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http://dx.doi.org/10.1111/bjh.18229 | DOI Listing |
Leuk Res
September 2024
Division of Hematology and Oncology, Vanderbilt University School of Medicine and Vanderbilt-Ingram Cancer Center, Nashville, TN, USA. Electronic address:
Haematologica
September 2024
Division of Hematology-Oncology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Azacitidine/venetoclax is an active regimen in patients with newly diagnosed acute myeloid leukemia (AML). However, primary or secondary resistance to azacitidine/venetoclax is an area of unmet need and overexpression of MCL1 is suggested to be a potential resistance mechanism. Pevonedistat inhibits MCL1 through activation of NOXA, and pevonedistat/azacitidine has previously shown activity in AML.
View Article and Find Full Text PDFClin Lymphoma Myeloma Leuk
June 2024
Department of Malignant Hematology, Moffitt Cancer Center and Research Institute, Tampa, FL. Electronic address:
Background: Hypomethylating agent + venetoclax is an effective frontline combination for acute myeloid leukemia, but its efficacy and safety in post-allogeneic hematopoietic cell transplant (alloHCT) relapse remain underexplored. Outcomes have been poor for this population, with no standard treatment.
Patients And Methods: We retrospectively analyzed 72 Ven-naïve patients who received hypomethylating agents + venetoclax at relapse following alloHCT and aimed to evaluate the rates of complete remission with or without hematologic recovery (CR/CRi) and minimal residual disease (MRD) negativity, CR/CRi duration, and overall survival.
Leuk Lymphoma
March 2024
Department of Hematology and Hematopoietic Cell Transplantation, City of Hope, Duarte, California, USA.
Blood Cancer J
September 2023
Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
FLT3 is the most frequently mutated gene in acute myeloid leukemia (AML), with FLT3 internal tandem duplication (ITD) mutations being associated with a more aggressive clinical course. While two large, randomized clinical trials have shown a survival benefit with the frontline use of an oral FLT3 inhibitor (midostaurin or quizartinib) in patients with FLT3-mutated AML, the role of FLT3 inhibitors in older adults with newly diagnosed FLT3-mutated AML remains unclear. A definitive improvement in survival has not been observed in intensively treated patients over 60 years of age receiving frontline FLT3 inhibitors.
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