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Fungal secondary metabolites as a potential inhibitor of T315I- BCR::ABL1 mutant in chronic myeloid leukemia by molecular docking, molecular dynamics simulation and binding free energy exploration approaches.
J Genet Eng Biotechnol
December 2024
Hematologic Disease Center, The First Affiliated Hospital of Xinjiang Medical University, Xinjiang Medical University, Urumqi 830011, China. Electronic address:
Background: Chronic Myeloid Leukemia (CML) is particularly challenging to treat due to the T315I BCR::ABL1 mutation. Although fungal metabolites are known for their pharmaceutical potential, none are approved for CML. Our study screened approximately 2000 fungal secondary metabolites to discover inhibitors targeting the T315I- BCR::ABL1 mutant protein.
View Article and Find Full Text PDFExploring Inhibition Mechanisms in Wildtype and T315I BCR-ABL1: An In Silico Approach Integrating Virtual Screening, MD Simulations, and MM-GBSA Analysis.
J Comput Chem
January 2025
Department of Bioinformatics, Institute of Health Sciences, Karadeniz Technical University, Trabzon, Turkey.
The BCR-ABL tyrosine kinase which is responsible for the pathogenesis of chronic myeloid leukemia (CML), has emerged as a promising therapeutic target. To address this issue, we employed a comprehensive computational approach integrating virtual screening, molecular dynamics (MD) simulations, and MM-GBSA (Molecular Mechanics/Generalized Born Surface Area) analysis to identify potential inhibitors and elucidate their binding mechanisms. Initially, virtual screening was conducted on 994 compounds from the ZINC database and, these compounds were docked against wildtype and T315I mutant ABL1 for the Type I and Type II ABL1 kinase inhibition mechanisms.
View Article and Find Full Text PDFPonatinib vs. asciminib in post-second-generation tyrosine kinase inhibitor therapy for chronic-phase chronic myeloid leukemia: a matching-adjusted indirect comparison.
Front Oncol
November 2024
Department of Leukemia, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Article Synopsis
- Ponatinib and asciminib are both approved for treating chronic-phase chronic myeloid leukemia (CP-CML) in the U.S., specifically for patients who have not responded to other therapies or have the T315I mutation, with ponatinib also available in Europe for this mutation.
- A systematic review identified clinical trials comparing the effectiveness of ponatinib and asciminib for patients who have relapsed or are resistant to treatments, and a statistical analysis was used to compare their response rates after matching patient characteristics.
- Results showed ponatinib had significantly higher response rates than asciminib, particularly in patients with the T315I mutation, indicating that ponatinib may be a more effective treatment option in these cases.
Critical role of protein kinase CK2 in chronic myeloid leukemia cells harboring the T315I BCR::ABL1 mutation.
Int J Biol Macromol
December 2024
Dept. Biomedical Sciences, University of Padova, Padova, Italy. Electronic address:
Chronic myeloid leukemia (CML) is characterized by the fusion protein BCR::ABL1, a constitutively active tyrosine kinase. The frontline treatment, represented by tyrosine kinase inhibitors (TKIs), has dramatically improved the clinical outcomes of patients. However, TKI resistance through various mechanisms has been reported.
View Article and Find Full Text PDFOlverembatinib After Failure of Tyrosine Kinase Inhibitors, Including Ponatinib or Asciminib: A Phase 1b Randomized Clinical Trial.
JAMA Oncol
November 2024
Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston.
Article Synopsis
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