Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: results of a phase II study.

By C. Sawyers, Andreas Hochhaus, E. Feldman, J. Goldman, Carole B. Miller, O. Ottmann, C. Schiffer, M. Talpaz, F. Guilhot, M. Deininger and 21 more. Blood, 2002

1,213 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Public Health, Environmental and Occupational Health

View Paper: https://www.semanticscholar.org/paper/2df1398251a8b7198971cfe315385682113b81c7

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. C. Ashby
2. C. Sawyers
3. Zhesheng Chen
4. Y. Luqmani

In Hematology

1. C. Ashby
2. Zhesheng Chen
3. Brian J. Druker
4. E. Scholar
5. A. Arora
6. Y. Luqmani

In Public Health, Environmental and Occupational Health

1. Y. Luqmani

Citations in the corpus

• BCR-ABL tyrosine kinase inhibitors in the treatment of Philadelphia chromosome positive chronic myeloid leukemia: a review. (2010, methodology): “[21] Sawyers CL, Hochhaus A, Feldman E, Goldman JM, Miller CB, Ottmann OG, et al.”
• 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. (2002, background): “The ability of BCR- continued therapy (Druker et al., 2001a; Sawyers et al., 2002).”
• Glucocorticoid Receptor Confers Resistance to Anti-Androgens by Bypassing Androgen Receptor Blockade (2013, neutral): “Clinical success of kinase inhibitors in other tumors such as melanoma, lung cancer, leukemia, and sarcoma is similarly transient (Sawyers et al., 2002; Chapman et al., 2011; Demetri et al., 2002; Maemondo et al., 2010), resulting in numerous efforts to define mechanisms of acquired resistance.”
• Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia. (2007, background): “Durable responses are the rule in early chronic phase, but the exception in blast crisis.(1,6,7) Responses to second-line inhibitors (dasatinib(11,38,39,50) and nilotinib(10,41)) are based on limited preliminary evidence (green trace).”
• Chronic Myeloid Leukemia (2007, neutral): “Phase II trials have investigated the efficacy of front-line imatinib 400-800 mg/day in AP-CML 66-69 and BC-CML 70,71 .”
• Neuronal and glioma-derived stem cell factor induces angiogenesis within the brain. (2006, background): “…activity against certain systemic solid tumors, such as gastrointestinal stromal tumors (GIST), and chronic myelogenous leukemia (CML) may be in part a result of its antiangiogenic as well as its direct antitumor effects (Demetri et al., 2002; Kantarjian et al., 2002; Sawyers et al., 2002).”
• Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. (2005, background): “In contrast, patients diagnosed with Ph+ ALL, as well as many patients with more advanced stage CML (accelerated phase and blast crisis), fail to achieve a complete cytogenetic response and frequently develop resistance to therapy and relapse (Sawyers et al., 2002; Ottmann et al., 2002).”