AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance.

By T. O'hare, W. Shakespeare, Xiaotian Zhu, C. Eide, V. Rivera, Frank Y. Wang, Lauren T. Adrian, Tianjun Zhou, Wei‐Sheng Huang, Qihong Xu and 18 more. Cancer Cell, 2009

1,220 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/a5ae6c382d4e46455e380e3f5937dae3f52e958d

How researchers see this paper

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In Genetics

1. Brian J. Druker
2. J. Cortes
3. William C. Hahn
4. Andreas Hochhaus
5. H. Kantarjian
6. M. Baccarani

In Hematology

1. Brian J. Druker
2. J. Cortes
3. J. Goldman
4. J. Apperley
5. Levi A. Garraway
6. Andreas Hochhaus
7. H. Kantarjian
8. M. Baccarani

In Rheumatology

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

Citations in the corpus

• Ponatinib in Refractory Philadelphia Chromosome–Positive Leukemias (2012, background): “Moreover, in these preclinical experiments, ponatinib suppressed the emergence of any mutation at a concentration of 40 nM. 20 These data support the characterization of ponatinib as a pan–BCR-ABL inhibitor and suggest that ponatinib may have substantial clinical utility in the treatment of…”
• A Phase 2 Trial of Ponatinib in Philadelphia Chromosome–Positive Leukemias (2013, neutral): “Fatigue 51 (19) 4 (1) 17 (20) 1 (1) 7 (11) 2 (3) 3 (9) 0”
• Targeting the cancer kinome through polypharmacology (2010, neutral): “These agents are effective in preclinical models of drug-resistant CML 36–39 , and four such compounds are currently in clinical trials.”
• Dissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling. (2011, background): “inhibit gatekeeper mutations remains an area of intense study.(97,102)”
• European LeukemiaNet recommendations for the management of chronic myeloid leukemia: 2013. (2013, background): “T315I is also resistant to bosutinib,(34,68) whereas ponatinib inhibits T315I in vitro and is effective in patients with T315 in vivo.(49-52) Table 4 reports the in vitro sensitivity of the most common BCR-ABL1 mutants to imatinib, nilotinib, dasatinib, bosutinib, and ponatinib, expressed as half-ma”