Conner Wiggins (sushizoo60)

9% vs. 6.5%, P less then 0.001; median OS not reached vs. 9.6 months, log-rank P less then 0.001; median PFS 9.6 vs. 2.8 months, log-rank P less then 0.001). In multivariate analysis, AFP response was an independent factor associated with good OS (hazard ratio [HR]=0.301, P=0.001) and PFS (HR=0.332, P less then 0.001). Moreover, AFP responders had higher ORR and better OS as well as PFS than non-responders, regardless of nivolumab as a first- or more than a second-line therapy (all P less then 0.05). In conclusion, the novel 50-10 rule of AFP response provides practical guidance for nivolumab monotherapy in unresectable HCC patients. However, this algorithm remains to be verified in a large prospective cohort.A recent JCOG1104, OPAS-1 trial revealed the significance of S-1 duration. However, the significance of cumulative total S-1 dose (CTSD) remains unclear. In this study, we designed to evaluate the prognostic effect of CTSD on adjuvant chemotherapy after curative gastrectomy. We retrospectively analyzed 77 consecutive pStage II and III gastric cancer (GC) patients, who underwent curative gastrectomy followed by adjuvant S-1 chemotherapy from 2008 through 2014. CTSD of 20000 mg was the upper-limit of cut-off value to stratify the prognosis (5-year relapse free survival (RFS); CTSD less then 20000 mg vs. CTSD ≥ 20000 mg 51.9% vs. 85.1%, P = 0.004). Compared patients with CTSD more than 20000 mg, those with CTSD less than 20000 mg had a significantly higher rate of preoperative anemia (P = 0.041), low nutrition (P = 0.008) and open gastrectomy (P = 0.012). Multivariate Cox's proportional hazards model for RFS proved that CTSD less than 20000 mg was an independent prognostic factor [P = 0.031, HR 3.32 (95% CI 1.11-11.1)] although S-1 intensity and duration were not independent prognostic factors. The cumulative total S-1 dose more than 20000 mg might contribute to better prognosis.Mitochondria have attracted attention in cancer research as organelles associated with tumor development and response to therapy. We recently reported acquisition of resistance to cisplatin (DDP) associated with a metabolic rewiring in ovarian cancer patient-derived xenografts (PDXs) models. DDP-resistant PDXs models were obtained mimicking the clinical setting, treating mice bearing sensitive-DDP tumors with multiple cycles of DDP until the development of resistance. To further characterize the metabolic rewiring, the present study focused on tumor mitochondria. We analysed by transmission electron microscopy the mitochondria structure in two models of DDP-resistant and the corresponding DDP-sensitive PDXs and evaluated tumor mDNA content, the expression of genes and proteins involved in mitochondria functionality, and mitochondria fitness-related processes, such as autophagy. We observed a decrease in the number of mitochondria paralleled by an increased volume in DDP-resistant versus DDP-sensitive PDXs. DDP-resistant PDXs presented a higher percentage of damaged mitochondria, in particular of type 2 (concave-shape), and type 3 (cristolysis) damage. We found no difference in the mDNA content, and the expression of genes involved in mitochondrial biogenesis was similar between the sensitive and resistant PDXs. An upregulation of some genes involved in mitochondrial fitness in DDP-R versus DDP-S PDXs was observed. At protein level, no difference in the expression of proteins involved in mitochondrial function and biogenesis, and in autophagy/mitophagy was found. We here reported that the acquisition of DDP resistance is associated with morphological alterations in mitochondria, even if we couldn't find any dysregulation in the studied genes/proteins that could explain the observed differences.Siglec15 is a recently characterized immunosuppressive transmembrane protein, which expresses in various types of solid tumors and promotes cancer development. Several studies reported that Siglec15 is a prognostic biomarker of cancer patients, and targeting S