Chronic Myeloid Leukemia
The latest news, research, and perspectives in chronic myeloid leukemia (CML). CML is caused by the BCR-ABL1 fusion gene, which is formed by a translocation between chromosomes 9 and 22 (the Philadelphia chromosome), that produces abnormal proteins leading to the development of leukemic cells.
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Ponatinib demonstrated long-term efficacy and manageable safety in patients with highly resistant, chronic phase CML.
Achieving deep molecular response has allowed for treatment discontinuation, making TFR a main goal of therapy.
Olverembatinib was well tolerated and showed strong antileukemic activity in patients with chronic phase CML.
Asciminib continues to demonstrate favorable safety and tolerability compared to TKIs in patients with chronic phase CML.
Age ≥65 years, arrhythmia, and cardiogenic shock were associated with a significantly higher rate of acute heart failure.
The rate of response was “significantly higher” with asciminib compared with tyrosine kinase inhibitors.
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Sangeetha Venugopal, MD, engages outstanding issues in chronic myeloid leukemia treatment research.
In this executive editor's message, Elias Jabbour, MD, writes about redefining leukemias as curable or less curable.
Palliative care facilitates communication and helps with symptom management, the researchers noted.
The goal of PedAL is to establish a data-driven developmental therapeutics program.
The trial's treatment regimen included single-agent dasatinib for the first three months, followed by venetoclax.
The study determined the maximum tolerated dose of asciminib with dasatinib and prednisone.
Mice with CML who were given a synthetic version of miR-142 lived much longer and were even cured.
Dr. Cortes chats about the “boom” in treatments for chronic myeloid leukemia (CML), and where he sees a need for balance.
Dr. Radich reflects on lessons in cowboy medicine, the genetics of luck, and a serendipitous meeting.
The FDA also announced it approved a new capsule dosage form of bosutinib.
Dr. Cortes speaks about the plenary session he delivered during the Eleventh Annual Meeting of SOHO.
Researchers reviewed data from 107 patients with CML who developed a T315I mutation in BCR-ABL1.
From Houston, Texas, to Beirut, Lebanon, the SOHO global community continues to grow thanks to its Ambassador Program.
In this poor-risk population of patients, 73% responded to the triplet.
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Editorial Board
Sagar Lonial, MD, FACPEditor-in-Chief | Chief Medical Officer of Winship Cancer Institute at Emory University School of Medicine
Guillermo Garcia-Manero, MDAssociate Editor | Chief, Section of Myelodysplastic Syndromes, The University of Texas MD Anderson Cancer Center
Elias Jabbour, MDExecutive Editor | DB Lane Cancer Research Fund Distinguished Professor in Leukemia Research, MD Anderson Cancer Center
Kami Maddocks, MDAssociate Editor | Professor of Clinical Internal Medicine in the Division of Hematology at The Ohio State University
Thomas Martin, MDAssociate Editor | Clinical Research Director, UCSF Helen Diller Family Comprehensive Cancer Center
Jerald Radich, MDAssociate Editor | Professor in the Clinical Research Division and Kurt Enslein Endowed Chair at Fred Hutch
Laurie Sehn, MD, MPHAssociate Editor | Clinical Professor of Medical Oncology, British Columbia Cancer Centre for Lymphoid Cancer
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