Research Topic

Chronic Myeloid Leukemia

About this Research Topic

Chronic myeloid leukemia (CML) is a neoplastic disease characterized by a reciprocal balanced translocation between chromosomes 9 and 22, namely the Philadelphia chromosome, which encodes the BCR-ABL1 fusion protein, a constitutively active tyrosine kinase. Five tyrosine kinase inhibitors (TKIs) targeting the ATP-catalytic site of the BCR-ABL1 protein are approved: the introduction of these drugs into clinical practice drastically changed the outcome of CML patients, with a lifespan actually similar to that of general population. Imatinib, the first generation TKI, has improved the overall survival to more than 90%: some patients develop resistance and half of clinical resistance is due to the onset of mutations of ATP-binding site, but also intolerance in the long-term can be associated to treatment failure. Second and third generation TKIs entered into clinical practice, able to rescue about 40-50% of resistant patients, but with increasing probabilities of off-target effects in the long term. Recent studies showed that about 40-50% patients that achieved stable and deep molecular responses with every drug available can remain disease free after treatment discontinuation, but with the evidence of persistence of Ph+ leukemic stem cells and residual disease.

The special issue on chronic myeloid leukemia will cover the following topics:

1. The biology of CML disease: characteristics of Ph+ leukemic stem cells
2. Monitoring CML in 2018: cytogenetic, molecular (RQ-PCR and ddPCR) and mutation analysis
3. Tyrosine kinase inhibitors available for CML treatment: safety and efficacy
4. Treatment-free remission in CML: new endpoint for all patients?
5. New approaches and combination for CML treatment
6. The management of CML in advanced phase


Keywords: Chronic myeloid leukemia, BCR-ABL1, tyrosine kinase inhibitors, Philadelphia chromosome, ATP


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Chronic myeloid leukemia (CML) is a neoplastic disease characterized by a reciprocal balanced translocation between chromosomes 9 and 22, namely the Philadelphia chromosome, which encodes the BCR-ABL1 fusion protein, a constitutively active tyrosine kinase. Five tyrosine kinase inhibitors (TKIs) targeting the ATP-catalytic site of the BCR-ABL1 protein are approved: the introduction of these drugs into clinical practice drastically changed the outcome of CML patients, with a lifespan actually similar to that of general population. Imatinib, the first generation TKI, has improved the overall survival to more than 90%: some patients develop resistance and half of clinical resistance is due to the onset of mutations of ATP-binding site, but also intolerance in the long-term can be associated to treatment failure. Second and third generation TKIs entered into clinical practice, able to rescue about 40-50% of resistant patients, but with increasing probabilities of off-target effects in the long term. Recent studies showed that about 40-50% patients that achieved stable and deep molecular responses with every drug available can remain disease free after treatment discontinuation, but with the evidence of persistence of Ph+ leukemic stem cells and residual disease.

The special issue on chronic myeloid leukemia will cover the following topics:

1. The biology of CML disease: characteristics of Ph+ leukemic stem cells
2. Monitoring CML in 2018: cytogenetic, molecular (RQ-PCR and ddPCR) and mutation analysis
3. Tyrosine kinase inhibitors available for CML treatment: safety and efficacy
4. Treatment-free remission in CML: new endpoint for all patients?
5. New approaches and combination for CML treatment
6. The management of CML in advanced phase


Keywords: Chronic myeloid leukemia, BCR-ABL1, tyrosine kinase inhibitors, Philadelphia chromosome, ATP


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

28 January 2019 Manuscript

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Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

28 January 2019 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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