Our results demonstrate that dapagliflozin not only enhances the antitumor efficacy of sunitinib against renal cell carcinoma but also alleviates sunitinib-induced cardiac toxicity in mice via modulation of the AMPKα-PPARα axis.

Notably, this is the first report of ArtiSential articulated forceps utilized in TAMIS, demonstrating their innovative potential in enhancing surgical precision and outcomes in challenging pelvic procedures. The online version contains supplementary material available at 10.1007/s13691-025-00786-7.

Oral melanocytic neoplasms are rare and have distinct clinicopathological features. Despite this, a gap exists in molecular data regarding ODN and AMP. Conversely, OMN and OMM have distinct profiles; in particular, the latter may benefit modestly from tyrosine kinase inhibitor treatment, as KIT and BRAF mutations are sensitive to imatinib and vemurafenib, respectively.

A fragment-assisted screen then delivered a phenalene-dicarbonitrile chemotype, S1g-2, and optimized analogs that displace Bim with sub-micromolar potency, dismantle Hsp70-client hubs, and resensitize resistant xenografts to imatinib or tamoxifen without global proteostasis collapse. Future directions include covalent or macrocyclic wedges, degrader hybrids, and adaptive pulse-dose regimens guided by proximity-ligation assays. Collectively, chemical disarming of the Hsp70-Bim alliance exemplifies how precision targeting of chaperone PPIs can recalibrate apoptotic thresholds and unlock new therapeutic space in oncology.

Moreover, we showed that telatinib-mediated STING activation contributed to the antitumor effects in tumor-bearing mouse models. In summary, our results reveal that telatinib, a previously identified VEGFR2 inhibitor, activates STING signaling, highlighting its potential in cancer immunotherapy.

Cardiac involvement in hypereosinophilic syndromes requires multidisciplinary management combining cytoreductive therapy, anticoagulation when thrombus is present, and serial cardiac magnetic resonance. Testing for FIP1L1-platelet-derived growth factor receptor α is disease-defining and therapy-guiding given the marked response to imatinib.

Primary gallbladder EGISTs are exceedingly rare, with insidious onset and nonspecific clinical manifestations. Histopathological examination combined with immunohistochemistry remains the cornerstone of definitive diagnosis.

The rare genetic co-occurrence of t(15;17)/PML::RARA and t(9;22)/BCR::ABL1 translocations may be identified in a single patient with acute promyelocytic leukaemia (APL).Successful induction using all-trans retinoic acid (ATRA) together with imatinib achieved effective control of both leukemic clones.The patient demonstrated rapid haematologic remission and favourable clinical recovery, suggesting a positive outcome with this therapeutic approach.

Since 2004, patients receiving imatinib with relapse in non-marrow sites were given dasatinib to preserve control of leukemic marrow. Dasatinib is a potentially practice-changing targeted therapy for EML. Finding and eradicating EML could increase the possibility of lengthy disease-free survival.

However, the toxicity and resistance associated with the use of imatinib, a first-generation Bcr-Abl inhibitor, in cases where the T315I mutation exists, necessitates the need for new tyrosine kinase inhibitors...However, investigating different combined scaffolds enhances the chance of successfully developing novel drug candidates. Overall, the information provided in this review can be beneficial to researchers with an interest in chronic myeloid leukemia and tyrosine kinase inhibitors.

The advent of targeted therapy, notably the first tyrosine kinase inhibitor (TKI) imatinib, has revolutionized the treatment landscape for GISTs...This commentary highlights discrepancies in the recommendations for managing GISTs as outlined in these major guidelines. Based on emerging new evidence from recent studies, the authors propose recommendations to be considered for inclusion in future guideline updates to optimize management strategies and ultimately improve the outcomes of patients with GISTs.

Definitive diagnosis of seminoma was established through expanded immunohistochemistry (OCT4+/SALL4+/PLAP+/D2-40+) and molecular confirmation of the characteristic KIT p.D816Y mutation, which concurrently explains the observed imatinib resistance. In conclusion, the findings of the present study highlighted the imperative of integrating morphology, immunohistochemistry and context-specific molecular profiling to avoid diagnostic in CD117-positive tumors.