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

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

Through the open door: Preferential binding of dasatinib to the active form of BCR-ABL unveiled by in silico experiments

(2013) Erik Laurini et al.   Molecular Oncology

Ponatinib Is a Pan-BCR-ABL Kinase Inhibitor: MD Simulations and SIE Study

(2013) Karunakar Tanneeru et al.   PLoS One

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

(2012) J. S. Khorashad et al.   BLOOD

Ponatinib in Refractory Philadelphia Chromosome–Positive Leukemias

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

BCR-ABL kinase domain mutation analysis in chronic myeloid leukemia patients treated with tyrosine kinase inhibitors: recommendations from an expert panel on behalf of European LeukemiaNet

(2011) S. Soverini et al.   BLOOD

The rise and fall of gatekeeper mutations? TheBCR-ABL1T315I paradigm

(2011) Don L. Gibbons et al.   CANCER

Inhibitors of the Abl kinase directed at either the ATP- or myristate-binding site

(2010) Doriano Fabbro et al.   BIOCHIMICA ET BIOPHYSICA ACTA-PROTEINS AND PROTEOMICS

Assessing the Performance of the MM/PBSA and MM/GBSA Methods. 1. The Accuracy of Binding Free Energy Calculations Based on Molecular Dynamics Simulations

(2010) Tingjun Hou et al.   Journal of Chemical Information and Modeling

ON012380, a putative BCR-ABL kinase inhibitor with a unique mechanism of action in imatinib-resistant cells

(2010) J Wu et al.   LEUKEMIA

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

Computations of Standard Binding Free Energies with Molecular Dynamics Simulations

(2009) Yuqing Deng et al.   JOURNAL OF PHYSICAL CHEMISTRY B

Failure to achieve a major cytogenetic response by 12 months defines inadequate response in patients receiving nilotinib or dasatinib as second or subsequent line therapy for chronic myeloid leukemia

(2008) C. S. Tam et al.   BLOOD

Association Between Imatinib-Resistant BCR-ABL Mutation-Negative Leukemia and Persistent Activation of LYN Kinase

(2008) Ji Wu et al.   JNCI-Journal of the National Cancer Institute

SGX393 inhibits the CML mutant Bcr-AblT315I and preempts in vitro resistance when combined with nilotinib or dasatinib

(2008) T. O'Hare et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA