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Venetoclax and azacitidine in combination with homoharringtonine, cytarabine, and aclarubicin for salvage therapy of relapsed/refractory T cell acute lymphoblastic leukemia.
Int J Hematol
January 2025
Department of Hematology, The 920th Hospital of Joint Logistics Support Force, No.212, Da Guan Road, Xishan District, Kunming, 650100, Yunnan, China.
Background: The treatment of relapsed/refractory T cell acute lymphoblastic leukemia (R/R T-ALL) is a significant challenge in hematologic oncology, and no standard salvage treatment plan exists. Both Chinese and international clinical guidelines recommend combination chemotherapy including venetoclax.
Methods: Efficacy and safety of venetoclax, azacitidine, homoharringtonine, cytarabine, and aclarubicin (VA-HAA) combination therapy were retrospectively analyzed in 3 patients with R/R T-ALL at the Department of Hematology, 920th Hospital of the Joint Logistics Support Force, Chinese People's Liberation Army.
Treating Hematological Malignancies With OR-2100, an Orally Bioavailable Prodrug of Decitabine.
Cancer Sci
January 2025
Department of Drug Discovery and Biomedical Sciences, Faculty of Medicine, Saga University, Saga, Japan.
DNA methylation is an enzyme-driven epigenetic modification that must be precisely regulated to maintain cellular homeostasis. Aberrant methylation status, especially hypermethylation of the promoter sites of tumor-suppressor genes, is observed in human malignancies and is a proven target for cancer therapy. The first-generation DNA demethylating agents, azacitidine and decitabine, are widely used for treating several hematological malignancies.
View Article and Find Full Text PDFHypoxia impairs decitabine-induced expression of HLA-DR in acute myeloid leukaemia cell lines.
Clin Epigenetics
January 2025
School of Biomedical Sciences and Pharmacy, The University of Newcastle, Callaghan, NSW, 2308, Australia.
Background: Hypomethylating agents (HMA), such as azacytidine (AZA) and decitabine (DAC), are epigenetic therapies used to treat some patients with acute myeloid leukaemia (AML) and myelodysplastic syndrome. HMAs act in a replication-dependent manner to remove DNA methylation from the genome. However, AML cells targeted by HMA therapy are often quiescent within the bone marrow, where oxygen levels are low.
View Article and Find Full Text PDFHypomethylating agents as emerging therapeutics for triple-negative breast cancer.
Life Sci
January 2025
Department of Immunology, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia. Electronic address:
Triple-negative breast cancer (TNBC) is recognized as the most aggressive subtype of breast cancer. Epigenetic silencing, such as DNA methylation mediated by DNA methyltransferases (DNMTs) plays key roles in TNBC tumorigenesis. Hypomethylating agents (HMAs) such as azacitidine, decitabine, and guadecitabine are key inhibitors of DNMTs, and accumulating evidence has shown their immunogenicity properties.
View Article and Find Full Text PDFOlutasidenib in combination with azacitidine induces durable complete remissions in patients with relapsed or refractory mIDH1 acute myeloid leukemia: a multicohort open-label phase 1/2 trial.
J Hematol Oncol
January 2025
Sylvester Comprehensive Cancer Center, University of Miami, Miami, FL, USA.
Background: Olutasidenib is a potent, selective, oral, small molecule inhibitor of mutant IDH1 (mIDH1) which induced durable remissions in high-risk, relapsed/refractory (R/R) mIDH1 AML patients in a phase 1/2 trial. We present a pooled analysis from multiple cohorts of the phase 1/2 trial of patients with R/R AML who received combination olutasidenib and azacitidine therapy.
Methods: Adult patients with mIDH1 AML received 150 mg olutasidenib twice daily plus standard-of-care azacitidine (OLU + AZA) and were evaluated for response and safety.
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