Lymphoplasmacytic Lymphoma

P2, N=25, Not yet recruiting, University of Utah

P=N/A, N=50, Peking University Shenzhen Hospital; Peking University Shenzhen Hospital

To our knowledge, there have been only two cases previously described in the literature of LPL/WM involvement in the female genital tract; both of which had prominent involvement of the ovaries. Although exceedingly rare, LPL/WM involvement of the female genital tract should be considered on the differential diagnosis if atypical lymphoid cells or dense lymphoid aggregates are observed.

Expression of IRTA1 alone, or either IRTA1+ or MNDA+, was less frequent among MZL with plasma cell differentiation than among MZL with classical cell morphology (p=0.063 and 0.071, respectively), albeit not significantly. IRTA1 and MNDA are sensitive and specific markers for the differential diagnosis of MZL, and they may be helpful in distinguishing MZL from histologic mimics.

P1/2, N=146, Recruiting, BeiGene | Trial completion date: Sep 2027 --> Jan 2029 | Trial primary completion date: Feb 2026 --> Jan 2029

P1, N=36, Recruiting, Verismo Therapeutics | N=18 --> 36

P1/2, N=28, Not yet recruiting, Hemato-Oncologie voor Volwassenen Nederland (Hovon) Stichting | N=14 --> 28

P1, N=16, Completed, Calibr, a division of Scripps Research | N=36 --> 16 | Trial completion date: Aug 2036 --> Oct 2025 | Trial primary completion date: Aug 2036 --> Oct 2025 | Enrolling by invitation --> Completed

Aberrant B cell receptor signaling occurs in several B cell neoplasms including follicular lymphoma (treated with zanubrutinib, a BTK inhibitor), mantle cell lymphoma (acalabrutinib, pirtobrutinib, zanubrutinib), marginal zone lymphoma (zanubrutinib), chronic lymphocytic leukemia and small lymphocytic lymphoma (ibrutinib, acalabrutinib, zanubrutinib, pirtobrutinib), and Waldenström macroglobulinemia (ibrutinib, zanubrutinib)...Pirtobrutinib fails to form a covalent bond and is a reversible BTK inhibitor. The FDA-approvals of rilzabrutinib and remibrutinib (2025) represent the first nononcologic authorizations for BTK antagonists.

Furthermore, this review positions mavorixafor within the broader CXCR4-targeted therapeutic landscape, identifying current research gaps and suggesting directions for future studies. In conclusion, by integrating mechanistic insights with preclinical and clinical findings, this article highlights mavorixafor's promise as a targeted therapy with the potential to transform treatment paradigms for CXCR4-driven diseases.