Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Transl Med. Nov 28, 2026; 12(4): 125122
Published online Nov 28, 2026. doi: 10.5528/wjtm.125122
Published online Nov 28, 2026. doi: 10.5528/wjtm.125122
Molecular mechanisms of BCR::ABL1 in chronic myeloid leukaemia: From treatment-free remission to curative therapy
Temilola Oludunmomi Owojuyigbe, Muheez Alani Durosinmi, Department of Haematology and Immunology, Obafemi Awolowo University, Ile-Ife 220, Osun, Nigeria
Temilola Oludunmomi Owojuyigbe, Muheez Alani Durosinmi, Department of Haematology and Blood Transfusion, Obafemi Awolowo University Teaching Hospitals Complex, Ile-Ife 220, Osun, Nigeria
Author contributions: Owojuyigbe TO conceptualised the manuscript, conducted the literature search and review, drafted the manuscript; Durosinmi MA critically revised the content; and all authors reviewed the final version, and approved it for publication.
AI contribution statement: No AI tools were used in the preparation of this document.
Conflict-of-interest statement: All authors declare that they have no conflict of interest to disclose.
Corresponding author: Temilola Oludunmomi Owojuyigbe, MD, PhD, Assistant Professor, Consultant, Lecturer, Department of Haematology and Immunology, Obafemi Awolowo University, Faculty of Basic Clinical Sciences College of Health Sciences, Ile-Ife 220, Osun, Nigeria. temilolly@yahoo.com
Received: July 1, 2026
Revised: August 25, 2026
Accepted: October 9, 2026
Published online: November 28, 2026
Processing time: 128 Days and 9 Hours
Revised: August 25, 2026
Accepted: October 9, 2026
Published online: November 28, 2026
Processing time: 128 Days and 9 Hours
Core Tip
Core Tip: Chronic myeloid leukaemia is a clonal haematological malignancy with a well-defined aetiology: The Philadelphia chromosome. The backbone of therapy are the tyrosine kinase inhibitors (TKIs) which have transformed the disease from a fatal cancer into a manageable, chronic disease. The TKIs produced remarkable cytogenetic and molecular remission but they do not produce cure in about half of the patients due to the non-eradication of leukaemia stem cells. This review evaluates the molecular mechanisms underlying BCR::ABL1 signalling and leukaemia stem cell survival, providing a framework that distinguishes guideline-supported operational remission from investigational “double-hit” therapies aimed at leukaemic clone eradication.