MOESM1 of SMAD4 Y353C promotes the progression of PDAC

Additional file 1: Figure S1. The whole exons of SMAD4 gene primers for details. Figure S2. SMAD4 gene 1~11 exons’ PCR products electrophoresis results. Figure S3. SMAD4 mutation analysis. (A) c.6C>T (p.D2D=); (B) c.29C>T (p.P10L); (C) c.34A>G (p.S12G); (D) c.112A>G (p.R38G); (E) c.153_d3elA [Frameshift, stop at codon 57(TAA)]; (F) c.201 T>C (p.H67H=); (G) c.352_363delGCGTTTGACTTA (A118_L121del, Frameshift); (H)c.1058A>G(p.Y353C); (I)c.1103_1104insG [(Frameshift and stop at codon 377(TGA)]; (J) c.1242-1245delAGAC [(L414_D415del, Framashift and stop at codon 434(TAA)]. Figure S4. SMAD4 Y353C has no effects to cell proliferation in vitro. (A, B) The proliferation ability of the SW1990 and PANC-1 cell line was detected and the results showed that there was no significant difference between the negative control group (NC), SMAD4 wt group and SMAD4 Y353C group. All data are shown as mean ± SD of 3 independent experiments performed in triplicate (one-way ANOVA, p>0.05)

Figure S2 from A Zebrafish Model Discovers a Novel Mechanism of Stromal Fibroblast-Mediated Cancer Metastasis

Mouse CAFs promote breast cancer metastasis</p

Hyperuricemia Predisposes to the Onset of Diabetes via Promoting Pancreatic β-Cell Death in Uricase Deficiency Male Mice

Clinical studies have shown a link between hyperuricemia (HU) and diabetes, while the exact effect of soluble serum urate on glucose metabolism remains elusive. This study aims to characterize the glucose metabolic phenotypes and investigate the underlying molecular mechanisms using a novel spontaneous HU mouse model which is in absence of Uricase (Uox) gene. In an attempt to study the role of HU in glycometabolism, we implemented external stimulation on Uox-knockout (KO) and wild-type (WT) males with high-fat diet (HFD) and (/or) multiple-low-dose streptozotocin (MLD-STZ) to provoke the potential role of urate. Notably, while Uox-KO mice developed glucose intolerance in basal condition, none had spontaneously developed into diabetes even with aging. HFD-fed Uox-KO mice manifested similar insulin sensitivity compared with WT controls. HU augmented the existing glycometabolism abnormality induced by MLD-STZ, and eventually lead to diabetes evidenced by the increased random glucose. Reduced β cell masses and increased the terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) positive β cells suggested HU-mediated diabetes was cell death dependent. However, urate-lowering treatment (ULT) cannot ameliorate the diabetes incidence nor reverse β-cell apoptosis with significance. While, ULT displayed a significant therapeutic effect of hyperuricemic-crystal associated kidney injury and tubulointerstitial damage in diabetes. Moreover, we present transcriptomic analysis of isolated islets, using Uox-KO versus WT mice and streptozotocin-induced diabetic WT (STZ-WT) versus diabetic Uox-KO (STZ-KO) mice. Shared differentially expressed genes of HU primacy revealed Stk17β is a possible target gene in HU related β-cell death. Together, this study suggests that HU accelerates but not causes diabetes by inhibiting islet β-cell survival

Figure S5 from A Zebrafish Model Discovers a Novel Mechanism of Stromal Fibroblast-Mediated Cancer Metastasis

Gene expression in PDGF-BB stimulated fibroblasts</p

Supplementary Information from A Zebrafish Model Discovers a Novel Mechanism of Stromal Fibroblast-Mediated Cancer Metastasis

Supplementary Figure Legends</p

Additional file 3 of Construction of a survival prediction model for high-and low -grade UTUC after tumor resection based on “SEER database”: a multicenter study

Additional file 3: Appendix Figure 1. (a-d) X-tile plots of age at diagnosis, identifying the best risk score cut-off based on the overall survival (OS) in the high- and low-grades; (e-h)X-tile plots of tumor size, identifying the best risk score cut-off based on the OS in the high- and low-grades

Additional file 1 of Construction of a survival prediction model for high-and low -grade UTUC after tumor resection based on “SEER database”: a multicenter study

Additional file 1: Appendix Table 1. Cox regression coefficients of the two models of the SEER training set. AJCC: the American Joint Committee on Cancer; CI: confidence interval; HR: Hazard Ratio; Ln_surg: Lymph node dissection; SEER: the Surveillance Epidemiology, and End Results database

Additional file 2 of Construction of a survival prediction model for high-and low -grade UTUC after tumor resection based on “SEER database”: a multicenter study

Additional file 2: Appendix Table 2. A table showing the percentage of surgical procedures. Partial nephrectomy: Partial or subtotal nephrectomy (kidney or renal pelvis) or partial ureterectomy; RNU:Complete/total/simple nephrectomy - for kidney parenchyma Nephroureterectomy; Any nephrectomy: Any nephrectomy (simple, subtotal, complete, partial, total, radical) PLUS an en bloc:resection of other organ(s) (colon, bladder); Nephrectomy, NOS:Nephrectomy, NOS;Ureterectomy, NOS

Figure S1 from A Zebrafish Model Discovers a Novel Mechanism of Stromal Fibroblast-Mediated Cancer Metastasis

Human CRC tumor fibrosis and isolation of CAFs</p

Dissemination of CAF-cancer cell complex from A Zebrafish Model Discovers a Novel Mechanism of Stromal Fibroblast-Mediated Cancer Metastasis

Video - Dissemination of CAF-cancer cell complex</p