daunorubicin

P2, N=60, Not yet recruiting, Institute of Hematology & Blood Diseases Hospital, China

P1, N=18, Active, not recruiting, Uma Borate | Recruiting --> Active, not recruiting | Trial completion date: Jan 2025 --> Dec 2025 | Trial primary completion date: Jan 2025 --> Jun 2025

P3, N=1656, Not yet recruiting, Children's Oncology Group | Initiation date: Dec 2024 --> Mar 2025

P3, N=300, Not yet recruiting, Institute of Hematology & Blood Diseases Hospital, China

P2, N=125, Not yet recruiting, University of Washington

P2, N=30, Not yet recruiting, University of Washington

P3, N=727, Completed, ECOG-ACRIN Cancer Research Group | Active, not recruiting --> Completed

P2/3, N=745, Completed, Universitätsklinikum Hamburg-Eppendorf | Active, not recruiting --> Completed

Furthermore, in vivo experiments demonstrated that blocking CCL20 effectively restores the sensitivity of AML cells to daunorubicin chemotherapy. Collectively, these findings underscore the complex interplay between M2 macrophages, CCL20 signaling, and chemotherapy resistance in AML, highlighting potential therapeutic avenues for intervention.

This study presents the important role of FLT3-ITD mutation via its downstream signaling (PI3K/AKT) in the outcome of D3A7 induction therapy. The FLT3-ITD mutation plays an important role in the 12-month survival of AML patients after D3A7 therapy. However, the outcome of D3A7 therapy and FLT3-ITD mutation were not associated with leukemia stem cells.

P3, N=110, Not yet recruiting, Children's Oncology Group | Initiation date: Dec 2024 --> Mar 2025

P3, N=700, Recruiting, Daiichi Sankyo | Not yet recruiting --> Recruiting

P3, N=537, Active, not recruiting, Children's Oncology Group | Trial completion date: Jun 2026 --> Dec 2026 | Trial primary completion date: Jun 2026 --> Dec 2026

P3, N=488, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Dec 2024 --> Mar 2025

P3, N=312, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Sep 2024 --> Sep 2025

P2, N=50, Active, not recruiting, National Cancer Institute (NCI) | Recruiting --> Active, not recruiting

These data suggest that combination therapy involving bortezomib and the DA regimen may represent a promising strategy for HL-AML.

P3, N=5949, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Sep 2024 --> Oct 2025

P3, N=847, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Sep 2024 --> Sep 2025

Simultaneously, the elevation of GSTP1 and JNK complex may reduce the expression of p-JNK and inhibit the activation of JNK pathway, which might inhibit cell apoptosis. In conclusion, our experiments suggested that upregulated SPAG6 might mitigate the pro-apoptotic effects of DNR through ROS/JNK MAPK axis in a GSTP1-dependent manner.

P2, N=155, Active, not recruiting, City of Hope Medical Center | Trial completion date: Sep 2024 --> Dec 2024 | Trial primary completion date: Sep 2024 --> Dec 2024

P1/2, N=55, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Aug 2024 --> Oct 2025 | Trial primary completion date: Aug 2024 --> Oct 2025

P1, N=24, Recruiting, City of Hope Medical Center | Active, not recruiting --> Recruiting | Trial completion date: Aug 2025 --> Feb 2026 | Trial primary completion date: Aug 2025 --> Feb 2026

The "7+3 regimen", which consists of 7 days of cytarabine in combination with daunorubicin during the first 3 days, is a widely used therapy protocol. These simulations are in line with the clinical finding that G-CSF priming can improve the treatment outcome. Furthermore, our model suggests that a decline of HSC counts during remission might serve as an indication for salvage therapy in patients lacking MRD (minimal residual disease) markers.

P1, N=200, Recruiting, Janssen Research & Development, LLC | N=150 --> 200

Mechanistically, the NF-κB signaling pathway regulates the expression of miR-133 in HL-60/ADR cells, and the targeting of CXCL12 by miR-133 enhances the resistance of HL-60/ADR cells to DNR. In conclusion, the NF-κB signaling pathway regulates the expression of miR-133, and inhibiting miR-133 expression can target CXCL12 to increase the sensitivity of HL-60/ADR cells to DNR.

P3, N=110, Not yet recruiting, Children's Oncology Group

Remarkably, the cytotoxicity induced by BOPs triggers the release of DAMPs, particularly HMGB1, IFN-β and ATP, by dying cells, persisting longer than the cytotoxicity of conventional chemotherapeutic agents such as irinotecan and daunorubicin. An in vivo assay in nude mice showed an encouraging 20% inhibition of tumor grafting and growth in a pancreatic cancer model by BOP9.

P2, N=42, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Sep 2024 --> Sep 2025

P2, N=171, Not yet recruiting, National Cancer Institute (NCI) | Trial completion date: Dec 2027 --> Dec 2028 | Initiation date: Oct 2024 --> Jan 2025 | Trial primary completion date: Dec 2027 --> Dec 2028

P3, N=537, Active, not recruiting, Children's Oncology Group | Phase classification: P2/3 --> P3

P3; Initiation date: Jul 2024 --> Feb 2025

Moreover, combined treatment with TRF and daunorubicin (DNR) significantly reduced cell viability and promoted apoptosis in DNR-resistant T-ALL cells. Our study provides valuable insights into the critical role of TRF in treating T-ALL while increasing the sensitivity of DNR-resistant T-ALL cells to DNR.

This is the first evidence that SC, a milk protein, may inhibit proliferation and induce apoptosis in cytarabine-resistant cells.

This report discusses a case of CML that progressed to a megakaryoblastic phase and the patient's death within a month despite receiving one cycle of daunorubicin, cytarabine, and TKI chemotherapy. A 39-year-old female with CML (CP) initially achieved hematological remission with nilotinib but later presented with B symptoms and cytopenias indicative of disease progression...While BCR-ABL1 positivity is typically associated with CML (90-95%), the additional findings point towards a transformation to acute megakaryoblastic leukemia (AMKL or AML-M7). The rare instance of CML's transformation to AMKL highlights the need for megakaryocytic markers in diagnostic panels to ensure accurate diagnosis and timely, tailored therapies for improved outcomes.

Increased nuclear translocation of Nrf2 leads to a significant increase in the expression of its target gene TXN1, but not the NQO1, GPX1, and HMOX1 genes, the increased expression of which can lead to the development of resistance to anthracycline antibiotics. Redox-active CPA micelles have great potential for the development of nanoparticles for the transport of anthracycline antibiotics in experimental tumor chemotherapy, and also as promising activators of Nrf2 transcription factor.

In this study, we designed a multifunctional DNA tetrahedron (MB-MUC1-TD) for the targeted delivery of combined daunorubicin (DAU) + toluidine blue O (TBO)...In vitro cytotoxicity showed better gene therapy efficacy of MB on MCF-7 cells, better biocompatibility of loaded DAU and TBO on LO2 cells, and stronger synergistic cytotoxicity of DAU + TBO on MCF-7/ADR cells. This study may establish a theoretical foundation for co-loading CTPT combination drugs based on multifunctional DNA nanostructures.

P1, N=221, Terminated, M.D. Anderson Cancer Center | Trial completion date: Dec 2024 --> Sep 2024 | Active, not recruiting --> Terminated | Trial primary completion date: Dec 2024 --> Sep 2024; Administratively Complete

P1, N=15, Active, not recruiting, AIDS Malignancy Consortium | Recruiting --> Active, not recruiting

Fat is an expandable tissue that can sequester and detoxify DNR when stimulated by obesity, likely through the upregulation of DNR-metabolizing enzymes AKR1C3 and CBR1. Our data partially explains why obese ALL patients may be more likely to become chemoresistant towards DNR, and provides evidence for potential clinical investigation targeting obesity to reduce DNR chemoresistance.

P1, N=68, Recruiting, University of Washington | Suspended --> Recruiting

P2, N=39, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Aug 2024 --> Aug 2025 | Trial primary completion date: Aug 2024 --> Aug 2025