Chronic Myeloid Leukemia: Advances in Understanding Disease Biology and Mechanisms of Resistance to Tyrosine Kinase Inhibitors

No abstract is available for this paper.

• Publication year

  2015

• Venue

  Current Hematologic Malignancy Reports

• Publication date

  2015-02-21

• Fields of study

  Medicine

• Identifiers
  DOI 10.1007/s11899-015-0248-3PMID 25700679PMCID PMC4447524
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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• Many BCR-ABL1 compound mutations reported in chronic myeloid leukemia patients may actually be artifacts due to PCR-mediated recombination.

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• Selectins and their ligands are required for homing and engraftment of BCR-ABL1+ leukemic stem cells in the bone marrow niche.

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• Early molecular response predicts outcomes in patients with chronic myeloid leukemia in chronic phase treated with frontline nilotinib or imatinib.

  2014cited by this paper
• Combined STAT3 and BCR-ABL1 Inhibition Induces Synthetic Lethality in Therapy-Resistant Chronic Myeloid Leukemia

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• Molecular dynamics reveal BCR-ABL1 polymutants as a unique mechanism of resistance to PAN-BCR-ABL1 kinase inhibitor therapy

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• A therapeutically targetable mechanism of BCR-ABL–independent imatinib resistance in chronic myeloid leukemia

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• Loss of major molecular response as a trigger for restarting tyrosine kinase inhibitor therapy in patients with chronic-phase chronic myelogenous leukemia who have stopped imatinib after durable undetectable disease.

  2014cited by this paper
• BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia.

  2014cited by this paper
• Deep molecular responses achieved in patients with CML-CP who are switched to nilotinib after long-term imatinib.

  2014cited by this paper
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  2014cited by this paper
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• MEK-dependent negative feedback underlies BCR-ABL-mediated oncogene addiction.

  2014cited by this paper
• Arachidonate 15-lipoxygenase is required for chronic myeloid leukemia stem cell survival.

  2014cited by this paper
• BCR‐ABL residues interacting with ponatinib are critical to preserve the tumorigenic potential of the oncoprotein

  2014cited by this paper
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  2013cited by this paper
• A phase 2 trial of ponatinib in Philadelphia chromosome-positive leukemias.

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• Role of ABL family kinases in cancer: from leukaemia to solid tumours

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• BCR-ABL1 compound mutations in tyrosine kinase inhibitor-resistant CML: frequency and clonal relationships.

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• Activity of ponatinib against clinically-relevant AC220-resistant kinase domain mutants of FLT3-ITD.

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• Unraveling the complexity of tyrosine kinase inhibitor-resistant populations by ultra-deep sequencing of the BCR-ABL kinase domain.

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• Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukaemia

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• Chronic myeloid leukemia stem cells are not dependent on Bcr-Abl kinase activity for their survival.

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• Pushing the limits of targeted therapy in chronic myeloid leukaemia

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• Low BCR-ABL expression levels in hematopoietic precursor cells enable persistence of chronic myeloid leukemia under imatinib.

  2012cited by this paper
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  2011cited by this paper
• Gastrointestinal stromal tumours: origin and molecular oncology

  2011cited by this paper
• Physiologic hypoxia promotes maintenance of CML stem cells despite effective BCR-ABL1 inhibition.

  2011cited by this paper
• Nilotinib and MEK inhibitors induce synthetic lethality through paradoxical activation of RAF in drug-resistant chronic myeloid leukemia.

  2011cited by this paper
• Allosteric Interactions between the Myristate- and ATP-Site of the Abl Kinase

  2011cited by this paper
• Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity.

  2011cited by this paper
• Quantitative phosphoproteomics revealed interplay between Syk and Lyn in the resistance to nilotinib in chronic myeloid leukemia cells.

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• Targeting Bcr–Abl by combining allosteric with ATP-binding-site inhibitors

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• Poor outcome after reintroduction of imatinib in patients with chronic myeloid leukemia who interrupt therapy on account of pregnancy without having achieved an optimal response.

  2010cited by this paper
• Wnt/Ca2+/NFAT signaling maintains survival of Ph+ leukemia cells upon inhibition of Bcr-Abl.

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• Mechanisms of resistance to imatinib and sunitinib in gastrointestinal stromal tumor

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• Mechanisms of Resistance to Imatinib and Second-Generation Tyrosine Inhibitors in Chronic Myeloid Leukemia

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• AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance.

  2009cited by this paper
• BCR–ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros

  2008cited by this paper
• Stat3 contributes to resistance toward BCR-ABL inhibitors in a bone marrow microenvironment model of drug resistance

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• An activating KRAS mutation in imatinib-resistant chronic myeloid leukemia

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• Part I: mechanisms of resistance to imatinib in chronic myeloid leukaemia.

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• Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency.

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• An Activating KRAS Mutation in Imatinib Resistant Chronic Myeloid Leukemia.

  2007cited by this paper
• Adaptive secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF) mediates imatinib and nilotinib resistance in BCR/ABL+ progenitors via JAK-2/STAT-5 pathway activation.

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• Mechanisms of BCR–ABL in the pathogenesis of chronic myelogenous leukaemia

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• Inhibition of Tumoral VISTA to Overcome TKI Resistance via Downregulation of the AKT/mTOR and JAK2/STAT5 Pathways in Chronic Myeloid Leukemia

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• Combining the Allosteric Inhibitor Asciminib with Ponatinib Suppresses Emergence of and Restores Efficacy against Highly Resistant BCR-ABL1 Mutants.

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• The effect of the additional cytogenetic abnormalities on major molecular response and BCR-ABL kinase domain mutations in long-term follow-up chronic myeloid leukemia patients, a cross sectional study

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