Leukemia & Lymphoma最新文献

Bruton tyrosine kinase inhibitors (BTKi) have a unique cardiovascular toxicity profile. We investigated pericardial effusion and tamponade (PE/T) as a potential cardiac complication associated with BTKi therapy. We employed a multi-modal approach: (1) a case series (2) a prevalence analysis using institutional and National Health Oragnization Maintanance (HMO) registry data; and (3) a systematic review and meta-analysis of randomized controlled trials (RCTs) comparing BTKi- and non-BTKi-based regimens in CLL. We identified 15 cases of PE/T during BTKi therapy. In our institutional cohort (n = 750), PE/T prevalence was 2.6% among BTKi-treated patients vs. 0.17% in non-BTKi-treated patients (RR 15.48; p = 0.0072). In the HMO registry (n = 5917), BTKi-associated PE/T prevalence was 0.78%, with an RR of 3.09 (p = 0.029). The meta-analysis showed a significantly increased risk of PE/T with BTKi therapy (OR 3.25; 95% CI 1.02-10.35; p = 0.01; I²=0%). These results suggest that PE/T may represent a rare but clinically meaningful cardiac toxicity of BTKi therapy.

Pneumocystis jirovecii pneumonia (PJP) after autologous stem cell transplantation (ASCT) remains insufficiently characterized. We retrospectively analyzed 304 ASCT recipients (2005-2024) at a single center (B-cell lymphoma n = 138; plasma cell tumor n = 126). Fourteen patients (4.6%) developed PJP at a median of 143 days (86-286) post-ASCT; none were on prophylaxis at diagnosis. The 1-year cumulative incidence was 5.2% overall, and varied by disease: 24% in follicular lymphoma (FL), 5.9% in other B-cell lymphomas, 1.9% in plasma cell tumor, and 0% in T-cell lymphomas. Prior rituximab exposure (HR 6.75; 95% CI 1.50-30.2) and FL diagnosis (HR 7.26; 95% CI 2.51-20.9) were associated with higher risk; age, purine analogs, lymphocyte count, globulin/IgG, and conditioning were not. No death was directly attributable to PJP. These data suggest, diagnosis-dependent risk after ASCT; prophylaxis may be considered for rituximab-treated patients, especially FL, while the optimal duration warrants further study.

Multiple myeloma (MM) is a plasma cell cancer characterized by genomic instability and drug resistance. The FOXM1 transcription factor and the BUB1B kinase are pivotal drivers of this malignancy. FOXM1 promotes cell cycle progression and is upregulated by oncogenic pathways like mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/AKT, correlating with aggressive disease. BUB1B ensures proper chromosome segregation, and its dysregulation fuels genomic instability. Critically, FOXM1 transcriptionally regulates BUB1B, forming an oncogenic axis that enhances proliferation, drug resistance, and survival. This FOXM1-BUB1B pathway is a promising therapeutic target, with inhibitors under preclinical investigation. Future research must validate its clinical relevance, explore combination therapies, and assess its potential as a biomarker to overcome challenges like toxicity and resistance.

Waldenström macroglobulinemia (WM) is the most common malignancy associated with an IgM paraprotein, but in rare cases, a clonal IgM may be the result of IgM multiple myeloma (IgM-MM). Although there are some overlapping features associated with these two entities, there are specific characteristics that can help differentiate IgM-MM from WM. In each patient a thorough clinical, pathologic, and genomic evaluation is required to distinguish these conditions and allow for accurate diagnosis and appropriate treatment.

Tonsillar enlargement in chronic lymphocytic leukemia (CLL) either with or without symptoms has been rarely reported. We describe 22 cases of CLL with tonsillar involvement and demonstrate this is a CLL disease site that may be under-recognized in routine practice. Tonsillar involvement can be divided into three categories: (1) symptomatic CLL tonsillar involvement with upper airway obstruction (UAO) requiring therapy managed with: (a) tonsillectomy without systemic therapy when tonsillar enlargement is disproportionate to overall disease state, (b) tonsillectomy and systemic CLL therapy, and (c) standard systemic CLL therapy alone for both UAO and overall CLL state; (2) asymptomatic CLL tonsillar enlargement in proportion to other CLL disease sites not necessarily requiring imminent therapy; and finally, (3) tonsils as the site of Richter's transformation (RT). Tonsillar involvement in CLL can be evaluated by simple clinical examination in most cases, with imaging utilized if there is concern for UAO or RT.