Published Paper Details:

The Philadelphia chromosome and the bcr-abl fusion gene cause aberrant myeloid cell proliferation, which is the hallmark of chronic myeloid leukemia (cml), a Myeloproliferative disease. Patient outcomes have significantly improved over the past 20 years due to considerable breakthroughs in treatment, especially with the development of tyrosine kinase inhibitors (tkis) like Imatinib. Tkis are now the mainstay of cml treatment, allowing 85-95% of patients to survive during the chronic periods while achieving a long-term remission. Patients who do not respond to first-generation tkis are treated with second- and third-generation tkis, such as dasatinib, nilotinib, andponatinib. For individuals who do not react to tkis, stem cell transplantation is still a curative option, albeit with increased risks. Leukapheresis, chemotherapy, and interferon-alpha are further treatments that are generally saved for particular situations or crises. It is essential to regularly assess hematologic, cytogenetic, and molecular responses in order to modify treatment and sustain remission. With improved survival rates and quality of life, cml is no longer a fatal disease for the majority of patients, thanks to treatment advancements.