Molecular work up and monitoring of CML patients
EHA Library. CROSS N. 06/14/17; 185026
Topic: 2Aa Chronic myeloid leukemia, BCR-ABL1-positive
Prof. Nick CROSS
Contributions
Contributions
Learning Objectives
Simona Soverini - Chair Introduction
Three generations of tyrosine kinase inhibitors (TKIs) are now available for the treatment of chronic myeloid leukemia (CML) patients. None of them, however, is capable to eradicate leukemic stem cells (LSCs), whose persistence is though to be the main obstacle to successful treatment discontinuation and may, in some patients on therapy, trigger disease progression. Intense research has thus been devoted, over the past years, to the understanding of how LSCs survive, how we can identify and count them, and which therapeutic strategies may realistically be devised to eliminate LSCs while not impairing excessively treatment tolerability and patients quality of life. Another field of active research aims to identify (pre-treatment) biomarkers enabling us to predict which patients will do well, which patients will not, which patients will be able to stop treatment without experiencing disease recurrence. While work is in progress, thorough molecular monitoring of patients remains the key to therapeutic success and novel technologies might further improve accuracy and sensitivity. Choice between imatinib, dasatinib and nilotinib in newly diagnosed CML cases should be the result of a patient- and disease-centered algorithm taking into account age, risk, comorbidities, treatment endpoints, costs. Change of the TKI might be needed in case of intolerance or resistance; in some cases, transplant is still an option. New treatment modalities are still being explored in clinical trials: a novel inhibitor with allosteric binding mode (ABL001) appears to be the most promising one.
Learning Objectives of the manuscript
After viewing this presentation the participant will be able to:
- To review the key mechanisms underlying LSC persistence in CML and how we can therapeutically interfere with them
- To discuss the diagnostic work-up for newly diagnosed CML patients, the role of predictive and prognostic factors and the clinical value of molecular monitoring with current and novel technologies
- To review the factors to be considered when choosing the TKI and how toxicity and resistance should be managed
Learning Objectives of the presentation
After viewing this presentation the participant will be able to:
- Describe the essential elements for the diagnostic work of CML patients.
- Discuss factors associated with heterogeneous response to TKI therapy.
- Understand the role of molecular monitoring for personalised treatment, and how this process is standardised.
Three generations of tyrosine kinase inhibitors (TKIs) are now available for the treatment of chronic myeloid leukemia (CML) patients. None of them, however, is capable to eradicate leukemic stem cells (LSCs), whose persistence is though to be the main obstacle to successful treatment discontinuation and may, in some patients on therapy, trigger disease progression. Intense research has thus been devoted, over the past years, to the understanding of how LSCs survive, how we can identify and count them, and which therapeutic strategies may realistically be devised to eliminate LSCs while not impairing excessively treatment tolerability and patients quality of life. Another field of active research aims to identify (pre-treatment) biomarkers enabling us to predict which patients will do well, which patients will not, which patients will be able to stop treatment without experiencing disease recurrence. While work is in progress, thorough molecular monitoring of patients remains the key to therapeutic success and novel technologies might further improve accuracy and sensitivity. Choice between imatinib, dasatinib and nilotinib in newly diagnosed CML cases should be the result of a patient- and disease-centered algorithm taking into account age, risk, comorbidities, treatment endpoints, costs. Change of the TKI might be needed in case of intolerance or resistance; in some cases, transplant is still an option. New treatment modalities are still being explored in clinical trials: a novel inhibitor with allosteric binding mode (ABL001) appears to be the most promising one.
Learning Objectives of the manuscript
After viewing this presentation the participant will be able to:
- To review the key mechanisms underlying LSC persistence in CML and how we can therapeutically interfere with them
- To discuss the diagnostic work-up for newly diagnosed CML patients, the role of predictive and prognostic factors and the clinical value of molecular monitoring with current and novel technologies
- To review the factors to be considered when choosing the TKI and how toxicity and resistance should be managed
Learning Objectives of the presentation
After viewing this presentation the participant will be able to:
- Describe the essential elements for the diagnostic work of CML patients.
- Discuss factors associated with heterogeneous response to TKI therapy.
- Understand the role of molecular monitoring for personalised treatment, and how this process is standardised.
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