Waldenstrom Macroglobulinemia

P1/2, N=190, Active, not recruiting, ArQule, Inc., a subsidiary of Merck Sharp & Dohme LLC, a subsidiary of Merck & Co., Inc. (Rahway, NJ USA) | Trial completion date: Sep 2026 --> Sep 2027 | Trial primary completion date: Sep 2026 --> Sep 2027

The patient received six cycles of bendamustine and rituximab (BR), leading to a reduction in hepatic lesions and IgM levels, though treatment was complicated by persistent cytopenias. Comprehensive histopathological and molecular evaluation is critical for accurate diagnosis and appropriate therapy. Our report expands the spectrum of extramedullary WM and highlights the potential for favorable response to BR despite unusual presentation.

P1, N=85, Recruiting, Exscientia AI Ltd., a wholly owned subsidiary of Recursion Pharmaceuticals, Inc. | N=50 --> 85

After six cycles of azacitidine, she achieved remission of MDS but rapidly progressed to AML and ultimately died. This case provides a key clinical lesson: persistent cytopenias during ibrutinib therapy were attributable to MDS progression rather than SWM, underscoring the importance of re-evaluation. Furthermore, it completely documents clonal evolution from 2.5% blasts (MDS with low blasts) to 6% blasts (MDS with increased blasts-1) and ultimately to AML (66% blasts), and it introduces the emergence of an FLT3-ITD mutation that rapidly drove the disease into AML even after the patient had achieved MDS remission. We also review the rare coexistence of WM and MDS/AML, and MGUS with MDS.

This case of WM with renal AHL amyloidosis highlights the importance of keeping renal amyloidosis in mind in patients with proteinuria. The favourable hematologic and renal response to treatment with bendamustine and rituximab in this case adds valuable data for the management of WM complicated by renal amyloidosis.

It highlights the diagnostic challenge of seronegative RPGN, in which MIDD should be included in the differential diagnosis. The case underscores the importance of integrated histopathology and hematologic genomics in identifying rare MGRS entities, recognizing that severe kidney injury may evolve rapidly despite appropriate management.

This case highlights the diagnostic complexity of composite indolent B-cell lymphomas and underscores the importance of integrated clinical, morphologic, immunophenotypic, and molecular assessment to inform management and surveillance.

In DLBCL MYD88 L265P mutation is found in 32% of cases and it is significantly more prevalent in cases with the non-GCB phenotype (OR 5.78 p value = 2.07 × 10⁻⁵) and in DLBCL of extranodal locations (OR = 5.44 p value p < 0.001), including, not only immuneprivileged sites but also the skin, breast, upper respiratory tract, adrenal gland and bone and soft tissues. MYD88L265P mutation is highly specific of the non-GCB type DLBCL, likely reflecting MCD/C5 genetic features in a subset of non-GCB/ABC DLBCL.

P3, N=700, Recruiting, Janssen Research & Development, LLC | Trial completion date: Aug 2027 --> Dec 2029

P=N/A, N=10, Completed, British Columbia Cancer Agency | Not yet recruiting --> Completed | N=30 --> 10

P2, N=46, Active, not recruiting, Dana-Farber Cancer Institute | Recruiting --> Active, not recruiting