incidence rate (AIR), the crude incidence rate (CIR), and the age-standardised incidence rate (ASIR) stratified by age group, year of diagnosis, and region. Methods A retrospective descriptive epidemiological analysis of all liver cancer cases documented in the Saudi Cancer Registry (SCR) between 2004 and 2014 was performed. The data were analysed using descriptive statistics, t-test, Kruskal-Wallis, and sex ratio with the Statistical Package for the Social Sciences version 20.0 (SPSS). Results A total of 4723 liver cancer cases were registered in the SCR between January 2004 and December 2014. The highest overall ASIR of liver cancer among Saudi males was observed in the regions of Riyadh, Najran, and Tabuk at 10.4, 7.7, and 7.0 per 100,000 males, respectively. Furthermore, Riyadh, Eastern Region, and Tabuk recorded the highest overall ASIR among Saudi females at 4.