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Asciminib add-on to imatinib demonstrates sustained high rates of ongoing therapy and deep molecular responses with prolonged follow-up in the ASC4MORE study.
J Hematol Oncol
December 2024
Georgia Cancer Center, Augusta, GA, USA.
Background: Up to 65% of patients with chronic myeloid leukemia (CML) who are treated with imatinib do not achieve sustained deep molecular response, which is required to attempt treatment-free remission. Asciminib is the only approved BCR::ABL1 inhibitor that Specifically Targets the ABL Myristoyl Pocket. This unique mechanism of action allows asciminib to be combined with adenosine triphosphate-competitive tyrosine kinase inhibitors to prevent resistance and enhance efficacy.
View Article and Find Full Text PDFAsciminib monotherapy as frontline treatment of chronic-phase chronic myeloid leukemia: results from the ASCEND study.
Blood
November 2024
Haematology Department, Royal Adelaide Hospital, Adelaide Medical School, University of Adelaide and Precision Cancer Medicine Theme, South Australian Health and Medical Research Institute, Adelaide, Australia.
Asciminib is a myristoyl site BCR::ABL1 inhibitor approved for patients with chronic-phase chronic myeloid leukemia (CP-CML) failing ≥2 prior lines of therapy. The Australasian Leukaemia and Lymphoma Group conducted the Asciminib Evaluation in Newly Diagnosed CML study to assess efficacy of asciminib for newly diagnosed CP-CML. Patients commenced asciminib 40 mg twice daily.
View Article and Find Full Text PDFConcentration of low-density lipoproteins (LDL) is significantly reduced after nilotinib discontinuation.
Sci Rep
July 2023
Vascular Risk Unit, Internal Medicine, Virgen de Las Nieves Hospital, Avenida de Las Fuerzas Armadas 2, 18014, Granada, Spain.
Dyslipidemia is a frequent side effect associated with nilotinib treatment. Patients with chronic myeloid leukemia (CML) under treatment with nilotinib who develop dyslipidemia have been shown to have a higher risk of presenting atherosclerotic cardiovascular disease (ACVD). Therapeutic discontinuation in selected individuals could be a strategy in order to prevent the development of ACVD.
View Article and Find Full Text PDFCombination of tyrosine kinase inhibitors and the MCL1 inhibitor S63845 exerts synergistic antitumorigenic effects on CML cells.
Cell Death Dis
September 2021
Department of Women's and Children's Health, Karolinska Institute, Stockholm, Sweden.
Tyrosine kinase inhibitor (TKI) treatment has dramatically improved the survival of chronic myeloid leukemia (CML) patients, but measurable residual disease typically persists. To more effectively eradicate leukemia cells, simultaneous targeting of BCR-ABL1 and additional CML-related survival proteins has been proposed. Notably, several highly specific myeloid cell leukemia 1 (MCL1) inhibitors have recently entered clinical trials for various hematologic malignancies, although not for CML, reflecting the insensitivity of CML cell lines to single MCL1 inhibition.
View Article and Find Full Text PDFTargeted Therapy for Chordoma: Key Molecular Signaling Pathways and the Role of Multimodal Therapy.
Target Oncol
May 2021
Brain Tumor Stem Cell Laboratory, Department of Neurologic Surgery, Mayo Clinic, 4500 San Pablo Rd. S, Jacksonville, FL, 32224, USA.
Background: Chordoma is a rare but devastating tumor that arises in the cranial skull base or spine. There are currently no US Food and Drug Administration-approved targeted therapies for chordoma, and little understanding of whether using more than one therapy has benefit over monotherapy.
Objective: The objective of this study was to systematically review the current status of clinical trials completed for patients with chordoma to determine if multimodal therapy offers a benefit in progression-free survival over monomodal therapy.
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