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: Oncotarget

Article Title: The addition of abemaciclib to sunitinib induces regression of renal cell carcinoma xenograft tumors

doi: 10.18632/oncotarget.19618

Figure Lengend Snippet: 786-O (A) and Caki-1 (B) cells were treated with single agent therapy, or in combination with sunitinib. Cellular viability was determined by CellTiter-Glo ® .

Article Snippet: After 5 weeks of treatment, mice in the vehicle cohort and mice in the sunitinib cohort were treated with the combination of sunitinib 40 mg/kg and abemaciclib 100 mg/kg (HY-16297, Medchemexpress) for an additional 4 weeks.

Techniques:

Journal: Oncotarget

Article Title: The addition of abemaciclib to sunitinib induces regression of renal cell carcinoma xenograft tumors

doi: 10.18632/oncotarget.19618

Figure Lengend Snippet: 786-O cells were treated with DMSO (A) , sunitinib (B) , abemaciclib (C) , or abemaciclib + sunitinib (D) . Cells were stained for annexin V and positivity determined by flow cytometry.

Article Snippet: After 5 weeks of treatment, mice in the vehicle cohort and mice in the sunitinib cohort were treated with the combination of sunitinib 40 mg/kg and abemaciclib 100 mg/kg (HY-16297, Medchemexpress) for an additional 4 weeks.

Techniques: Staining, Flow Cytometry

Journal: Oncotarget

Article Title: The addition of abemaciclib to sunitinib induces regression of renal cell carcinoma xenograft tumors

doi: 10.18632/oncotarget.19618

Figure Lengend Snippet: In 786-O cells (A) and Caki-1 cells (B) abemaciclib exposure results in increased PARP cleavage. This effect is more rapid and pronounced when abemaciclib is combined with sunitinib.

Article Snippet: After 5 weeks of treatment, mice in the vehicle cohort and mice in the sunitinib cohort were treated with the combination of sunitinib 40 mg/kg and abemaciclib 100 mg/kg (HY-16297, Medchemexpress) for an additional 4 weeks.

Techniques:

Journal: Oncotarget

Article Title: The addition of abemaciclib to sunitinib induces regression of renal cell carcinoma xenograft tumors

doi: 10.18632/oncotarget.19618

Figure Lengend Snippet: 786-O cells were treated with DMSO (A) , sunitinib (B) , abemaciclib (C) , or abemaciclib + sunitinib (D) . Pictures were taken after 24 hours of treatment. Magnification factor is 20X.

Article Snippet: After 5 weeks of treatment, mice in the vehicle cohort and mice in the sunitinib cohort were treated with the combination of sunitinib 40 mg/kg and abemaciclib 100 mg/kg (HY-16297, Medchemexpress) for an additional 4 weeks.

Techniques:

Journal: Oncotarget

Article Title: The addition of abemaciclib to sunitinib induces regression of renal cell carcinoma xenograft tumors

doi: 10.18632/oncotarget.19618

Figure Lengend Snippet: Mice with xenograft RCC tumors were treated with sunitinib or vehicle. (A) Tumor size in individual mice. Mice were treated with vehicle or sunitinib as labelled and tumor size measured with calipers. (B) Mean tumor size in each treatment cohort. Error bars are standard deviation. The trend lines are shown within each group. P-value is for difference in slope over the course of the therapy.

Article Snippet: After 5 weeks of treatment, mice in the vehicle cohort and mice in the sunitinib cohort were treated with the combination of sunitinib 40 mg/kg and abemaciclib 100 mg/kg (HY-16297, Medchemexpress) for an additional 4 weeks.

Techniques: Standard Deviation

Journal: Oncotarget

Article Title: The addition of abemaciclib to sunitinib induces regression of renal cell carcinoma xenograft tumors

doi: 10.18632/oncotarget.19618

Figure Lengend Snippet: Mice with xenograft RCC tumors were first treated with sunitinib or vehicle. At the end of treatment, all mice were treated with combination abemaciclib/sunitinib. (A) Tumor size in individual mice. (B) Mean tumor size in each treatment cohort. Error bars represent standard deviation. The trend lines are shown within each group.

Article Snippet: After 5 weeks of treatment, mice in the vehicle cohort and mice in the sunitinib cohort were treated with the combination of sunitinib 40 mg/kg and abemaciclib 100 mg/kg (HY-16297, Medchemexpress) for an additional 4 weeks.

Techniques: Standard Deviation

Journal: Oncotarget

Article Title: The addition of abemaciclib to sunitinib induces regression of renal cell carcinoma xenograft tumors

doi: 10.18632/oncotarget.19618

Figure Lengend Snippet: After a course of sunitinib, mice were subsequently treated with combination abemaciclib/sunitinib and tumor response determined by measurement with calipers. (A) Individual responses, each line represents an individual mouse. (B) Mean response of cohort. Error bars represent standard error of the mean.

Article Snippet: After 5 weeks of treatment, mice in the vehicle cohort and mice in the sunitinib cohort were treated with the combination of sunitinib 40 mg/kg and abemaciclib 100 mg/kg (HY-16297, Medchemexpress) for an additional 4 weeks.

Techniques:

Journal: Human molecular genetics

Article Title: High-throughput screening uncovers miRNAs enhancing glioblastoma cell susceptibility to tyrosine kinase inhibitors.

doi: 10.1093/hmg/ddx323

Figure Lengend Snippet: Figure 1. MiR-302/520 miRNA family increases susceptibility of GBM cells to sunitinib treatment. a) Overview

Article Snippet: Temozolomide and the multitargeted tyrosine kinase inhibitors sunitinib malate and axitinib were acquired from Selleckchem (Houston, USA) and stored at 20 C in DMSO.

Techniques:

Journal: Human molecular genetics

Article Title: High-throughput screening uncovers miRNAs enhancing glioblastoma cell susceptibility to tyrosine kinase inhibitors.

doi: 10.1093/hmg/ddx323

Figure Lengend Snippet: Figure 3. Combination of miRNA-302a/520b expression with multitargeted tyrosine kinase inhibitors decreases GBM cell viability. U87 and DBTRG cells were transfected with 50 nM of miRNA-302a, miR-520b or

Article Snippet: Temozolomide and the multitargeted tyrosine kinase inhibitors sunitinib malate and axitinib were acquired from Selleckchem (Houston, USA) and stored at 20 C in DMSO.

Techniques: Expressing, Transfection

Journal: Human molecular genetics

Article Title: High-throughput screening uncovers miRNAs enhancing glioblastoma cell susceptibility to tyrosine kinase inhibitors.

doi: 10.1093/hmg/ddx323

Figure Lengend Snippet: Figure 5. Cellular DNA content increases upon miR-302a transfection and treatment with multitargeted tyrosine kinase inhibitors. Cells were incubated with miR-302a or control miRNA (cel-miR-239b) mimics for

Article Snippet: Temozolomide and the multitargeted tyrosine kinase inhibitors sunitinib malate and axitinib were acquired from Selleckchem (Houston, USA) and stored at 20 C in DMSO.

Techniques: Transfection, Incubation, Control

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: Molecules (Basel, Switzerland)

Article Title: Shikonin Causes an Apoptotic Effect on Human Kidney Cancer Cells through Ras/MAPK and PI3K/AKT Pathways.

doi: 10.3390/molecules28186725

Figure Lengend Snippet: Figure 1. Cell proliferation activity of A-498 and CAKI-2 human renal cancer cells treated with shikonin or sunitinib: (A,B) A-498 and (C,D) CAKI-2 cells were plated into 96-well plates and treated with increasing doses of shikonin or sunitinib over 72 h. DMSO was used as a vehicle for nontreated control group. The cell proliferation activity was detected by Cell Titer Blue Assay. * p < 0.05—mean significant inhibition of cell growth.

Article Snippet: Shikonin and sunitinib (purity > 98%) (Supplementary Figure S1A,B) were purchased from Santa Cruz Biotechnology (Dallas, TX, USA), dissolved in DMSO, and stored as a stock solution in aliquots at −20 ◦C.

Techniques: Activity Assay, Control, Inhibition

Journal: Molecules (Basel, Switzerland)

Article Title: Shikonin Causes an Apoptotic Effect on Human Kidney Cancer Cells through Ras/MAPK and PI3K/AKT Pathways.

doi: 10.3390/molecules28186725

Figure Lengend Snippet: Figure 2. Inhibition of colony formation of CAKI-2 and A-498 human renal cancer cells by shikonin treatment. Cells plated into 6-well plates were treated with (A,B) sunitinib and (C,D) shikonin at the same time. After administration of the drugs, cells were cultivated for 14 days at 37 ◦C in a 5% CO2 incubator with 95% air. After termination of the experiment, the cells were fixed and visualized by 0.1% crystal violet solution. The colonies resuspended in 2% SDS solution were quantified by determination of absorbance at 570 nm. (E,F) Quantification of colonies formed by cells treated with sunitinib and shikonin in case of two different cell lines. **, p < 0.005; ***, p < 0.0005.

Article Snippet: Shikonin and sunitinib (purity > 98%) (Supplementary Figure S1A,B) were purchased from Santa Cruz Biotechnology (Dallas, TX, USA), dissolved in DMSO, and stored as a stock solution in aliquots at −20 ◦C.

Techniques: Inhibition

Journal: Molecules (Basel, Switzerland)

Article Title: Shikonin Causes an Apoptotic Effect on Human Kidney Cancer Cells through Ras/MAPK and PI3K/AKT Pathways.

doi: 10.3390/molecules28186725

Figure Lengend Snippet: Figure 3. Effect of shikonin on apoptosis of CAKI-2 and A-498 human renal cancer cells. The cells were treated with shikonin and sunitinib over 48 h; the apoptosis was detected by measuring caspase-3 and -7 activity of the cells. * p < 0.05.

Article Snippet: Shikonin and sunitinib (purity > 98%) (Supplementary Figure S1A,B) were purchased from Santa Cruz Biotechnology (Dallas, TX, USA), dissolved in DMSO, and stored as a stock solution in aliquots at −20 ◦C.

Techniques: Activity Assay