Pharmacologic AC inhibition with the ceramide analog SACLAC enhanced single-agent venetoclax cytotoxicity and the venetoclax + cytarabine combination in AML cell lines with primary or acquired venetoclax resistance. Importantly, AC knockdown sensitized AML cells to venetoclax and induced NOXA protein accumulation, whereas NOXA knockdown protected against AC and BCL-2 cotargeting. Collectively, these findings demonstrate the efficacy of cotargeting AC and BCL-2, and rationalize targeting AC as a therapeutic approach for venetoclax-sensitive and -resistant AML.

In this randomized, double-blind, placebo-controlled phase II trial (NCT02502968; registered at ClinicalTrials.gov), 128 patients in first remission received high‑dose cytarabine (HiDAC) plus Motixafortide or placebo. Taken together, combining functional MRD profiling with biomarker-driven patient selection, such as CXCR4 expression, may enable more precise and effective post-remission interventions in AML. This clinical trial is registered at EudraCT number: 2014-002702-21.

Postoperatively, the patient was managed with standard AML therapy (chemotherapy with cytarabine plus an anthracycline was initiated)...Early recognition requires high clinical suspicion, and diagnosis depends on pathology. Further studies are needed to guide optimal management strategies.

Downregulation of IL16 also reduced cell viability and decreased the IC50 of cytarabine (Ara-C) across different concentrations...High IL16 expression was observed in malignant cells from patients with AML. Downregulation of IL16 promotes degradation of mutant TP53 and induces apoptosis, thereby increasing the sensitivity of AML cells to various chemotherapeutic agents in vitro.

Moreover, GSC-selective expression of a combination of cytotoxic (HSV-TK and ganciclovir) and immunomodulatory (IL-12) payloads, delivered using adeno-associated virus vectors, as a single treatment led to curative outcomes in a mouse model of aggressive glioblastoma...In summary, SSEs harness the unique core transcriptional programs that define the GSC phenotype and enable precision immune activation. This approach may have broader applications in other contexts when precise control of transgene expression in specific cell states is necessary.

Drug sensitivity prediction indicated lower IC50 values in high-risk patients for Camptothecin (p = 0.00031), Cytarabine (p = 0.013), Sorafenib (p = 0.000083), and SN-38 (p = 0.0042). This study delineates ICD-related transcriptional heterogeneity in osteosarcoma at single-cell resolution and establishes a robust ICD-based prognostic signature. The findings suggest that ICD reflects an integrated tumor state shaped by cellular programs and microenvironmental interactions, providing preliminary evidence for its utility in risk stratification and therapeutic exploration, which warrants further prospective validation.

P2, N=117, Not yet recruiting, University of California, San Francisco

P2, N=24, Not yet recruiting, National Institute of Neurological Disorders and Stroke (NINDS)

Entecavir antiviral therapy led to suppressed viral replication and improved liver function during follow-up. This case emphasizes the need for HBV screening and close monitoring of viral markers/liver function in asymptomatic HBV carriers receiving dalpiciclib, as early antiviral intervention prevents severe liver complications. It also highlights the importance of clinical pharmacist-led medication follow-up management for outpatients receiving targeted anticancer therapy to avoid oversight of comorbidities and associated prophylactic treatment.

In Jurkat xenograft models, SAp-CD28 demonstrated potent antitumor activity, and its combination with cytarabine resulted in near-complete tumor suppression, highlighting its potential for T-ALL treatment. This work introduces a CD28-targeted, enzyme-activated nanotherapeutic strategy that synergizes biochemical and mechanical mechanisms to selectively eliminate T-ALL cells. This multi-mechanistic tumor-killing strategy can also be extended to inspire therapeutic approaches for other diseases.

To develop novel anti-leukemia therapies, a CNN model identified C191-0266 targeting METTL3, which exhibited potent anti-leukemia activity. It inhibited the proliferation of OCI-AML3, MOLM-13, and THP-1 cell lines with IC50 values of 16.91 μM, 19.01 μM, and 24.99 μM respectively, showed strong METTL3 binding (KD = 7.28 μM) and enzymatic inhibition (IC50 = 7.639 μM), enhanced Ara-C's cytotoxicity by suppressing Ara-C-induced protective autophagy, maintained stable binding to METTL3, regulated the NF-κB pathway to inhibit TNF-α overexpression in Ara-C-resistant cell lines, and had favorable pharmacokinetics and safety profiles via ADME assessments, thus holding promise as an anti-leukemia drug candidate.

This facilitates autophagolysosome formation and enhances autophagic flux to reduce AraC-induced apoptosis, resulting in drug resistance. Targeting LAPTM5 represents a promising strategy to overcome this autophagy-mediated resistance.