Year |
Citation |
Score |
2011 |
Leder K, Foo J, Skaggs B, Gorre M, Sawyers CL, Michor F. Fitness conferred by BCR-ABL kinase domain mutations determines the risk of pre-existing resistance in chronic myeloid leukemia. Plos One. 6: e27682. PMID 22140458 DOI: 10.1371/Journal.Pone.0027682 |
0.555 |
|
2006 |
Skaggs BJ, Gorre ME, Ryvkin A, Burgess MR, Xie Y, Han Y, Komisopoulou E, Brown LM, Loo JA, Landaw EM, Sawyers CL, Graeber TG. Phosphorylation of the ATP-binding loop directs oncogenicity of drug-resistant BCR-ABL mutants. Proceedings of the National Academy of Sciences of the United States of America. 103: 19466-71. PMID 17164333 DOI: 10.1073/Pnas.0609239103 |
0.536 |
|
2006 |
Chandra J, Tracy J, Loegering D, Flatten K, Verstovsek S, Beran M, Gorre M, Estrov Z, Donato N, Talpaz M, Sawyers C, Bhalla K, Karp J, Sausville E, Kaufmann SH. Adaphostin-induced oxidative stress overcomes BCR/ABL mutation-dependent and -independent imatinib resistance. Blood. 107: 2501-6. PMID 16291594 DOI: 10.1182/Blood-2005-07-2966 |
0.53 |
|
2005 |
Skaggs BJ, Burgess MR, Gorre ME, Graeber TG, Sawyers CL. Altered Oncogenic Fitness of Imatinib- and Dasatinib-Resistant BCR-ABL Mutants Is Due to Differential Intrinsic Kinase Activity and Signaling Pathway Selection Defined by Phosphoproteome Profiling. Blood. 106: 692-692. DOI: 10.1182/Blood.V106.11.692.692 |
0.409 |
|
2004 |
Gorre ME, Skaggs BJ, Sawyers CL. Imatinib-Resistant BCR-ABL Mutations Alter Oncogenic Potency, Kinase Activity and Substrate Selection. Blood. 104: 556-556. DOI: 10.1182/Blood.V104.11.556.556 |
0.409 |
|
2004 |
Chandra J, Tracy J, Gorre M, Talpaz M, Griffin J, Verstovsek S, Beran M, Sawyers C, Sausville E, Kaufmann S. Effects of Adaphostin, a Novel Tyrphostin Inhibitor, in Diverse Models of Imatinib Mesylate Resistance. Blood. 104: 2097-2097. DOI: 10.1182/Blood.V104.11.2097.2097 |
0.409 |
|
2003 |
Huron DR, Gorre ME, Kraker AJ, Sawyers CL, Rosen N, Moasser MM. A novel pyridopyrimidine inhibitor of abl kinase is a picomolar inhibitor of Bcr-abl-driven K562 cells and is effective against STI571-resistant Bcr-abl mutants. Clinical Cancer Research : An Official Journal of the American Association For Cancer Research. 9: 1267-73. PMID 12684394 |
0.513 |
|
2002 |
Gorre ME, Ellwood-Yen K, Chiosis G, Rosen N, Sawyers CL. BCR-ABL point mutants isolated from patients with imatinib mesylate-resistant chronic myeloid leukemia remain sensitive to inhibitors of the BCR-ABL chaperone heat shock protein 90. Blood. 100: 3041-4. PMID 12351420 DOI: 10.1182/Blood-2002-05-1361 |
0.533 |
|
2002 |
Shah NP, Nicoll JM, Nagar B, Gorre ME, Paquette RL, Kuriyan J, Sawyers CL. Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia. Cancer Cell. 2: 117-25. PMID 12204532 DOI: 10.1016/S1535-6108(02)00096-X |
0.529 |
|
2002 |
Roumiantsev S, Shah NP, Gorre ME, Nicoll J, Brasher BB, Sawyers CL, Van Etten RA. Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop. Proceedings of the National Academy of Sciences of the United States of America. 99: 10700-5. PMID 12149456 DOI: 10.1073/Pnas.162140299 |
0.538 |
|
2002 |
Gorre ME, Sawyers CL. Molecular mechanisms of resistance to STI571 in chronic myeloid leukemia. Current Opinion in Hematology. 9: 303-7. PMID 12042704 DOI: 10.1097/00062752-200207000-00007 |
0.524 |
|
2001 |
Gorre ME, Mohammed M, Ellwood K, Hsu N, Paquette R, Rao PN, Sawyers CL. Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Science (New York, N.Y.). 293: 876-80. PMID 11423618 DOI: 10.1126/Science.1062538 |
0.54 |
|
Show low-probability matches. |