Hematological Malignancies

P1, N=114, Completed, Janssen Research & Development, LLC | Active, not recruiting --> Completed

P2, N=30, Active, not recruiting, University of Pennsylvania | Recruiting --> Active, not recruiting

P2, N=26, Recruiting, University of Miami | Not yet recruiting --> Recruiting

P1/2, N=30, Completed, Southern Cross University | Recruiting --> Completed

P=N/A, N=500, Recruiting, Peter MacCallum Cancer Centre | N=300 --> 500

P=N/A, N=88, Recruiting, Rajshekhar Chakraborty, MD | Trial completion date: Nov 2025 --> Jun 2026 | Trial primary completion date: Nov 2025 --> Feb 2026

P1, N=28, Terminated, Century Therapeutics, Inc. | Trial completion date: Aug 2027 --> Jul 2025 | Active, not recruiting --> Terminated; Strategic decision

P=N/A, N=80, Enrolling by invitation, University of Pennsylvania | Not yet recruiting --> Enrolling by invitation

All three tested derivatives demonstrated moderate to strong binding to bovine serum albumin (BSA), with preferential occupation of subdomain IIA (site I), as supported both experimentally and through docking studies. The interaction study of these compounds with DNA indicated their ability to interact with ct-DNA through the minor groove.

Beyond IL-1 release, NLRP3 may interface with cellular stress responses and pyroptosis, thereby influencing both AML cells and their microenvironment through multiple mechanisms. Inflammasome signaling may act as a driver of therapy resistance while also representing a promising therapeutic target.

Notably, NPM1 expression correlates with elevated WNT signaling and proliferation in human colorectal cancer (CRC), while CRCs harboring NPM1 deletions exhibit preferential TP53 inactivation, underscoring the clinical relevance of our findings. Being dispensable for adult epithelial homeostasis, NPM1 represents a promising therapeutic target in p53-proficient WNT-driven tumors, including treatment-refractory KRAS-mutant CRC, and hepatic cancers.

Intact pRBCs strongly inhibit megakaryocytic differentiation and disrupt PLP function through transcriptional dysregulation and inflammatory activation, whereas under our experimental conditions, RBC-EVs exert milder modulatory effects. These findings highlight defective platelet production as a novel mechanism contributing to malaria-associated thrombocytopenia.