Undetectable minimal residual disease (uMRD) has emerged as a critical prognostic and potentially predictive biomarker in chronic lymphocytic leukemia (CLL), particularly in venetoclax-based time-limited regimens...Ongoing trials will further define the role of MRD-adapted therapy duration in first-line CLL treatment. Overall, MRD is a powerful tool to move beyond one-size-fits-all regimens and may become integral in personalizing CLL management across diverse therapeutic regimens.

P1, N=50, Active, not recruiting, Dana-Farber Cancer Institute | Recruiting --> Active, not recruiting | Trial primary completion date: Dec 2025 --> Feb 2025

Morusin induces CRC cell senescence via the DNMT1/CDK2/p53 axis, and renders the cells vulnerable to senolytic agents. This study not only broadens the development and utilization of morusin but also provides a novel sequential therapeutic strategy for combating CRC.

P=N/A, N=100, Active, not recruiting, AbbVie | Recruiting --> Active, not recruiting

Pathway and perturbation analyses suggested that NCI-LYM-1 harbored a strong dependency on apoptotic pathways, which was confirmed by in vitro organoid testing with the BCL-2/BCL-xL inhibitor navitoclax (IC 50 : 0.27 µM) and the MCL-1 inhibitor AZD-5991 (IC 50 : 0.060 µM). Overall, NCI-LYM-1 recapitulates the clinical aggressiveness and heterogeneity of AVPC, providing a tractable platform to identify novel precision therapies.

P2, N=400, Not yet recruiting, Australasian Leukaemia and Lymphoma Group (ALLG) | Phase classification: P --> P2 | N=50 --> 400

In vitro treatment of primary HRS cells with BCL2 inhibitor, venetoclax, augmented induction of apoptosis in HRS cells and other cells of the HL immune microenvironment. These findings support further study of targeting apoptosis resistance as a potential approach to eliminate malignant HRS cells and dismantle inflammatory lesion formation in pediatric HL.

Venetoclax combination regimen achieved excellent efficacy and safety in the treatment of relapsed/refractory multiple myeloma with t(11;14) in this case. The treatment of patients with relapsed and refractory multiple myeloma with t(11;14) by venetoclax still needs to be confirmed by more clinical studies.

P2, N=40, Not yet recruiting, Canadian Cancer Trials Group

P1/2, N=75, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Dec 2025 --> Dec 2027 | Trial primary completion date: Dec 2025 --> Dec 2027

This approach is demonstrated in the recent promising results achieved utilizing venetoclax, a BCL2 inhibitor, in patients with PICALM::MLLT10 acute leukemia. Herein, we provide updates on the pathophysiology, clinical presentation, prognosis, and treatment of PICALM::MLLT10 acute leukemia.

The B-cell lymphoma 2 (BCL-2) inhibitor venetoclax (VEN) in combination with hypomethylating agents (HMAs) has improved treatment outcomes for acute myeloid leukemia (AML) patients unfit for intensive chemotherapy and is increasingly used in the relapsed/refractory setting. Ex vivo treatment with the combination of navitoclax and SMAC mimetics further enhanced the eradication of VEN-HMA refractory blasts, although toxicity was also observed in healthy CD34+ cells. In conclusion, our integrative analysis identifies molecular signatures associated with primary VEN-HMA resistance and highlights BCL-2/BCL-XL inhibition and SMAC mimetics as therapeutic strategies to target resistance.