Journal: Clinical Cancer Research

Article Title: Establishment of Patient-Derived Succinate Dehydrogenase–Deficient Gastrointestinal Stromal Tumor Models for Predicting Therapeutic Response

doi: 10.1158/1078-0432.ccr-21-2092

Figure Lengend Snippet: Figure 4. Temozolomide reduces cell viability of mSDH GIST models by induction of DNA DSBs and impairing DNA repair. Cell viability of mSDH GIST models determined by CellTiter-Glo viability assay after treatment by imatinib (A), sunitinib (B), and temozolomide (C). Viability was measured after 3 days of treatment for imatinib and sunitinib and on 7 days of temozolomide treatment. Data are presented as mean SD. D, Representative images of a neutral comet assay for mSDH GIST models treated with either DMSO or 500 mmol/L temozolomide for 72 hours. Comet tail lengths were measured (n ¼ 100þ cells per group) and plotted. E, Representative immunofluorescence images of mSDH GIST models treated with DMSO or temozolomide (500 mmol/L) and stained for g-H2AXþ nuclei. Quantification of g-H2AXþ cells in mSDH GIST models treated with DMSO or temozolomide for 72 hours. For each GIST model, g-H2AXþ nuclei were quantified and shown as % of total nuclei. Mann–Whitney t test was performed for statistical analysis with , P < 0.01; , P < 0.001, , P < 0.0001. F, Immunoblots of mSDH GIST models treated with DMSO or temozolomide (500 mmol/L) for 3 days and probed for indicated proteins. G, Immunoblots of mSDH GIST models treated with DMSO or temozolomide (500 mmol/L) for 7 days and probed for indicated proteins. CC3 denotes cleaved caspase 3.

Article Snippet: Drugs used include temozolomide (Selleckchem, S1237), 2-deoxy-D-glucose (Selleckchem, 25972), 6-aminonicotinamide (Thermo Fisher Scientific, AAL0669203), imatinib (Chemietek), and sunitinib malate (Thermo Fisher Scientific, 341031-54- 7 RS046).

Techniques: Viability Assay, Neutral Comet Assay, Staining, MANN-WHITNEY, Western Blot

Journal: PeerJ

Article Title: Endothelial cell-initiated extravasation of cancer cells visualized in zebrafish

doi: 10.7717/peerj.688

Figure Lengend Snippet: (A) Intersegmental vessels were severely deteriorated by treatment with sunitinib. (B) Extravasation of RFP-HeLa cells in the presence of sunitinib. The numbers indicate the elapsed time in minutes. (C) The incidence of the 2 processes of extravasation. Seven larvae in which RFP-HeLa cells formed severe emboli were observed in the presence of sunitinib. Nine extravasation events were counted during 11-h observations. (D) The sum of the area of extravasated cancer cell images was calculated from all of the 7 movies recorded in RFP-HeLa cells with and without sunitinib treatments. Bars, 100 µm (A) or 40 µm (B). (E, G) Scanning electron micrographs of the arteries in the control and sunitinib-treated larvae. Sunitinib-treated larvae showed thicker vascular walls. (F) The magnified image of the luminal face on the endothelial wall of a control larva. The endothelial wall showed many holes or fenestration-like structures (arrowhead). (H) The magnified image of the luminal face on the endothelial wall of a sunitinib-treated larva. The endothelial wall showed no fenestration-like structures. Bars, 10 µm (E, G) or 0.5 µm (F, H).

Article Snippet: Sunitinib (Toronto Research Chemicals, Toronto), an orally active VEGFR tyrosine kinase inhibitor, was dissolved in dimethyl sulfoxide (DMSO) to make a stock solution of 10 mM.

Techniques: Control

Journal: Acta Dermato-Venereologica

Article Title: Possible Clinical Effects of Ketoconazole on Sorafenib-induced Hand–Foot Skin Reaction and Cytoprotection Mechanisms of Antifungal Agents against Multikinase Inhibitor-induced Keratinocyte Toxicity

doi: 10.2340/actadv.v105.40697

Figure Lengend Snippet: Cytotoxicity of MKI and capecitabine in NHEK. Various concentrations of MKI (sorafenib, regorafenib, lenvatinib, sunitinib) or the anticancer drug capecitabine were added to cultured NHEK. After overnight incubation, cell viability was assessed using the Cell Counting Kit-8 assay. Data were analysed using two-way ANOVA followed by Dunnett’s test; **** p < 0.0001, ** p < 0.01 and * p < 0.05 (vs control). Results are expressed as the mean ± SD of quadruplicate experiments.

Article Snippet: Lenvatinib was from MedChem Express (Monmouth Junction, NJ, USA); sorafenib from Santa Cruz Biotechnology (Dallas, TX, USA); ketoconazole and itraconazole from Sigma-Aldrich (Saint Louis, MO, USA); sunitinib from Tocris Bioscience (Bristol, UK); regorafenib from Tokyo Chemical Industry (Tokyo, Japan); and capecitabine from Toronto Research Chemicals (Toronto, Canada).

Techniques: Cell Culture, Incubation, Cell Counting, Control

Journal: Biological & pharmaceutical bulletin

Article Title: Pharmacokinetic-pharmacodynamic analysis of sunitinib-induced thrombocytopenia in Japanese patients with renal cell carcinoma.

doi: 10.1248/bpb.b14-00636

Figure Lengend Snippet: Fig. 1. Schematic Representation of the PK–PD Model of Sunitinib-Induced Thrombocytopenia

Article Snippet: Determination of Sunitinib and Its Active Metabolite The sunitinib (Toronto Research Chemicals Inc., Toronto, Canada) and N-desethyl sunitinib (Toronto Research Chemicals Inc., Toronto, Canada) assays were performed according to a previously described method14) with minor modifications.

Techniques:

Journal: Biological & pharmaceutical bulletin

Article Title: Pharmacokinetic-pharmacodynamic analysis of sunitinib-induced thrombocytopenia in Japanese patients with renal cell carcinoma.

doi: 10.1248/bpb.b14-00636

Figure Lengend Snippet: Fig. 4. Simulation of Sunitinib-Induced Thrombocytopenia with Reduced Doses of Sunitinib

Article Snippet: Determination of Sunitinib and Its Active Metabolite The sunitinib (Toronto Research Chemicals Inc., Toronto, Canada) and N-desethyl sunitinib (Toronto Research Chemicals Inc., Toronto, Canada) assays were performed according to a previously described method14) with minor modifications.

Techniques: