sunitinib

Our study confirmed FADS3 as a key intermediate protein regulating fatty acid metabolism and tumor progression, which was expected to be a potential diagnostic and prognostic biomarker for ccRCC.

This study reveals that GA inhibits LDHA-driven glycolysis and disrupts the HIF-1α/VEGFA/VEGFR2 signaling pathway in RCC. By enhancing the therapeutic efficacy of sunitinib and overcoming drug resistance, GA offers a promising metabolic-targeted adjuvant strategy for RCC treatment.

Clinical observations in patients treated with sunitinib confirmed a significant reduction in prostate volume and improvement in BPH-related urinary symptoms. Collectively, these findings establish a fibroblast/CSF1R/RTK signaling axis that contributes to BPH pathogenesis and support the potential of RTK inhibition as a therapeutic strategy.

Therapeutic options include somatostatin analogs, multi-targeted tyrosine kinase inhibitors (e.g., sunitinib), or mammalian targets of rapamycin (mTOR) inhibitors (e.g., everolimus), telotristat ethyl, chemotherapy, and peptide-receptor radionuclide therapy. Biomarkers may assist in both the diagnosis and post-treatment follow-up in patients with GEP-NETs. The next decade of research on GEP-NETs is promising and should provide new insights into the molecular underpinnings of this disease, therapy selection, and the sequencing of the available therapies, along with the potential role of AL in NET pharmacotherapy.

Tyrosine kinase inhibitors (TKIs), such as sunitinib and sorafenib, are standard treatments for renal cell carcinoma (RCC). RNA sequencing (RNA-seq) and bioinformatic analyses showed that niclosamide modulated critical pathways, including BRIP1- and FANCA-mediated DNA repair and E2F2-regulated cell cycle progression. These findings provide proof-of-concept that niclosamide enhances TKI efficacy through modulation of DNA repair and cell cycle pathways, supporting the rationale for DNA damage response (DDR)-targeted combination strategies in RCC.

Radiopharmaceuticals such as 131I-MIBG and 177Lu-DOTATATE continue to play a pivotal role, achieving disease control in many patients. Cytotoxic regimens, particularly temozolomide, remain relevant, with some studies suggesting that SDHB-mutated PPGLs demonstrate a heightened sensitivity associated with MGMT promoter hypermethylation and reduced MGMT expression. Targeted agents are increasingly important: multi-kinase inhibitors such as sunitinib, anlotinib, and cabozantinib have shown meaningful activity. The landmark approval of belzutifan, a HIF-2α inhibitor, in 2025 represents the first oral targeted therapy for advanced/metastatic PPGL, which is particularly relevant for pseudohypoxic Cluster 1 tumors...This review summarizes current evidence and highlights ongoing clinical trials, underscoring a paradigm shift toward precision medicine and rational combination strategies. Collectively, these advances bring cautious optimism that metastatic PPGLs may soon become a more manageable chronic disease with improved survival and quality of life.

P3, N=442, Active, not recruiting, Cogent Biosciences, Inc. | Trial primary completion date: Jul 2025 --> Sep 2025

The patient was treated with immunization and targeted therapy (Sunitinib and Tislelizumab injection) and subsequently received a robotic radical nephrectomy. Patients with similar conditions might initially present gynecology for uterine fibroids, easily ignored due to their rarity, missing the time window for diagnosing and treating RCC. This case underscores the need for early genetic screening in patients with recurrent uterine leiomyomas suggestive of FH deficiency.

We described the concentration dependence of neurological and endocrine toxicity. NCT02404584, registered 26 March 2015.

SDH deficient GIST is a unique subtype of gastrointestinal stromal tumor with distinct clinic-pathological features, diagnostic modalities, therapeutic strategies, and genetic implications as compared to C-kit/PDGFR-alpha mutated GIST.

Second- and third-line TKIs, such as sunitinib and regorafenib, provide limited benefits, highlighting the urgent need to address resistance mechanisms. These findings uncover a TGF-β1/CCN2/Rack1/PGK1 mechanism linking CAF-mediated metabolic reprogramming to imatinib resistance in GISTs. Targeting CAF-GIST interactions and key metabolic pathways presents a promising therapeutic strategy.