Dae Hyun Lee

Cardiovascular adverse events (CVAEs) associated with bispecific T‐cell engaging antibodies (BsAbs) have not been systematically investigated across approved agents. In this disproportionality analysis of FAERS (December 2014–September 2025), reports listing BsAbs as the primary suspected drug ( n = 7647) were compared with all other drugs in the database ( N = 7 289 316) and appropriate active comparators. Adjusted reporting odds ratios (aRORs) were estimated using multivariable logistic regression, adjusting for age, sex, cardiovascular comorbidity, disease, and concomitant cardiotoxic medications. Among 7647 BsAb‐associated reports (median age: 60 [36–71] years; 44.6% female), 1408 (18.4%) involved a CVAE and 447 (5.8%) were fatal. BsAbs showed increased reporting of DIC (aROR: 4.35 [3.18–5.96]; n = 49), hypotension (1.61 [1.38–1.89]; n = 181), and fatal CVAEs (1.63 [1.47–1.80]; n = 447). MM‐directed BsAbs were associated with shock (2.09 [1.65–2.66]) and myocarditis (3.68 [1.49–9.10]). Blinatumomab was associated with DIC (4.41 [3.05–6.37]) and hypotension (1.46 [1.18–1.81]). Teclistamab showed the strongest myocarditis signal (5.95 [2.16–16.43]; n = 4). Mosunetuzumab showed increased reporting of atrial fibrillation (2.25 [1.15–4.38]) and supraventricular tachycardia (2.21 [1.17–4.15]). CVAEs occurred earlier than non‐CVAEs (median 7 vs. 15 days; p < 0.001). The majority of hypotension (56.4%) and heart failure (44.2%) reports occurred independently of both CRS and infection. Case fatality proportions for shock (60.1%), DIC (51.0%), and heart failure (48.1%) exceeded those for CRS (24.3%). BsAb‐associated cardiovascular signals, particularly DIC, hemodynamic events, and fatal CVAEs, varied by agent and target antigen. These findings support the need for cardiovascular‐specific monitoring during therapy.

Figure S5. Changes in signaling in BM of trisomy 8+ TN-MF patient and MYC MF mice. Figure S6. Effects of silencing S100a9 in MYC-driven MF or overexpression of S100a9. Figure S7. Effects of inhibition of S100a9 or MYC in MYC-driven MF. Figure S8. Synthesis and Characterization of Tasquinimod. Figure S9. Synthesis and Characterization of MYCi975.

Comparison of gene expression profiles of Mx1-Cre+/-;Rosa26LSL-MYC/LSL-MYC vs. Mx1-Cre+/-;Rosa26+/+ mouse.

Cell-cell interaction analyses.

Figure S1. Landscape of somatic mutations and cytogenetics in Moffitt MF cohort. Figure S2. Effects of enforced MYC expression in HSCs in vivo. Figure S3. MYC-induced changes in hematopoietic sub-populations and colony forming potential. Figure S4. The JAK/STAT, PI3K/AKT, MEK/ERK, and alarmin pathways in MYC-driven MF.

Table S1. Demographics of Moffitt Total Cancer Care MF patients. Table S2. Demographic Profile of trisomy 8+ TN-MF patients and HDs used in scRNA-seq analysis and PDX studies. Table S3. List of genes used for PROGENy analysis of human BM cells. Table S4. Demographics of TN-MF patients. Table S5. Clinical parameters of Mx1-Cre+/-;Rosa26LSL-MYC/LSL-MYC studies. Table S6. Clinical parameters of Scl-CreERT+/-;Rosa26LSL-MYC/LSL-MYC in vivo studies. Table S7. Clinical parameters in competitive transplant studies. Table S8. Comparison of gene expression profiles of Mx1-Cre+/-;Rosa26LSL-MYC/LSL-MYC vs. Mx1-Cre+/-;Rosa26+/+ mouse. Table S9. List of genes used for PROGENy analysis of mouse BM cells. Table S10. Cell-cell interaction analyses. Table S11. Clinical parameters of Mx1-Cre+/-;Rosa26LSL-MYC/LSL-MYC;S100a9-/- studies. Table S12. Clinical parameters of S100a9 transgenic mouse studies. Table S13. Clinical parameters of Tasquinimod efficacy studies in MYC-driven MF. Table S14. Clinical parameters of MYCi975 efficacy studies in MYC-driven MF. Table S15: Key Resources Table. Table S16: Sequence Information.

Background: Venetoclax, a potent B‐cell leukemia/lymphoma‐2 inhibitor, is an antineoplastic agent used in various hematologic malignancies, including acute myeloid leukemia (AML). The aim of the study is to evaluate the incidence, risk factors, and outcomes of major adverse cardiac events (MACEs) among patients with newly diagnosed AML receiving venetoclax‐based therapy. Methods: We conducted a retrospective, single‐center cohort study of 214 patients with newly diagnosed AML treated with venetoclax. MACE was defined as a composite of new‐onset heart failure, heart failure exacerbation requiring hospitalization, myocardial infarction/coronary revascularization, or stroke/transient ischemic attack during active venetoclax‐based therapy. The Fine–Gray subdistribution hazard model determined the association between baseline clinical characteristics and MACEs, with noncardiovascular death as a competing risk. A Cox proportional hazard model determined the association between time‐dependent MACEs and overall survival. Results: Among 214 patients (mean age, 71.5 years; 41% women), MACEs occurred in 14 (6.5%) patients. Patients with non–de novo (secondary /treatment‐related) AML had a higher incidence of MACEs compared with de novo AML (85.7% versus 14.3%; subdistribution hazard ratio [HR], 7.1 [95% CI, 1.5–33]; P <0.01). Time‐dependent MACE was independently associated with inferior overall survival (adjusted HR, 2.75 [95% CI, 1.41–5.35]). Conclusions: In conclusion, MACE is a clinically significant event that occurs in 6.5% of patients with AML treated with venetoclax and is a higher‐risk event for patients with secondary AML or treatment‐related AML.

Myelofibrosis (MF) is a subgroup of Philadelphia chromosome-negative myeloproliferative neoplasms that are associated with an increased risk of cardiovascu