Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification

Gorre, M.; Mohammed, Mansoor; Ellwood, Katharine; Hsu, Nancy; Paquette, Ron; Rao, P. Nagesh; Sawyers, Charles L.

doi:10.1126/science.1062538

Cited by 2,878 publications

(2,188 citation statements)

References 31 publications

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“…49), in cardiomyocytes, and found that it partially rescued the cells from imatinib-induced toxicity 4 . Because ABL is known to induce apoptosis, the fact that it seemed to provide a survival signal in cardiomyocytes was surprising.…”

Section: R E V I E W Smentioning

confidence: 99%

Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition

2007

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Section: R E V I E W Smentioning

confidence: 99%

Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition

2007

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“…23 The most common cause of secondary imatinib resistance is point mutations in BCR-ABL that prevent effective binding of imatinib but may retain kinase activity. [35][36][37][38][39] These mutations are clustered primarily within the kinase domain of BCR-ABL (ABL exons 4-10). 40 They exhibit differential relative resistance to imatinib in vitro.…”

Section: Imatinib Nilotinib Dasatinibmentioning

confidence: 99%

Optimizing therapy for patients with chronic myelogenous leukemia in chronic phase

Kantarjian

Cortés

Rosée

et al. 2010

Cancer

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Identification of BCR‐ABL as the defining leukemogenic event in chronic myelogenous leukemia (CML) revolutionized the treatment of the disease. Imatinib, a potent BCR‐ABL inhibitor, is the standard of care for the first‐line treatment of patients with chronic‐phase CML because of its high long‐term response rates and favorable tolerability profile compared with previous standard therapies. However, resistance to imatinib develops in 2% to 4% of patients annually. For patients with acquired cytogenetic resistance to standard‐dose imatinib (400 mg daily), imatinib dose escalation (600‐800 mg daily) is an excellent first option for managing patients and achieving cytogenetic responses. However, for patients with primary resistance to imatinib, hematologic disease recurrence, or emergent BCR‐ABL kinase domain mutations, imatinib dose escalation may not be sufficient to control the disease. For these patients, the potent second‐generation tyrosine kinase inhibitors dasatinib and nilotinib are available. Both agents provide effective therapeutic options for patients with imatinib resistance or intolerance. For the current overview, the authors reviewed the data supporting the use of both dasatinib and nilotinib in imatinib‐resistant or imatinib‐intolerant patients, and they have highlighted the future of CML therapy. Overall, the article is intended to offer physicians a comprehensive review of the current literature and to provide data supporting various treatment options for patients with CML throughout the course of imatinib therapy and beyond. Cancer 2010. © 2010 American Cancer Society.

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“…However, acquired resistance to imatinib develops in a substantial fraction of patients. In 70 -80% of these cases, acquired resistance is caused by point mutations in the ABL kinase domain (Gorre et al, 2001). So far, about 40 different point mutations have been discovered, each of which is sufficient to cause resistance to imatinib (Branford et al, 2003a).…”

Section: Dynamics Of CMLmentioning

confidence: 99%

Mathematical models of targeted cancer therapy

Abbott

Michor

2006

Br J Cancer

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Improved understanding of the molecular underpinnings of cancer initiation and progression has led to the development of targeted cancer therapies. The importance of these new methods of cancer treatment necessitates further research into the dynamic interactions between cancer cells and therapeutic agents, as well as a means of analysing their relationship quantitatively. The present review outlines the application of mathematical modelling to the dynamics of targeted cancer therapy, focusing particular attention on chronic myeloid leukaemia and its treatment with imatinib (Glivec).

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Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification

Cited by 2,878 publications

References 31 publications

Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition

Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition

Optimizing therapy for patients with chronic myelogenous leukemia in chronic phase

Mathematical models of targeted cancer therapy

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