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Conclusions The WC, WHR, WHtR, BF%, FM and FFM apparently do not add significant information related to the levels of cardiovascular biomarkers or the calculated CV-risks. © 2020 Aleksandra Markova et al., published by De Gruyter.Background Previous studies have shown that NF2 plays a key role in tumorigenesis. NF2 has been illustrated to be downregulated in several types of human cancer. However, the role of NF2 in breast cancer remains unclear. Methods We used UALCAN and KM-plotter database to study NF2 expression in human breast cancer and corresponding normal tissues and analyzed its relationship with clinicopathological parameters. We investigated the role of NF2 in breast cancer cells behavior by inhibiting its expression in MDA-MB-231 and MCF-7 cells. Results In this study, we found that NF2 was downregulated in breast cancer tissues compared to the adjacent normal tissues. We found that the low expression of NF2 was related with the tumor stage. NF2 overexpression inhibited the cell colon formation and stemness. Conclusion Our results indicate a role of NF2 in the progression of breast cancer. © 2020 Zhibao Wang et al., published by De Gruyter.Objective Programmed cell death-ligand 1 (PD-L1) expression has been shown to play important roles in various types of cancer. However, the role of PD-L1 expression has not been conclusively reported in patients with oral squamous cell carcinoma (OSCC). Accordingly, in this meta-analysis, we investigated the clinicopathological value of PD-L1 expression in patients with OSCC. Methods Google Scholar, PubMed, EMBASE, and CNKI databases were searched to find relevant studies published through to September 16, 2019. The relationships between PD-L1 expression in patients with OSCC and clinicopathological features were assessed using risk ratio (RR) and 95% confidence intervals (CIs). Results Sixteen studies including 1989 participants were included. The results indicated that high PD-L1 expression was correlated with sex (RR = 1.28, 95% CI 1.16-1.42, P less then 0.001), N stage (RR = 1.19, 95% CI 1.06-1.33, P = 0.003), M stage (RR = 1.64, 95% CI 1.01-2.66, P = 0.044), low differentiation (RR = 1.16, 95% CI 1.01-1.33, P = 0.034), and human papilloma virus infection (RR = 1.38, 95% CI 1.14-1.68, P = 0.001), but unrelated to TNM stage or T stage. There was no significant publication bias in the studies included in this analysis. Conclusions This meta-analysis revealed that high PD-L1 expression in patients with OSCC was correlated with clinicopathological features. Further large-scale studies are necessary to confirm our results. © 2020 Yong-Xin Cui, Xian-Shuang Su, published by De Gruyter.To examine whether combining arsenic trioxide (ARS) and pamidronate (PAM), anticancer drugs that generate reactive oxygen species (ROS), enhanced targeting of redox sensitive growth signals, we studied cloning efficiency, protein tyrosine phosphatase (PTPase) activity, and epidermal growth factor receptor (EGFR) phosphorylation in DU-145 and PC-3 human prostate cancer cells in response to treatment with ARS and/or PAM for 24 h. IC50 concentrations in a clonogenic assay for ARS and PAM were 9 and 20 μM, respectively, in DU-145 cells; and 2 and 12 μM, in PC-3 cells. When combined, ARS and PAM demonstrated additive cytotoxicity in the DU-145 line (combination index [CI] of 1.10) and synergy for PC-3 cells (CI of 0.86). ARS (20 μM for 24 h) inhibited PTPase activity by 36 ± 7 %, p less then 0.05 vs. untreated controls, in DU-145 cells; and by 58 ± 8%, p less then 0.05, in the PC-3 line. [https://www.selleckchem.com/products/shr0302.html STAT inhibitor] PAM (20 μM for 24 h) decreased PTPase activity by 24 ± 9%, p = 0.06, and 8 ± 1%, p less then 0.01, in DU-145 and PC-3 cells, respectively. Combining ARS and PAM significantly inhibited PTPase activity in both cell lines at lower concentrations of each drug. Pretreatment with N-acetyl-L-cysteine reversed ARS- and PAM-induced inhibition of PTPase activity. PTPase inhibition by ARS and/or PAM treatment in both DU-145 and PC-3 cells was associated with prolonged EGFR activation. These experiments demonstrate additive or synergistic cell killing by the ARS/PAM combination in DU-145 or PC-3 cells and suggest that enhanced antitumor activity may be related to alterations in receptor tyrosine kinase signaling that occur, in part, due to ROS-mediated PTPase inhibition.Objective Physical rehabilitation programs hold the potential to mitigate deterioration in health-related quality of life (HRQoL) in patients with head and neck cancer. The objective was to assess development in relevant domains of HRQoL following a physical exercise and nutrition intervention administrated during or after treatment. Methods In a pilot study, 41 patients were randomized to resistance training and oral nutritional supplements during (EN-DUR, n = 20) or after (EN-AF, n = 21) radiotherapy. Global health status/QoL (GHS) and physical functioning (PF) were measured by the European Organization for Research and Treatment of Cancer (EORTC) quality of life questionnaire at baseline, week 6, and week 14. Differences between the groups were assessed by analysis of covariance. A difference of ≥10 points in GHS and PF was interpreted as clinically relevant. Results No statistically significant differences were detected between the groups; however, clinically relevant changes and differences in GHS and PF were observed. From baseline to week 6, GHS decreased 9 points in the EN-DUR group and 23 points in the EN-AF group and PF decreased 13 points and 21 points, respectively. From week 6 to week 14, GHS increased 14 points in the EN-DUR group and 26 points EN-AF group and PF did not change (0 points) in the EN-DUR group and increased 16 points in the EN-AF group. Conclusion The findings from the present pilot study are promising and indicate that a physical rehabilitation program may have a positive impact on HRQoL during treatment and enhance recovery after treatment. A definitive randomized trial is warranted. Level of Evidence 1b-Individual randomized controlled trial. © 2020 The Authors. Laryngoscope Investigative Otolaryngology published by Wiley Periodicals, Inc. on behalf of The Triological Society.