Overriding Imatinib Resistance with a Novel ABL Kinase Inhibitor

By N. Shah, C. Tran, F. Lee, Ping Chen, Derek J. Norris, C. Sawyers. Science, 2004

1,888 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/a53335143581b3d708ff865ef5c1588ecc6e95e4

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. C. Ashby
3. Andreas Hochhaus
4. J. Massagué
5. Zhesheng Chen
6. H. Kantarjian

In Hematology

1. Brian J. Druker
2. M. Heinrich
3. William Pao
4. E. Scholar
5. C. Ashby
6. Adi F. Gazdar
7. Andreas Hochhaus
8. J. Massagué

In Rheumatology

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

Citations in the corpus

• Somatic mutations of epidermal growth factor receptor signaling pathway in lung cancers (2006, background): “cial, as seen in imatinib refractory chronic myeloid leukemia cases.(43) Several specific ERBB TKIs, pan-ERBB TKIs, monoclo-”
• In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutants. (2005, background): “As a basis of comparison, published values for BMS-354825 are included in Table 2 (14).”
• Acquired Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib Is Associated with a Second Mutation in the EGFR Kinase Domain (2005, background): “The new drugs bind to ABL in an ‘‘open’’ conformation, as opposed to imatinib, which binds ABL in a ‘‘closed’’ conformation [12,13].”
• AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance. (2009, background): “Longer term, a pan-BCR-ABL inhibitor such as AP24534 might offer important strategic advantages in a first-line capacity by minimizing BCR-ABL kinase domain mutation-based drug resistance. ancer Cell 16, 401–412, November 3, 2009 ª2009 Elsevier Inc. 401 imatinib family member nilotinib (Tasigna; AMN”
• 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)”
• The structure of Dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants. (2006, background): “effectively inhibited in the low nanomolar range (16).”
• Kinase-targeted cancer therapies: progress, challenges and future directions (2018, background): “, imatinib and dasatinib, produce more favorable outcome compared to conventional cytotoxic therapy [18, 19].”
• Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia. (2007, background): “…40% of reported mutations.3 Second, KD mutants may be gain-of-function or loss-of-function, which could influence their chances of survival.31,32 For example, compared with native Bcr-Abl, the 253Y F mutant has increased kinase activity and transformation potency, particularly in…”
• Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. (2005, background): “There has also been increasing interest in identifying new Bcr-Abl inhibitors with greater potency than imatinib, or that retain the ability to inhibit imatinib-resistant point mutants to Bcr-Abl (Mow et al., 2002; La Rosee et al., 2002; Shah et al., 2004; O’Hare et al., 2004).”