These findings indicate that the Leader assay provides a more reliable assessment of SHM status, with higher concordance with SS. Although the FR1 assay may offer additional information regarding clonal patterns, its results should be interpreted cautiously. Given the limited sample size, further studies are warranted to validate these findings. Overall, the Leader assay appears to be more suitable as a primary tool for SHM evaluation, with FR1 results serving a complementary role when interpreted in clinical context.
We illustrate four use cases of ASHOP: (1) stratification of DUX4-rearranged B-cell leukemias into Early/Multipotent and Committed subgroups with distinct outcomes, (2) characterization of HOXA/HOXB expression patterns in acute myeloid leukemias, (3) correlating mutational burden with mismatch repair deficiency and mutational signatures, (4) investigation of TP53 alteration landscape. ASHOP is an open-access resource to inform genomic and transcriptomic data interpretation for hematologic malignancies, and will expand to support additional diseases and data modalities from the ASH community.
The patient was treated with six cycles of rituximab-bendamustine, resulting in complete regression of the nasopharyngeal mass and reduction in splenomegaly, with minimal residual lymphadenopathy and good clinical and biological tolerance. This case highlights the importance of considering CLL in the differential diagnosis of nasopharyngeal masses and emphasizes the role of combined imaging, histology, and immunophenotyping in establishing an accurate diagnosis and guiding appropriate management.
NFκB acts downstream of the T-cell-mediated CD40L:CD40 stimulus, and indeed, CK1δ/ε inhibition efficiently blocked the proliferation of primary CLL triggered by CD40L across multiple patient groups, with lower efficacy in patients with TP53 defects. We propose that CK1δ/ε inhibitors act in the multiple-hit mode, striking both intrinsically via direct interference with cell cycle machinery and extrinsically via inhibition of multiple pro-proliferative stimuli.
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.
Noncovalent BTK inhibitors, particularly pirtobrutinib, has shown impressive activity in patients who have progressed on covalent BTKi. The FDA approval of lisocabtagene maraleucel represents a significant milestone in the treatment of double refractory CLL, providing a potentially curative option for eligible patients. The development of effective treatments for double refractory CLL represents an urgent unmet clinical need and the promising results from emerging therapies offer hope for improved outcomes in this challenging patient population.
P=N/A, N=38, Suspended, University of Wisconsin, Madison | Recruiting --> Suspended
4 days ago
Trial suspension
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HLA-DRB1 (Major Histocompatibility Complex, Class II, DR Beta 1) • HLA-B (Major Histocompatibility Complex, Class I, B) • HLA-C (Major Histocompatibility Complex, Class I, C)
In this review, we will describe the current status of CAR T/NK cell development for AML. We will also introduce a new CAR T-cell or NK-cell therapy that targets mismatched HLA-DRB1 in patients with AML who have relapsed following an allogeneic haematopoietic stem cell transplant.
P2, N=41, Recruiting, Milton S. Hershey Medical Center | Not yet recruiting --> Recruiting
4 days ago
Enrollment open
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HLA-DRB1 (Major Histocompatibility Complex, Class II, DR Beta 1) • HLA-B (Major Histocompatibility Complex, Class I, B) • HLA-C (Major Histocompatibility Complex, Class I, C)