Results 41 to 50 of about 410 (180)
Potential therapeutic targeting of BKCa channels in glioblastoma treatment
This review summarizes current insights into the role of BKCa and mitoBKCa channels in glioblastoma biology, their potential classification as oncochannels, and the emerging pharmacological strategies targeting these channels, emphasizing the translational challenges in developing BKCa‐directed therapies for glioblastoma treatment.
Kamila Maliszewska‐Olejniczak +4 more
wiley +1 more source
Monitoring circulating tumor DNA (ctDNA) in patients with operable breast cancer can reveal disease relapse earlier than radiology in a subset of patients. The failure to detect ctDNA in some patients with recurrent disease suggests that ctDNA could serve as a supplement to other monitoring approaches.
Kristin Løge Aanestad +35 more
wiley +1 more source
Cell surface interactome analysis identifies TSPAN4 as a negative regulator of PD‐L1 in melanoma
Using cell surface proximity biotinylation, we identified tetraspanin TSPAN4 within the PD‐L1 interactome of melanoma cells. TSPAN4 negatively regulates PD‐L1 expression and lateral mobility by limiting its interaction with CMTM6 and promoting PD‐L1 degradation.
Guus A. Franken +7 more
wiley +1 more source
Pharmacologic ascorbate (vitamin C) increases ROS, disrupts cellular metabolism, and induces DNA damage in CRPC cells. These effects sensitize tumors to PARP inhibition, producing synergistic growth suppression with olaparib in vitro and significantly delayed tumor progression in vivo. Pyruvate rescue confirms ROS‐dependent activity.
Nicolas Gordon +13 more
wiley +1 more source
Nanosecond infrared laser (NIRL) low‐volume sampling combined with shotgun lipidomics uncovers distinct lipidome alterations in oropharyngeal squamous cell carcinoma (OPSCC) of the palatine tonsil. Several lipid species consistently differentiate tumor from healthy tissue, highlighting their potential as diagnostic markers.
Leonard Kerkhoff +11 more
wiley +1 more source
Peroxidasin enables melanoma immune escape by inhibiting natural killer cell cytotoxicity
Peroxidasin (PXDN) is secreted by melanoma cells and binds the NK cell receptor NKG2D, thereby suppressing NK cell activation and cytotoxicity. PXDN depletion restores NKG2D signaling and enables effective NK cell–mediated melanoma killing. These findings identify PXDN as a previously unrecognized immune evasion factor and a potential target to improve
Hsu‐Min Sung +17 more
wiley +1 more source
Etoposide induces DNA damage, activating p53‐dependent apoptosis via caspase‐3/7, which cleaves PARP1. Dammarenediol II enhances this apoptotic pathway by suppressing O‐GlcNAc transferase activity, further decreasing O‐GlcNAcylation. The reduction in O‐GlcNAc levels boosts p53‐driven apoptosis and influences the Akt/GSK3β/mTOR signaling pathway ...
Jaehoon Lee +8 more
wiley +1 more source
Aptamers are used both therapeutically and as targeting agents in cancer treatment. We developed an aptamer‐targeted PLGA–TRAIL nanosystem that exhibited superior therapeutic efficacy in NOD/SCID breast cancer models. This nanosystem represents a novel biotechnological drug candidate for suppressing resistance development in breast cancer.
Gulen Melike Demirbolat +8 more
wiley +1 more source
The PI3Kδ inhibitor roginolisib (IOA‐244) preserves T‐cell function and activity
Identification of novel PI3K inhibitors with limited immune‐related adverse effects is highly sought after. We found that roginolisib and idelalisib inhibit chronic lymphocytic leukemia (CLL) cells and Treg suppressive functions to similar extents, but roginolisib affects cytotoxic T‐cell function and promotion of pro‐inflammatory T helper subsets to a
Elise Solli +7 more
wiley +1 more source
Basroparib inhibits YAP‐driven cancers by stabilizing angiomotin
Basroparib, a selective tankyrase inhibitor, suppresses Wnt signaling and attenuates YAP‐driven oncogenic programs by stabilizing angiomotin. It promotes AMOT–YAP complex formation, enforces cytoplasmic YAP sequestration, inhibits YAP/TEAD transcription, and sensitizes YAP‐active cancers, including KRAS‐mutant colorectal cancer, to MEK inhibition.
Young‐Ju Kwon +4 more
wiley +1 more source

