Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia.

By T. O'hare, C. Eide, M. Deininger. Blood, 2007

639 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/583d573087203c6d3a48041556f16f8f472eba3c

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In Genetics

1. Brian J. Druker
2. J. Cortes
3. H. Kantarjian

In Hematology

1. Brian J. Druker
2. J. Cortes
3. H. Kantarjian

In Rheumatology

1. Brian J. Druker
2. J. Cortes
3. H. Kantarjian

Citations in the corpus

• A Phase 2 Trial of Ponatinib in Philadelphia Chromosome–Positive Leukemias (2013, neutral): “Neutropenia 44 (16) 38 (14) 22 (26) 22 (26) 14 (23) 11 (18) 4 (12) 4 (12)”
• Ponatinib in Refractory Philadelphia Chromosome–Positive Leukemias (2012, background): “19,37 Imatinib, dasatinib, and nilotinib are all ineffective against the T315I mutant, a common mutation.”
• AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance. (2009, result): “no toxicity to normal hematopoietic cells at concentrations below 500 nM (Figure S2B), consistent with cellular proliferation assay data obtained using normal cells (Figure 4A).”