sunitinib

The LT-025 displayed superior cytotoxicity to the metastatic RCC cells, then standard RCC treatment by sunitinib...The combination therapy also showed an increased tumor growth inhibition in preclinical mouse model studies. A carefully designed KIM-1 targeting ADC can emerge as an effective treatment method for metastatic RCC.

She subsequently received systemic therapy, initially with temozolomide and later pazopanib, followed by sunitinib. This case illustrates the importance of molecular drivers of cancer in a benign soft-tissue tumor and the potential to offer targeted therapies to extend patient survival. This rare case highlights the potential malignant behavior of nodular fasciitis associated with PPP6R3-USP6 fusion.

P3, N=453, Active, not recruiting, Deciphera Pharmaceuticals, LLC | Trial completion date: Dec 2025 --> Dec 2026

Clinical data further verified that high ZEB1 expression is associated with poor prognosis in RCC and that ZEB1 promotes tumor progression by regulating SCD1 to activate the Wnt signaling pathway. In conclusion, APS enhances the sensitivity of RCC to sunitinib by targeting the ZEB1-SCD1-Wnt axis, thus providing a theoretical basis for the clinical application of this combined therapy.

P2, N=34, Completed, National Cancer Institute (NCI) | Active, not recruiting --> Completed

P3, N=861, Completed, Merck Sharp & Dohme LLC | Active, not recruiting --> Completed

Surveillance MRI at 3 months postoperatively revealed local recurrence, prompting combination therapy with sunitinib (VEGF inhibitor) and sintilimab (anti-PD-1 antibody). Follow-up imaging demonstrated significant regression at 1 month, with no evidence of disease progression at 12-month reassessment.

Importantly, PRKAB2 overexpression significantly restored sensitivity to tyrosine kinase inhibitors (TKIs) in sunitinib-resistant RCC cells...Overall, our findings identify PRKAB2 as a critical tumor suppressor in RCC, regulating both protein-protein interactions and lipid metabolism to suppress mitophagy. Targeting PRKAB2-associated pathways may provide a promising therapeutic strategy to enhance treatment efficacy and overcome drug resistance in RCC.

These NETs facilitate tumor cell migration and adhesion while conferring resistance to tyrosine kinase inhibitors (sunitinib and sorafenib) and anti-PD-1 therapy. In vivo, the treatment with DNase1 to disrupt NETs effectively reversed this therapeutic resistance. Our findings unveil the miR-301b-3p/ITPKB/PARP1/IL8/NETs axis as a novel mechanistic link between tumor-intrinsic signaling and neutrophil-driven immunosuppression, providing a solid experimental foundation for developing combination therapeutic strategies for advanced ccRCC.

PDGFRB was validated as a core node within the PTMRS network: activation of PDGFRβ in human colonic fibroblasts promoted CRC cell proliferation and migration, whereas sunitinib attenuated and reversed these effects...These findings suggest that PTMRS may help identify patients who could benefit from combining immunotherapy with therapies targeting PDGFRβ or other PTM-related pathways. Further validation in in vivo models and prospective clinical cohorts is needed.

The remaining patient had an unresectable tumor and received tyrosine kinase inhibitor therapy; however, sequential treatment with imatinib and sunitinib was clinically ineffective. However, their clinical behavior differs: D842Y-mutant GISTs consistently present as large, hypervascular tumors associated with acute complications. The therapeutic efficacy of tyrosine kinase inhibitors remains unclear, underscoring the need for further case accumulation to better define the clinical course and determine optimal treatment strategies for this rare subtype.

Several conjugates, particularly 3a (87.47 %) and 3 g (96.62 %) in MCF-7, induced late apoptosis, and 3c (98.57 %) in MDA-MB-231 induced the highest early apoptosis. Across both proteins (3G0E and 4AGD), 3c consistently shows stronger predicted binding than sunitinib, with more negative binding energies and lower Ki values in each case, supporting its promise as a lead together with 3a.