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European LeukemiaNet 2020 recommendations for treating chronic myeloid leukemia

Leukemia, 2020-04, Vol.34 (4), p.966-984

2020

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Response and Resistance to BCR-ABL1-Targeted Therapies

Cancer cell, 2020-04, Vol.37 (4), p.530-542

2020

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The allosteric inhibitor ABL001 enables dual targeting of BCR-ABL1

Nature (London), 2017-03, Vol.543 (7647), p.733-737

2017

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Deep Molecular Response Is Reached by the Majority of Patients Treated With Imatinib, Predicts Survival, and Is Achieved More Quickly by Optimized High-Dose Imatinib: Results From the Randomized CML-Study IV

Journal of clinical oncology, 2014-02, Vol.32 (5), p.415-423

2014

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Nilotinib versus imatinib for the treatment of patients with newly diagnosed chronic phase, Philadelphia chromosome-positive, chronic myeloid leukaemia: 24-month minimum follow-up of the phase 3 randomised ENESTnd trial

The lancet oncology, 2011-09, Vol.12 (9), p.841-851

2011

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Restoration of miR-424 suppresses BCR–ABL activity and sensitizes CML cells to imatinib treatment

Cancer letters, 2015-05, Vol.360 (2), p.245-256

2015

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Early molecular response and female sex strongly predict stable undetectable BCR-ABL1, the criteria for imatinib discontinuation in patients with CML

Blood, 2013-05, Vol.121 (19), p.3818-3824

2013

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The specificity of asciminib, a potential treatment for chronic myeloid leukemia, as a myristate-pocket binding ABL inhibitor and analysis of its interactions with mutant forms of BCR-ABL1 kinase

Leukemia research, 2020-11, Vol.98, p.106458, Article 106458

2020

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Treatment‐free remission with first‐ and second‐generation tyrosine kinase inhibitors

American journal of hematology, 2019-03, Vol.94 (3), p.346-357

2019

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Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation

Nature (London), 2015-03, Vol.519 (7541), p.102-105

2015

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Evidence that resistance to nilotinib may be due to BCR-ABL, Pgp, or Src kinase overexpression

Cancer research (Chicago, Ill.), 2008-12, Vol.68 (23), p.9809-9816

2008

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Mechanisms of resistance to BCR–ABL TKIs and the therapeutic strategies: A review

Critical reviews in oncology/hematology, 2015-03, Vol.93 (3), p.277-292

2015

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Discontinuation of imatinib in patients with chronic myeloid leukaemia who have maintained complete molecular remission for at least 2 years: the prospective, multicentre Stop Imatinib (STIM) trial

The lancet oncology, 2010-11, Vol.11 (11), p.1029-1035

2010

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Chronic myeloid leukemia: reminiscences and dreams

Haematologica (Roma), 2016-05, Vol.101 (5), p.541-558

2016

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Long-Term Follow-Up of the French Stop Imatinib (STIM1) Study in Patients With Chronic Myeloid Leukemia

Journal of clinical oncology, 2017-01, Vol.35 (3), p.298-305

2017

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Mechanisms of Disease Progression and Resistance to Tyrosine Kinase Inhibitor Therapy in Chronic Myeloid Leukemia: An Update

International journal of molecular sciences, 2019-12, Vol.20 (24), p.6141

2019

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Discovery of a highly potent kinase inhibitor capable of overcoming multiple imatinib-resistant ABL mutants for chronic myeloid leukemia (CML)

European journal of pharmacology, 2021-04, Vol.897, p.173944-173944, Article 173944

2021

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Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia

Blood, 2007-10, Vol.110 (7), p.2242-2249

2007

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Impact of BCR-ABL transcript type on outcome in patients with chronic-phase CML treated with tyrosine kinase inhibitors

Blood, 2016-03, Vol.127 (10), p.1269-1275

2016

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Lipid nanoparticle-mediated siRNA delivery for safe targeting of human CML in vivo

Annals of hematology, 2019-08, Vol.98 (8), p.1905-1918

2019

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

Blood, 2012-02, Vol.119 (6), p.1501-1510

2012

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Why chronic myeloid leukaemia cannot be cured by tyrosine kinase-inhibitors

Leukemia, 2021-08, Vol.35 (8), p.2199-2204

2021

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European LeukemiaNet 2020 recommendations for treating chronic myeloid leukemia

Response and Resistance to BCR-ABL1-Targeted Therapies

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

The allosteric inhibitor ABL001 enables dual targeting of BCR-ABL1

Deep Molecular Response Is Reached by the Majority of Patients Treated With Imatinib, Predicts Survival, and Is Achieved More Quickly by Optimized High-Dose Imatinib: Results From the Randomized CML-Study IV

Nilotinib versus imatinib for the treatment of patients with newly diagnosed chronic phase, Philadelphia chromosome-positive, chronic myeloid leukaemia: 24-month minimum follow-up of the phase 3 randomised ENESTnd trial

AP24534, a Pan-BCR-ABL Inhibitor for Chronic Myeloid Leukemia, Potently Inhibits the T315I Mutant and Overcomes Mutation-Based Resistance

Restoration of miR-424 suppresses BCR–ABL activity and sensitizes CML cells to imatinib treatment

Early molecular response and female sex strongly predict stable undetectable BCR-ABL1, the criteria for imatinib discontinuation in patients with CML

The specificity of asciminib, a potential treatment for chronic myeloid leukemia, as a myristate-pocket binding ABL inhibitor and analysis of its interactions with mutant forms of BCR-ABL1 kinase

Treatment‐free remission with first‐ and second‐generation tyrosine kinase inhibitors

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

Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation

Evidence that resistance to nilotinib may be due to BCR-ABL, Pgp, or Src kinase overexpression

Mechanisms of resistance to BCR–ABL TKIs and the therapeutic strategies: A review

Discontinuation of imatinib in patients with chronic myeloid leukaemia who have maintained complete molecular remission for at least 2 years: the prospective, multicentre Stop Imatinib (STIM) trial

Chronic myeloid leukemia: reminiscences and dreams

Long-Term Follow-Up of the French Stop Imatinib (STIM1) Study in Patients With Chronic Myeloid Leukemia

Mechanisms of Disease Progression and Resistance to Tyrosine Kinase Inhibitor Therapy in Chronic Myeloid Leukemia: An Update

Discovery of a highly potent kinase inhibitor capable of overcoming multiple imatinib-resistant ABL mutants for chronic myeloid leukemia (CML)

Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia

Impact of BCR-ABL transcript type on outcome in patients with chronic-phase CML treated with tyrosine kinase inhibitors

Lipid nanoparticle-mediated siRNA delivery for safe targeting of human CML in vivo

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

Why chronic myeloid leukaemia cannot be cured by tyrosine kinase-inhibitors

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