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Favorable tolerability of asciminib <i>versus</i> ATP-competitive tyrosine kinase inhibitors in the ASC4FIRST study of newly diagnosed patients with chronic-phase chronic myeloid leukemia.

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Direct measurement of in vivo BCR::ABL1 kinase inhibition reveals stronger potency of asciminib as compared with imatinib and nilotinib.

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Allosteric and ATP-Pocket BCR::ABL1 Inhibition In Vitro, and Characterising Ex Vivo Thrombo-Inflammatory Biomarkers and Thrombin Generation in Asciminib-Treated CML Patients.

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Identification of a Novel, Oncogenic and Targetable <i>TPR::ABL2</i> Fusion Gene in T-Cell Acute Lymphoblastic Leukaemia.

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Early Management of CML.

Naranie Shanmuganathan1,2,3,4,5, Timothy P Hughes6,7,8

  • 1Precision Medicine Theme, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia. naranie.shanmuganathan@sa.gov.au.

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Summary

Optimizing tyrosine kinase inhibitor (TKI) selection is crucial for managing chronic myeloid leukaemia (CML). Personalized TKI therapy considers patient-specific factors to achieve deep molecular response and potential treatment-free remission in CML patients.

Keywords:
Deep molecular responsesDrug toxicityTKITreatment-free remission

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Area of Science:

  • Hematology
  • Oncology
  • Pharmacology

Background:

  • Chronic myeloid leukaemia (CML) treatment has significantly improved due to targeted therapies like BCR-ABL1 inhibitors.
  • However, patient responses to these therapies are heterogeneous, necessitating individualized treatment strategies.

Purpose of the Study:

  • To explore the early management of CML, focusing on frontline therapy selection.
  • To highlight the complex decision-making process involved in choosing the optimal tyrosine kinase inhibitor (TKI) for each patient.

Main Methods:

  • Review of current clinical practices and treatment guidelines for CML.
  • Analysis of factors influencing TKI selection, including disease biology and patient comorbidities.

Main Results:

  • TKI selection requires balancing potent BCR-ABL1 inhibition with the need to avoid toxicity in patients with comorbidities.
  • Achieving deep molecular response is a key goal, paving the way for potential treatment-free remission.

Conclusions:

  • Personalized TKI selection is paramount for optimizing CML patient outcomes.
  • Early management and frontline therapy choices significantly impact long-term CML treatment success and remission potential.