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

Safety of bosutinib versus imatinib in the phase 3 BELA trial in newly diagnosed chronic phase chronic myeloid leukemia

(2014) Carlo Gambacorti-Passerini et al.   AMERICAN JOURNAL OF HEMATOLOGY

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

(2014) W. T. Parker et al.   BLOOD

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

(2014) D. S. Krause et al.   BLOOD

The IL-2/CD25 axis maintains distinct subsets of chronic myeloid leukemia-initiating cells

(2014) C. I. Kobayashi et al.   BLOOD

Physiologic hypoxia promotes maintenance of CML stem cells despite effective BCR-ABL1 inhibition

(2014) K. P. Ng et al.   BLOOD

Deep molecular responses achieved in patients with CML-CP who are switched to nilotinib after long-term imatinib

(2014) T. P. Hughes et al.   BLOOD

Long-term outcome with dasatinib after imatinib failure in chronic-phase chronic myeloid leukemia: follow-up of a phase 3 study

(2014) N. P. Shah et al.   BLOOD

BCR-ABL1 Compound Mutations Combining Key Kinase Domain Positions Confer Clinical Resistance to Ponatinib in Ph Chromosome-Positive Leukemia

(2014) Matthew S. Zabriskie et al.   CANCER CELL

Drug Resistance via Feedback Activation of Stat3 in Oncogene-Addicted Cancer Cells

(2014) Ho-June Lee et al.   CANCER CELL

Arachidonate 15-lipoxygenase is required for chronic myeloid leukemia stem cell survival

(2014) Yaoyu Chen et al.   JOURNAL OF CLINICAL INVESTIGATION

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

(2014) Don L. Gibbons et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

The ecology in the hematopoietic stem cell niche determines the clinical outcome in chronic myeloid leukemia

(2014) A. L. MacLean et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

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

(2014) L. Ma et al.   Science Translational Medicine

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

(2013) C. C. Smith et al.   BLOOD

Small molecule Me6TREN mobilizes hematopoietic stem/progenitor cells by activating MMP-9 expression and disrupting SDF-1/CXCR4 axis

(2013) J. Zhang et al.   BLOOD

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

(2013) T. P. Hughes et al.   BLOOD

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

(2013) S. Soverini et al.   BLOOD

Bosutinib safety and management of toxicity in leukemia patients with resistance or intolerance to imatinib and other tyrosine kinase inhibitors

(2013) H. M. Kantarjian et al.   BLOOD

Early response with dasatinib or imatinib in chronic myeloid leukemia: 3-year follow-up from a randomized phase 3 trial (DASISION)

(2013) E. Jabbour et al.   BLOOD

Microenvironmental protection of CML stem and progenitor cells from tyrosine kinase inhibitors through N-cadherin and Wnt- -catenin signaling

(2013) B. Zhang et al.   BLOOD

Safety and efficacy of imatinib cessation for CML patients with stable undetectable minimal residual disease: results from the TWISTER study

(2013) D. M. Ross et al.   BLOOD

Ponatinib in patients with refractory acute myeloid leukaemia: findings from a phase 1 study

(2013) Neil P. Shah et al.   BRITISH JOURNAL OF HAEMATOLOGY

Deep Molecular Response in Chronic Myeloid Leukemia: The New Goal of Therapy?

(2013) F.-X. Mahon et al.   CLINICAL CANCER RESEARCH

Rapid identification of compound mutations in patients with Philadelphia-positive leukaemias by long-range next generation sequencing

(2013) R. Kastner et al.   EUROPEAN JOURNAL OF CANCER

BCR-ABL residues interacting with ponatinib are critical to preserve the tumorigenic potential of the oncoprotein

(2013) Pietro Buffa et al.   FASEB JOURNAL

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

(2013) Philippe Rousselot et al.   JOURNAL OF CLINICAL ONCOLOGY

A Phase 2 Trial of Ponatinib in Philadelphia Chromosome–Positive Leukemias

(2013) J.E. Cortes et al.   NEW ENGLAND JOURNAL OF MEDICINE

MEK-Dependent Negative Feedback Underlies BCR-ABL-Mediated Oncogene Addiction

(2013) J. Asmussen et al.   Cancer Discovery

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

(2012) J. S. Khorashad et al.   BLOOD

Overcoming Bcr-Abl T315I mutation by combination of GNF-2 and ATP competitors in an Abl-independent mechanism

(2012) Mamduh Khateb et al.   BMC CANCER

Standardized definitions of molecular response in chronic myeloid leukemia

(2012) N C P Cross et al.   LEUKEMIA

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

(2012) Catherine C. Smith et al.   NATURE

Ponatinib in Refractory Philadelphia Chromosome–Positive Leukemias

(2012) Jorge E. Cortes et al.   NEW ENGLAND JOURNAL OF MEDICINE

Quantitative phosphoproteomics revealed interplay between Syk and Lyn in the resistance to nilotinib in chronic myeloid leukemia cells

(2011) R. Gioia et al.   BLOOD

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

(2011) A. Hamilton et al.   BLOOD

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

(2011) A. Kumari et al.   BLOOD

Nilotinib and MEK Inhibitors Induce Synthetic Lethality through Paradoxical Activation of RAF in Drug-Resistant Chronic Myeloid Leukemia

(2011) Leisl M. Packer et al.   CANCER CELL

Blockade of JAK2-mediated extrinsic survival signals restores sensitivity of CML cells to ABL inhibitors

(2011) E Traer et al.   LEUKEMIA

Allosteric Interactions between the Myristate- and ATP-Site of the Abl Kinase

(2011) Roxana E. Iacob et al.   PLoS One

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

(2010) A. Kuwabara et al.   BLOOD

Wnt/Ca2+/NFAT Signaling Maintains Survival of Ph+ Leukemia Cells upon Inhibition of Bcr-Abl

(2010) Mark A. Gregory et al.   CANCER CELL

Mechanisms of resistance to imatinib and sunitinib in gastrointestinal stromal tumor

(2010) Wei-Lien Wang et al.   CANCER CHEMOTHERAPY AND PHARMACOLOGY

Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity

(2010) Amie S. Corbin et al.   JOURNAL OF CLINICAL INVESTIGATION

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

(2010) François-Xavier Mahon et al.   LANCET ONCOLOGY

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

(2010) Jianming Zhang et al.   NATURE

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

(2009) Thomas O'Hare et al.   CANCER CELL

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

(2009) D. Milojkovic et al.   CLINICAL CANCER RESEARCH

An activating KRAS mutation in imatinib-resistant chronic myeloid leukemia

(2008) A Agarwal et al.   LEUKEMIA

Stat3 contributes to resistance toward BCR-ABL inhibitors in a bone marrow microenvironment model of drug resistance

(2008) Nadine N. Bewry et al.   MOLECULAR CANCER THERAPEUTICS

BCR–ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros

(2008) Charles G. Mullighan et al.   NATURE