Hairy Cell Leukemia

P2, N=15, Completed, Scripps Health | Active, not recruiting --> Completed | Trial completion date: Dec 2026 --> Apr 2026 | Trial primary completion date: Dec 2026 --> Apr 2026

This case suggests that the combination of cladribine and low-dose rituximab may be an effective therapeutic strategy for classical HCL with TP53 abnormality, enabling deep molecular response and reversal of associated bone marrow fibrosis. Further prospective studies are warranted to validate these findings.

Aberrant expression of CD5 and CD23 is extremely rare. We present a case of classical HCL expressing both markers, along with a brief review of the literature emphasizing the diagnostic complexities associated with such aberrancy.

P1/2, N=50, Recruiting, Universita' Degli Studi Di Perugia | Not yet recruiting --> Recruiting

P1/2, N=55, Completed, University of Chicago | Active, not recruiting --> Completed

Building on this synthesis, we propose that the insights gained from well-characterized lymphoproliferative disorders may serve as a valuable foundation for investigating related yet poorly understood conditions, such as HCL. Furthermore, given the scarcity of both biological samples and reliable preclinical models for rare hematological malignancies, we highlight the strategic role of European biobanks in providing access to well-annotated clinical samples-an essential resource for fostering interdisciplinary collaboration and enabling advanced experimental modelling.

More recently, 2 BRAF(V600E)-based HCL mouse models have been developed that could be extremely useful both for functional studies and for testing the activity of new drugs. This review aims to summarize current understanding of key pathogenic mechanisms underlying HCL development and discusses major hurdles that need to be overcome in the context of other BRAF-mutated malignancies.

In this Mini Review, we summarize how stromal interactions, extracellular-matrix remodeling, and disrupted immune surveillance reinforce therapeutic resistance in HCL, and how BCR and MAPK signaling interact with these circuits. Further, we highlight emerging strategies, including agents that disrupt chemotaxis, adhesion, and immune checkpoints, designed to dismantle microenvironmental support and improve the depth and durability of remission in HCL.

P1, N=60, Recruiting, Newave Pharmaceutical Inc | Trial completion date: Dec 2025 --> Dec 2027 | Trial primary completion date: Jul 2025 --> Dec 2027

P2, N=30, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Jan 2026 --> Jan 2027 | Trial primary completion date: Jan 2026 --> Jan 2027