Annual Report on Status of Cancer from ACS, NCI, CDC, Cancer Registries: Targeted Focus on Latinos Will Likely Improve US Cancer Rates

Bladder cancer - the tenth most frequent cancer worldwide - has a heterogeneous natural history and clinical behaviour. The predominant histological subtype, urothelial bladder carcinoma, is characterized by high recurrence rates, progression and both primary and acquired resistance to platinum-based therapy, which impose a considerable economic burden on health-care systems and have substantial effects on the quality of life and the overall outcomes of patients with bladder cancer. The incidence of urothelial tumours is increasing owing to population growth and ageing, so novel therapeutic options are vital. Based on work by The Cancer Genome Atlas project, which has identified targetable vulnerabilities in bladder cancer, immune checkpoint inhibitors (ICIs) have arisen as an effective alternative for managing advanced disease. However, although ICIs have shown durable responses in a subset of patients with bladder cancer, the overall response rate is only ~15-25%, which increases the demand for biomarkers of response and therapeutic strategies that can overcome resistance to ICIs. In ICI non-responders, cancer cells use effective mechanisms to evade immune cell antitumour activity; the overlapping Warburg effect machinery of cancer and immune cells is a putative determinant of the immunosuppressive phenotype in bladder cancer. This energetic interplay between tumour and immune cells leads to metabolic competition in the tumour ecosystem, limiting nutrient availability and leading to microenvironmental acidosis, which hinders immune cell function. Thus, molecular hallmarks of cancer cell metabolism are potential therapeutic targets, not only to eliminate malignant cells but also to boost the efficacy of immunotherapy. In this sense, integrating the targeting of tumour metabolism into immunotherapy design seems a rational approach to improve the therapeutic efficacy of ICIs.

Competitive glucose metabolism as a target to boost bladder cancer immunotherapy.

Carvedilol attenuates liver fibrosis by suppressing autophagy and promoting apoptosis in hepatic stellate cells.

Activation of hepatic stellate cell (HSC) involves the transition from a quiescent to a proliferative, migratory, and fibrogenic phenotype (i.e., myofibroblast), which is characteristic of liver fibrogenesis. Multiple cellular and molecular signals which contribute to HSC activation have been identified. This review specially focuses on the metabolic changes which impact on HSC activation and fibrogenesis.

/pdf/role-of-metabolism-in-hepatic-stellate-cell-activation-and-20iwv374xk.pdf

Role of Metabolism in Hepatic Stellate Cell Activation and Fibrogenesis.

In diet-induced obesity, metformin (MF) has weight-lowering effect and improves glucose homeostasis and insulin sensitivity. However, there is no information on the efficiency of MF and the mechanisms of its action in melanocortin-type obesity. We studied the effect of the 10-day treatment with MF at the doses of 200, 400 and 600 mg/kg/day on the food intake and the metabolic and hormonal parameters in female C57Bl/6J (genotype Ay/a) agouti-mice with melanocortin-type obesity, and the influence of MF on the hypothalamic signaling in obese animals at the most effective metabolic dose (600 mg/kg/day). MF treatment led to a decrease in food intake, the body and fat weights, the plasma levels of glucose, insulin and leptin, all increased in agouti-mice, to an improvement of the lipid profile and glucose sensitivity, and to a reduced fatty liver degeneration. In the hypothalamus of obese agouti-mice, the leptin and insulin content was reduced and the expression of the genes encoding leptin receptor (LepR), MC3- and MC4-melanocortin receptors and pro-opiomelanocortin (POMC), the precursor of anorexigenic melanocortin peptides, was increased. The activities of AMP-activated kinase (AMPK) and the transcriptional factor STAT3 were increased, while Akt-kinase activity did not change from control C57Bl/6J (a/a) mice. In the hypothalamus of MF-treated agouti-mice (10 days, 600 mg/kg/day), the leptin and insulin content was restored, Akt-kinase activity was increased, and the activities of AMPK and STAT3 were reduced and did not differ from control mice. In the hypothalamus of MF-treated agouti-mice, the Pomc gene expression was six times higher than in control, while the gene expression for orexigenic neuropeptide Y was decreased by 39%. Thus, we first showed that MF treatment leads to an improvement of metabolic parameters and a decrease of hyperleptinemia and hyperinsulinaemia in genetically-induced melanocortin obesity, and the specific changes in the hypothalamic signaling makes a significant contribution to this effect of MF.

/pdf/the-evidence-of-metabolic-improving-effect-of-metformin-in-11tojkxhmp.pdf

The evidence of metabolic-improving effect of metformin in Ay/a mice with genetically-induced melanocortin obesity and the contribution of hypothalamic mechanisms to this effect.

Metformin attenuates motility, contraction, and fibrogenic response of hepatic stellate cells in vivo and in vitro by activating AMP-activated protein kinase

Metformin attenuates motility, contraction, and fibrogenic response of hepatic stellate cells in vivo and in vitro by activating AMP-activated protein kinase.

Background The study was conducted to investigate the effectiveness and cost of computed tomography (CT)-guided percutaneous microwave ablation (MWA) and thoracoscopic lobectomy for stage I non-small cell lung cancer (NSCLC) Methods We retrospectively analyzed the data of 46 and 85 patients with stage I NSCLC treated with CT-guided percutaneous MWA or thoracoscopic lobectomy, respectively, at our center from July 2013 to June 2015 Overall survival (OS), disease-free survival (DFS), local control rate, hospital stay, and cost were evaluated Survival curves were constructed using the Kaplan-Meier method and compared using the log-rank test Results The one and two-year OS rates were 9782% and 9130% and 9765% and 9059% in the MWA and lobectomy groups, respectively The one and two-year DFS rates were 9565% and 7609% and 9529% and 7529%, respectively No significant differences were observed in log-rank analysis between the groups (P = 0169) The hospital stays in the MWA and lobectomy groups were 662 ± 231 and 957 ± 319 days, respectively The costs of MWA and lobectomy were US$327450 ± US$23391 and US$467887 ± US$15596, respectively The differences were all significant (P = 0003) Conclusion MWA and thoracoscopic lobectomy for stage I NSCLC demonstrate similar one and two-year OS and DFS, with no significant differences between the two groups MWA involved a shorter hospital stay and lower cost, thus should be considered a better option for patients with severe cardiopulmonary comorbidity and patients unwilling to undergo surgery

Comparison between computed tomography-guided percutaneous microwave ablation and thoracoscopic lobectomy for stage I non-small cell lung cancer.

Background Scutellarin (SCU), a flavonoid isolated from Erigeron breviscapus (Vant.) Hand.-Mazz., increases autophagy and apoptosis in the adenocarcinoma A549 cell line, which is resistant to cisplatin. However, whether SCU alone has antitumor activity against non-small cell lung cancer (NSCLC) is unknown. Methods Cell Counting Kit-8, flow cytometry, colony formation, Hoechst 33258 staining, and Western blot analyses were used to examine the proliferation and apoptosis of A549 cells treated with SCU and the possible molecular mechanisms. Results The cell viability assay indicated that SCU markedly suppressed the proliferation of A549 cells in concentration and time-dependent manners. SCU caused significant G0/G1 phase arrest and apoptosis, as evidenced by flow cytometric analyses, Hoechst 33258 staining, and Western blot analyses of cyclin D1, cyclin E, BCL-2, cleaved-caspase-3, and BAX. Furthermore, SCU treatment reduced the level of pan-AKT, phosphorylated (p)-mTOR, mTOR, BCL-XL, STAT3, and p-STAT3, and increased the level of 4EBP1. Conclusions SCU can suppress proliferation and promote apoptosis in A549 cells through AKT/mTOR/4EBP1 and STAT3 pathways. This suggests that SCU may be developed into a promising antitumor agent for treating NSCLC.

Scutellarin suppresses proliferation and promotes apoptosis in A549 lung adenocarcinoma cells via AKT/mTOR/4EBP1 and STAT3 pathways

Percutaneous transhepatic extraction and balloon dilation for simultaneous gallbladder stones and common bile duct stones: A novel technique

Percutaneous transhepatic extraction and balloon dilation for simultaneous gallbladder stones and common bile duct stones: A novel technique.

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Metformin attenuates motility, contraction, and fibrogenic response of hepatic stellate cells in vivo and in vitro by activating AMP-activated protein kinase.

Comparison between computed tomography-guided percutaneous microwave ablation and thoracoscopic lobectomy for stage I non-small cell lung cancer.

Scutellarin suppresses proliferation and promotes apoptosis in A549 lung adenocarcinoma cells via AKT/mTOR/4EBP1 and STAT3 pathways

Percutaneous transhepatic extraction and balloon dilation for simultaneous gallbladder stones and common bile duct stones: A novel technique.