Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL.

By H. Kantarjian, F. Giles, L. Wunderle, K. Bhalla, S. O'brien, B. Wassmann, C. Tanaka, P. Manley, Patricia Rae, W. Mietlowski and 9 more. New England Journal of Medicine, 2006

1,311 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/63c397ff1e9cd1b4faded356154689f680dc1784

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. Brian J. Druker
2. J. Cortes
3. C. Ashby
4. Andreas Hochhaus
5. Nathanael S. Gray
6. Zhesheng Chen
7. D. J. Barnes
8. H. Kantarjian

In Hematology

1. Brian J. Druker
2. Jianming Zhang
3. J. Melo
4. J. Cortes
5. C. Ashby
6. Levi A. Garraway
7. Andreas Hochhaus
8. Nathanael S. Gray

In Rheumatology

1. Brian J. Druker
2. J. Cortes
3. Andreas Hochhaus
4. H. Kantarjian

Citations in the corpus

• Chronic myeloid leukaemia as a model of disease evolution in human cancer (2007, background): “For patients who develop resistance to imatinib, the new second-generation kinase inhibitors such as nilotinib and dasatinib offer a further opportunity to control the diseas”
• Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is effective in patients with Philadelphia chromosome-positive chronic myelogenous leukemia in chronic phase following imatinib resistance and intolerance. (2007, background): “Median duration of disease, mo (range) 57 (5-275)”
• Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition (2007, background): “Furthermore, rates of heart failure that are determined in trials before the approval of a drug by the US Food and Drug Administration (FDA), from which patients with co-morbidities, particularly cardiovascular disease, are often excluded (for examples, see Ref”
• Second generation inhibitors of BCR-ABL for the treatment of imatinib-resistant chronic myeloid leukaemia (2007, background): “Results of a phase I study of nilotinib in 97 patients with imatinib-resistant CML in chronic , accelerated , and blast phase , and 9 patients with Ph + ALL treated at doses ranging from 50 mg to 1,200 mg daily, have been reporte”
• MEK1 mutations confer resistance to MEK and B-RAF inhibition (2009, background): “Elaboration of such resistance mechanisms has enabled the design of secondgeneration inhibitors with enhanced potency against a range of resistant variants (25, 26).”
• Ponatinib in Refractory Philadelphia Chromosome–Positive Leukemias (2012, methodology): “Quantitative reverse-transcriptase–polymerase-chain-reaction assays for molecular response were performed on day 1 of cycles 3, 5, 7, and 9 and every 3 cycles thereafter.”
• Role of JAK2 in the pathogenesis and therapy of myeloproliferative disorders (2007, methodology): “This strategy has been used to design second-generation ABL inhibitors for the treatment of imatinib refractory CM”
• Kinase-targeted cancer therapies: progress, challenges and future directions (2018, background): “More active drugs, such as nilotinib, with a selectivity profile similar to imatinib, were approved for imatinibresistant CML [79, 80].”
• BCR-ABL tyrosine kinase inhibitors in the treatment of Philadelphia chromosome positive chronic myeloid leukemia: a review. (2010, background): “[82] Kantarjian H, Giles F, Wunderle L, Bhalla K, O’Brien S, Wassmann B, et al.”