Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia.

By N. Shah, J. Nicoll, B. Nagar, M. Gorre, R. Paquette, J. Kuriyan, C. Sawyers. Cancer Cell, 2002

1,712 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/3b97e992b88b27d2449ad88a4f7e31adea0abdd0

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In Genetics

1. K. Polyak
2. C. Ashby
3. Andreas Hochhaus
4. W. Kaelin
5. Zhesheng Chen
6. J. Engelman
7. Brian J. Druker
8. G. Semenza

In Hematology

1. William Pao
2. C. Ashby
3. Adi F. Gazdar
4. Andreas Hochhaus
5. W. Kaelin
6. Zhesheng Chen
7. P. Jänne
8. H. Shigematsu

In Rheumatology

1. Andreas Hochhaus
2. Brian J. Druker

Citations in the corpus

• Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. (2005, background): “…imatinib-resistant Bcr-Abl mutants Imatinib and AMN107 were compared for effects on cells expressing point mutants of Bcr-Abl associated with imatinib resistance in patients (Hofmann et al., 2002; Shah et al., 2002; 132 von Bubnoff et al., 2002; Branford et al., 2002; Roche-Lestienne et al., 2002).”
• The biology of CML blast crisis. (2004, background): “Last, point mutations can be found in blast crisis samples never exposed to tyrosine kinase inhibitors.(64) How does the acquisition of point mutations, resistance, and progression to blast crisis relate? The acquisition of point mutations may result from the genetic instability associated with Bcr-”
• Acquired Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib Is Associated with a Second Mutation in the EGFR Kinase Domain (2005, background): “It is also possible that EGFR amplification itself plays a role in acquired resistance, since imatinib-resistant clones have been shown to lack resistance mutations but contain amplified copies of BCR-ABL [11,28].”
• Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of BCR-ABL. (2003, positive): “Harvard Medical School and loop surrounding the active site (Barthe et al., 2001; Division of Pediatric Hematology/Oncology Branford et al., 2002; Gorre et al., 2001; Hochhaus et Children’s Hospital and al., 2001; Hofmann et al., 2002; Roche-Lestienne et al., Dana Farber Cancer Institute 2002; Shah”
• Tumor heterogeneity: causes and consequences (2009, background): “Analysis of patient samples collected before treatment often revealeds the presence of resistant subpopulations of leukemic cells; therefore, the treatment is thought to provide selective pressure that drives the expansion of these therapyinsensitive cells, causing the eventual relapse of the diseas”