Journal: Cell Communication and Signaling : CCS

Article Title: Establishment of a mouse hepatocellular carcinoma tumoroid panel recapitulating inter- and intra- heterogeneity for disease modelling and combinatorial drug discovery

doi: 10.1186/s12964-025-02391-w

Figure Lengend Snippet: Alb-R26 Met primary HCC cells are characterised by heterogeneous expression and phosphorylation levels of signals and by resistance to RTKi. ( A ) Western blot of the indicated signalling proteins. Actin or Tubulin were used for normalization. HCC13 cells were used as a positive control (34). Quantifications are reported in Fig. S5B. Full western blot and ponceau staining are shown in Fig. S10-12. ( B ) Dot plot reporting the percentage of viable cells after treatment (1, 3, 10 µM) with the indicated RTKi (cabozantinib, lenvatinib, sorafenib, and regorafenib). Statistical analyses were performed using one-way ANOVA followed by Tukey’s multiple comparison. Levels of significance: * p ≤ 0.05; ** p ≤ 0.01; *** p ≤ 0.001

Article Snippet: The drugs used on cell cultures were: cabozantinib, lenvatinib, regorafenib, and sorafenib (1, 3, and 10μM; TargetMol: #T2586, #T0520, #T1792, #T0093L, respectively).

Techniques: Expressing, Phospho-proteomics, Western Blot, Positive Control, Staining, Comparison

Journal: Cell Communication and Signaling : CCS

Article Title: Establishment of a mouse hepatocellular carcinoma tumoroid panel recapitulating inter- and intra- heterogeneity for disease modelling and combinatorial drug discovery

doi: 10.1186/s12964-025-02391-w

Figure Lengend Snippet: Responsiveness of Alb-R26 Met tumoroids to romidepsin alone or in combination with cabozantinib. ( A ) Graph reporting the viability of tumoroids to 1.3 µM of cabozantinib, a dose chosen for its clinical relevance in relation to the average amount of drug found in patient serum, and allowing comparative analyses with outcomes using patient-derived tumoroids (49). Values are compared to non-treated control conditions. Statistical analyses were performed using one-way ANOVA, followed by Dunnett’s multiple comparison. Levels of significance: * p ≤ 0.05; ** p ≤ 0.01; *** p ≤ 0.001. ( B ) Graphs reporting the viability of tumoroids at 1.3 µM of cabozantinib plus increasing concentration of romidepsin (0.001, 0.003, 0.01, 0.03 µM). Values are compared to non-treated control conditions. The IC 50 values are indicated on each graph. Statistical analyses were performed using two-way ANOVA, followed by Sidak’s multiple comparison. Data were further analysed using Bonferroni correction, showing same significance outcomes. Levels of significance: *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001. ( C ) Brightfield pictures of tumoroids at the indicated conditions. Regarding tHCC18 morphology, we observed some cystic structures developing under cabozantinib (1.3 µM) without and with romidepsin (0.01 µM), possibly related to a dying process in relation to the thinner tumoroid borders, different from cystic tumoroid structures (see as example tHCC20 and tHCC21 in Fig. A and S7B). ( D ) Graph reporting the viability of all tumoroids treated with romidepsin plus cabozantinib to compare the treatment efficacy among them. The IC 50 values for each tumoroids are reported. Experiments were performed in ultra-low adherent plates

Article Snippet: The drugs used on cell cultures were: cabozantinib, lenvatinib, regorafenib, and sorafenib (1, 3, and 10μM; TargetMol: #T2586, #T0520, #T1792, #T0093L, respectively).

Techniques: Derivative Assay, Control, Comparison, Concentration Assay

Journal: bioRxiv

Article Title: Fibroblast-derived Collagen VI shapes the structure and function of the tumor-immune microenvironment in clear cell renal cell carcinoma

doi: 10.64898/2026.03.19.712351

Figure Lengend Snippet: ( A ) Survival analysis for high or low expression of COL6A1 and COL6A2 in the CheckMate 025 study cohort of Nivolumab (anti-PD-1) or everolimus (mTOR inhibitor) treated patients . Graphs show Kaplan-Meier plots and Log-rank (Mantel-Cox) tests. (B-D) Analysis of COL6 deposition in CDMs treated with cabozantinib (Cabo.), sunitinib (Suni.), temsirolimus (Temsi.), or DMSO (Ctrl.) treated TK173 cells. (B) Dot plot depicting relative median fluorescence intensities (MFI) of COL6 in CDMs of respectively treated cells in the screening experiment (N=10 regions of interest, one-way ANOVA with Tukey’s multiple comparison test). (C) Dot plot depicting mean relative MFI of COL6 in CDMs of respectively treated TK173 cells (dots indicate mean of N=4 independent experiments, unpaired t test). (D) IF images stained for FN (green) and COL6 (violet) of synthesized CDMs of TK173 cells treated with the indicated drugs. (E) Schematic description of RNA sequencing analysis of cabozantinib or DMSO control-treated TK173 fibroblasts and acute organotypic slice cultures (OTSCs) of ccRCCs (Created in BioRender. Schell, C. (2026) https://BioRender.com/x5sqb3y ). (F&G) Volcano plot of differential gene expression analysis of matrisome genes in cabozantinib-treated TK173 cells and ccRCC OTSCs. The inserts depict a volcano plot of all genes. Red dots indicate significantly regulated genes with adjusted p<0.01 and log 2 fold change (FC) > |1|). (H) Heatmap analysis of significantly regulated matrisome genes in cabozantinib-treated TK173 cells and ccRCC OTSCs (genes with adjusted p<0.0001 and fold change > |2| are depicted for TK173 cells or with adjusted p<0.01 and fold change > |1.5| for OTSCs). (I) Heatmap analysis of log 2 expression fold changes (FC) of immunomodulatory genes in TK173 cells and ccRCC OTSCs (N/A – not announced). (J&K) IF validation of COL6 regulation in cabozantinib-treated ccRCC OTSCs. Images show IF staining for Nuclei by Hoechst (blue), CK (yellow) and COL6A1 (violet) of OTSCs treated with the indicated drugs. Quantification of COL6A1-positive areas in OTSCs of 10 ccRCC patients (dots indicate individual patients analyzed, ratio paired t test). (L) Schematic summary illustrating the findings of the study, highlighting COL6 expression in tumor stroma as well as the remodeling of the ECM architecture in dependence of COL6 abundance and the subsequent implications for cancer and immune cells (Created in BioRender. Schell, C. (2026) https://BioRender.com/x5sqb3y ).

Article Snippet: Inhibitors used and respective working concentrations are 5 μM cabozantinib (S1119, Selleck Chemicals, Houston, TX, USA), 10 μM sunitinib (S1042, Selleck Chemicals, Houston, TX, USA) and 10 μM temsirolimus (S1044, Selleck Chemicals, Houston, TX, USA), medium was changed every second day.

Techniques: Expressing, Fluorescence, Comparison, Staining, Synthesized, RNA Sequencing, Control, Gene Expression, Biomarker Discovery

Journal: European Thyroid Journal

Article Title: Patient-derived medullary thyroid cancer organoids: a potential model for mechanistic studies on diagnostics and therapy

doi: 10.1530/ETJ-24-0405

Figure Lengend Snippet: Effect of TKIs on calcitonin and CEA concentrations in culture medium from MTOs. (A) Schematic of MTC tissue isolation, primary tissue culture, and the drug screening experiment. MTOs exposed to (B) vandetanib, (C) cabozantinib, (D) selpercatinib, and (E) pralsetinib. All; n = 4 patients; error bars represent SEM, normalized to DMSO controls; dotted lines * P < 0.05.

Article Snippet: Vandetanib (Selleck Chemicals, USA), cabozantinib (LKT Laboratories Inc., USA.), selpercatinib (Selleck Chemicals), and pralsetinib (Selleck Chemicals) were added to the medium of the MZ-CRC-1 MTC cell-line derived spheroids, cultured in an ultra-low attachment U-bottom plate, in a logarithmic dose de-escalation per TKI, 1 week after start of culture.

Techniques: Isolation, Drug discovery

Journal: Advanced Science

Article Title: Micro‐Organ Chip Deciphers Tumor‐Derived G‐CSF as Remote Commander of Lung Pre‐Metastatic Niche via VEGFA‐KDR Cascade

doi: 10.1002/advs.202518584

Figure Lengend Snippet: Pharmacological inhibition of KDR disrupts PMN formation in vitro and in vivo. A) Schematic of assessing KDR inhibitor effect in micro‐organ chip in vitro co‐culture system (Top) and orthotopic 4T1 breast cancer in vivo model (Bottom) . B) Left : Representative fluorescence images showing 4T1‐GFP+ cell colonization in tumor‐co‐cultured lung tissue clusters after 3 days continuous treatment with either Cabozantinib or vehicle control. Right : Normalized colonization density (cells per clusters) in KDR inhibitor‐ versus vehicle‐treated groups. (Scale bars: 500 µm; *p < 0.05, **p < 0.01, ***p < 0.001 by two‐tailed t‐test). C) Left : Immunofluorescence analysis of PMN markers in micro‐organ chip cultured lung tissues. Nuclear staining (DAPI, blue), Vascular remodeling (CD31+, yellow, EMCN, red), KDR (green), ECM remodeling (Fibronectin, green; Vimentin, yellow). (Scale bars: 30 µm). Right : Quantitative analysis of CD31+, CD31+ and EMCN+, KDR+, Fibronectin, and Vimentin deposition. (n=3; *p < 0.05, **p < 0.01, ***p < 0.001 by two‐tailed t‐test). D) Representative longitudinal bioluminescence imaging (foci 10–15 days post 4T1‐GL injection) and quantitative fluorescence analysis of pulmonary metastases at 3–15 days post‐4T1‐GL cells injection. (n=4, p = 0.0140, Fisher's LSD post hoc test). E) IF analysis of lung tissues from orthotopic tumor‐bearing mice. Representative images of CD31 and EMCN (angiogenesis), KDR (target engagement), and Fibronectin (ECM remodeling) in lung sections and quantification results. (Scale bars: 60 µm n = 3 mice/group; * p < 0.05, **p < 0.01, ***p < 0.001 by two‐tailed t‐test).

Article Snippet: For pharmacological interventions, the system was treated with cabozantinib malate (XL184, 1.5 μ m ; Selleck) or vehicle (DMSO), recombinant VEGF164 (5 ng μL −1 ; MedChemExpress), anti‐mouse VEGF‐A neutralizing antibody (2G11‐2A05, 1 ng μL −1 ; Bio X Cell), recombinant G‐CSF (10 ng μL −1 ; Servicebio), or anti‐mouse G‐CSF antibody (MAB414, 1 ng μL −1 ; R&D Systems).

Techniques: Inhibition, In Vitro, In Vivo, Co-Culture Assay, Fluorescence, Cell Culture, Control, Two Tailed Test, Immunofluorescence, Staining, Imaging, Injection, Drug discovery

Journal: Advanced Science

Article Title: Micro‐Organ Chip Deciphers Tumor‐Derived G‐CSF as Remote Commander of Lung Pre‐Metastatic Niche via VEGFA‐KDR Cascade

doi: 10.1002/advs.202518584

Figure Lengend Snippet: The VEGFA‐KDR Signaling Axis Drives Pulmonary PMN Formation. A) Left : Schematic of the micro‐organ chip‐based experimental workflow for validating VEGFA‐induced PMN formation . Right : Representative fluorescence images of 4T1‐GFP+ cell colonization in PBS‐ versus VEGFA‐treated lung tissue clusters and normalized colonization density (cells per cluster). (Scale bars: 500 µm; n=3; * p < 0.05, ** p < 0.01, *** p < 0.001 by two‐tailed t‐test). B) Immunofluorescence analysis of lung tissues after PBS/VEGFA treatment: Nuclei (DAPI, blue), Angiogenesis (CD31, yellow), Microvasculature (EMCN, red), KDR expression (green), ECM remodeling (Fibronectin, green; Vimentin, yellow). (Scale bars: 30 µm), and quantification of CD31+, CD31+EMCN+ (CAP cells), KDR+ fractions in CAP cells, Fibronectin and Vimentin deposition. (n=3; *p < 0.05, **p < 0.01, ***p < 0.001 by two‐tailed t‐test). C) IF and IHC of in vivo lung sections from VEGFA‐infused mice showing CD31, KDR, and VEGFA expression, and marker‐positive area quantification. (Scale bars: 60 µm (IF), 40 µm (IHC); n=3 mice/group; *p < 0.05 , **p < 0.01 , ***p < 0.01 by t‐test). D) Schematic of the micro‐organ chip based experimental workflow for validating receptor‐dependent KDR activation, and signaling specificity of the VEGFA‐KDR axis. Top : 4T1‐GFP+ colonization in VEGFA protein and vehicle versus VEGFA protein and cabozantinib groups. Bottom : 4T1‐GFP+ colonization in tumor co‐cultured lung tissue clusters with isotype control versus αVEGFA antibody groups. E) Left : Normalized colonization density (cells per cluster) of 4T1‐GFP+ cell colonization in VEGFA protein and vehicle versus VEGFA protein and cabozantinib groups. Right : Normalized colonization density (cells per cluster) of 4T1‐GFP+ cell colonization in tumor‐lung co‐cultures with isotype control versus anti‐VEGFA. (Scale bars: 500 µm; n=3; *p < 0.05, **p < 0.01, ***p < 0.001 by two‐tailed t‐test). F) Quantification of CD31+EMCN+ (CAP cells), KDR+ fractions in CAP cells, Fibronectin deposition in VGEFA protein combine with cabozantinib or vehicle. (n=3; *p < 0.05, **p < 0.01, ***p < 0.001 by two‐tailed t‐test). G) IF and IHC analysis of lung tissues from orthotopic tumor‐bearing and VEGFA antibody or isotype control‐treated mice. Representative images of CD31 (angiogenesis), KDR (target engagement), and VEGFA (pro‐angiogenic signaling) in lung sections and quantification of marker‐positive areas. (Scale bars: 60 µm (IF), 100 and 40 µm (IHC); n = 3 mice/group; *p < 0.05, **p < 0.01, ***p < 0.001 by two‐tailed t‐test).

Article Snippet: For pharmacological interventions, the system was treated with cabozantinib malate (XL184, 1.5 μ m ; Selleck) or vehicle (DMSO), recombinant VEGF164 (5 ng μL −1 ; MedChemExpress), anti‐mouse VEGF‐A neutralizing antibody (2G11‐2A05, 1 ng μL −1 ; Bio X Cell), recombinant G‐CSF (10 ng μL −1 ; Servicebio), or anti‐mouse G‐CSF antibody (MAB414, 1 ng μL −1 ; R&D Systems).

Techniques: Fluorescence, Two Tailed Test, Immunofluorescence, Expressing, In Vivo, Marker, Activation Assay, Cell Culture, Control, Drug discovery

Journal: Advanced Science

Article Title: Micro‐Organ Chip Deciphers Tumor‐Derived G‐CSF as Remote Commander of Lung Pre‐Metastatic Niche via VEGFA‐KDR Cascade

doi: 10.1002/advs.202518584

Figure Lengend Snippet: Tumor‐derived G‐CSF regulates VEGFA‐KDR axis. A) ELISA quantification of VEGFA levels in conditioned media from differentially treated lung tissues. Tumor co‐culture and recombinant G‐CSF significantly increased VEGFA secretion compared to RPMI 1640 controls (n=3; *p < 0.05, **p < 0.01, ***p < 0.001 by one‐way ANOVA).B) Schematic of the experimental design for functional validation of G‐CSF‐mediated VEGFA‐KDR axis regulation in the micro‐organ chip system. Key interventions included: VEGFA neutralization (VEGFA antibody) and KDR inhibition (cabozantinib). C) Representative fluorescence images and quantitative analysis of 4T1‐GFP+ cell colonization in lung tissues treated with G‐CSF plus VEGFA antibody and parallel experiments with G‐CSF plus cabozantinib. Normalized colonization density (cells per cluster) demonstrates a significant reduction in tumor cell adhesion upon pathway disruption (Scale bar: 500 µm; n=3; two‐tailed t‐test, *p < 0.05, **p < 0.01, ***p < 0.01). D) Immunofluorescence analysis of lung tissues post‐treatment with G‐CSF combine with VEGFA antibody. Nuclei (DAPI, blue), angiogenesis (CD31, yellow), microvasculature (EMCN, red), and KDR expression (green). (Scale bars: 30 µm), and quantification of CD31+EMCN+ (CAP cells), KDR+ fractions in CAP cells. E) Immunofluorescence analysis of lung tissues post‐treatment with G‐CSF combined with VEGFA antibody. Nuclei (DAPI, blue), ECM remodeling (Fibronectin, green; Vimentin, yellow). (Scale bars: 30 µm), and quantification of Fibronectin deposition. F) Quantitative analysis of CD31+, CD31+EMCN+ (microvascular/CAP cells), KDR+ CAP cells, Fibronectin, and Vimentin deposition in G‐CSF‐cabozantinib. (n=3; two‐tailed t‐test, *p < 0.05, **p < 0.01, ***p < 0.001). G) Schematic illustration of how tumor‐secreted G‐CSF promotes pre‐metastatic niche formation in the lung by modulating the VEGFA‐KDR signaling axis.

Article Snippet: For pharmacological interventions, the system was treated with cabozantinib malate (XL184, 1.5 μ m ; Selleck) or vehicle (DMSO), recombinant VEGF164 (5 ng μL −1 ; MedChemExpress), anti‐mouse VEGF‐A neutralizing antibody (2G11‐2A05, 1 ng μL −1 ; Bio X Cell), recombinant G‐CSF (10 ng μL −1 ; Servicebio), or anti‐mouse G‐CSF antibody (MAB414, 1 ng μL −1 ; R&D Systems).

Techniques: Derivative Assay, Enzyme-linked Immunosorbent Assay, Co-Culture Assay, Recombinant, Functional Assay, Biomarker Discovery, Neutralization, Inhibition, Fluorescence, Disruption, Two Tailed Test, Immunofluorescence, Expressing

Journal: Cancer Research Communications

Article Title: Antiangiogenic Tyrosine Kinase Inhibitors have Differential Efficacy in Clear Cell Renal Cell Carcinoma in Bone

doi: 10.1158/2767-9764.CRC-24-0304

Figure Lengend Snippet: Efficacy of TKIs on tumor growth, in vitro and in vivo . A, Dose–response curve of axitinib, cabozantinib, and lenvatinib treatment of UM-RC-3 and RENCA VHL − , mean + SD, n = 5/group; control, 0 mmol/L TKIs, 1% DMSO; IC 50 values of cell viability are reported. B, Experimental design and timeline of treatment schedule. C and D, Response to TKIs by UM-RC-3 ( C ) and RENCA VHL − ( D ) tumor cells in tibiae at day 11 of treatment; representative bioluminescence images and quantification are shown, mean ± SEM, n = 16 tibiae/group. E, Response of tumor cells in lungs to TKIs at day 11 of treatment; representative bioluminescence images and quantification are shown, mean ± SEM, n = 8/group. F, Stereomicroscope images of lungs (brightfield and GFP–green); Bar, 1 cm. P values by one-way ANOVA with Tukey honestly significant difference post hoc test; *, P < 0.05; **, P < 0.01; ***, P < 0.001. Axi, axitinib; Cabo, cabozantinib; Conc, concentration; Lenv, lenvatinib; Veh, vehicle.

Article Snippet: TKIs (axitinib, cabozantinib, and lenvatinib >99% purity) were purchased from TargetMol.

Techniques: In Vitro, In Vivo, Control, Concentration Assay

Journal: Cancer Research Communications

Article Title: Antiangiogenic Tyrosine Kinase Inhibitors have Differential Efficacy in Clear Cell Renal Cell Carcinoma in Bone

doi: 10.1158/2767-9764.CRC-24-0304

Figure Lengend Snippet: In vitro and in vivo effects of TKIs on blood vessels. A, Dose–response curve of axitinib, cabozantinib, and lenvatinib treatment of HUVECs, mean ± SD, n = 4. B, Schematic representation of the experimental approach. C and D, Impact of TKIs on vascularization of RENCA VHL − tumors in bone evaluated by IF analysis; representative images acquired by confocal microscopy (green, GFP; blue, DAPI; yellow, endomucin; red, laminin; C ) and quantification are shown ( D ); dotted line, tumor area; mean ± SEM, n = 4–10/group; bar, 100 μm. E and F, Impact of TKIs on vascularization of RENCA VHL − tumors in lungs; representative images acquired by confocal microscopy (green, GFP; blue, DAPI; red, CD31; E ) and quantifications are shown; dotted line, tumor area; mean ± SEM, n = 4–10/group; ar, 100 μm. P values by one-way ANOVA with Tukey honestly significant difference post hoc test; *, P < 0.05; **, P < 0.01; ***, P < 0.001. A, axitinib; BV, blood vessel; C, cabozantinib; Endo/Endom, endomucin; L, lenvatinib; Lam, laminin; RV − , RENCA VHL; V, vehicle.

Article Snippet: TKIs (axitinib, cabozantinib, and lenvatinib >99% purity) were purchased from TargetMol.

Techniques: In Vitro, In Vivo, Confocal Microscopy

Journal: Cancer Research Communications

Article Title: Antiangiogenic Tyrosine Kinase Inhibitors have Differential Efficacy in Clear Cell Renal Cell Carcinoma in Bone

doi: 10.1158/2767-9764.CRC-24-0304

Figure Lengend Snippet: TKIs’ effect on immune cell infiltration in bone tumors. A, Impact of TKIs on CD8 infiltration in RENCA VHL − tumors in bone evaluated by IF analysis; representative images acquired at the confocal microscope (green, GFP; blue, DAPI; yellow, CD8; red, laminin) are shown; dotted line, tumor area. Bar, 100 μm. B, Quantification of the number and distribution of CD8 + cells associated with tumor; mean ± SEM, n = 6–12/group. C, Representative images and quantification ( D and E ) of immune subsets infiltrating bone tumors by multiplex imaging (COMET, Lunaphore) post-TKI treatment, mean ± SEM, n = 3/group P values by one-way ANOVA with Tukey honestly significant difference post hoc test; *, P < 0.05; **, P < 0.01; ***, P < 0.0001. Inner tumor region >25 μm from the tumor edge. A, axitinib; C, cabozantinib; Inner reg, inner region; L, lenvatinib; Lam, laminin; lymph, lymphocytes; myel, myeloid; V, vehicle.

Article Snippet: TKIs (axitinib, cabozantinib, and lenvatinib >99% purity) were purchased from TargetMol.

Techniques: Microscopy, Multiplex Assay, Imaging

Journal: Cancer Research Communications

Article Title: Antiangiogenic Tyrosine Kinase Inhibitors have Differential Efficacy in Clear Cell Renal Cell Carcinoma in Bone

doi: 10.1158/2767-9764.CRC-24-0304

Figure Lengend Snippet: Ex vivo µCT analysis of TKIs’ effects on bone microarchitecture. A, Representative μCT micrographs of tibial metaphysis cross-sections extracted from mice treated with axitinib, cabozantinib, and lenvatinib or vehicle, Bar, 300 μm. B, Quantification of key bone histomorphometry parameters extrapolated from μCT analysis, mean ± SEM, n = 4/group. C, Impact of TKIs on TRAP + cells in RENCA VHL − tumors in bone evaluated by IF analysis; representative images acquired at the confocal microscope (green, GFP; white, DAPI; red, TRAP) are shown; arrow, TRAP + cells. Bar, 250 μm. P values by one-way ANOVA with Tukey honestly significant difference post hoc test; *, P < 0.05. A, axitinib; C, cabozantinib; L, lenvatinib; TRAP, tartrate-resistant acid phosphatase; V, vehicle.

Article Snippet: TKIs (axitinib, cabozantinib, and lenvatinib >99% purity) were purchased from TargetMol.

Techniques: Ex Vivo, Microscopy

Journal: Cancer Research Communications

Article Title: Antiangiogenic Tyrosine Kinase Inhibitors have Differential Efficacy in Clear Cell Renal Cell Carcinoma in Bone

doi: 10.1158/2767-9764.CRC-24-0304

Figure Lengend Snippet: Prolonged treatment with TKIs followed by withdrawal and survival analysis. A, Schematic representation of experimental design. B, Representative images of bioluminescence signal in tibiae and lungs. C, Bioluminescence signal of tumors in bone quantified over time; single tumors are shown. D, Analysis of survival over time after TKI treatment based on bone tumors (photon flux values of 3 × 10 6 were considered as the end point). Absolute numbers are reported in the table. P value (one-way ANOVA with Tukey honestly significant difference post hoc test) and median OS are shown. E, Bioluminescence signal of tumors in lungs quantified over time; F, Estimation of survival over time after TKI treatment based on lung tumors. Absolute numbers are reported in the table. P value (one-way ANOVA with Tukey honestly significant difference post hoc test), median OS and 95% CI of ratio after the log-rank (Mantel–Cox) test are shown. Axi, axitinib; Cabo, cabozantinib; ; Lenv, lenvatinib; MBP, median bone progression; WD, withdrawal; Veh, vehicle.

Article Snippet: TKIs (axitinib, cabozantinib, and lenvatinib >99% purity) were purchased from TargetMol.

Techniques:

Journal: Cancer Research Communications

Article Title: Antiangiogenic Tyrosine Kinase Inhibitors have Differential Efficacy in Clear Cell Renal Cell Carcinoma in Bone

doi: 10.1158/2767-9764.CRC-24-0304

Figure Lengend Snippet: TKIs as a second-line treatment. A, Schematic representation of experimental design. B , D , and F, Representative images of bioluminescence signal in tibiae/lungs of mice and bioluminescence signal of tumors quantified over time; single tumors are shown. C , E , and G, Estimation of survival over time after TKI treatment based on bone and lung tumors. Absolute numbers are reported in the table. P value (one-way ANOVA with Tukey honestly significant difference post hoc test) with median OS and 95% CI of ratio after the log-rank (Mantel–Cox) test. Axi, axitinib; Cabo, cabozantinib; Lenv, lenvatinib; MBP, median bone progression; Rx, second-line treatment; WD, withdrawal.

Article Snippet: TKIs (axitinib, cabozantinib, and lenvatinib >99% purity) were purchased from TargetMol.

Techniques: