Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia chromosome.

By Brian J. Druker, C. Sawyers, H. Kantarjian, D. Resta, Sofia Fernandes Reese, J. Ford, R. Capdeville, M. Talpaz. New England Journal of Medicine, 2001

2,838 citations recorded by the source corpus.

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

View Paper: https://www.semanticscholar.org/paper/4eec29e9b67f376a2eddae9d7dd11361d39d8f6b

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In Hematology

1. E. Scholar
2. A. Arora
3. M. Greaves
4. Joe Wiemels
5. C. López‐Otín
6. Michael R. Stratton
7. J. Baselga
8. J. Cortes

In Public Health, Environmental and Occupational Health

1. F. S. Collins
2. Y. Luqmani

In Rheumatology

1. Michael R. Stratton
2. J. Cortes
3. H. Xue
4. Eric S. Lander

Citations in the corpus

• Clinical Pharmacokinetics of Imatinib (2005, neutral): “[21,25,39]”
• Molecular biology of bcr-abl1-positive chronic myeloid leukemia. (2009, background): “Quiescent BCR-ABL1–expressing LSCs account for approximately 0.5% of the CD34 population and, unlike their progeny, are refractory to chemotherapeutic agents, radiation,97 and BCR-ABL1 TKIs.98-100 The clearance of BCR-ABL1 transcripts during imatinib therapy follows a biphasic decline, reflecting th”
• Cancers predispose neutrophils to release extracellular DNA traps that contribute to cancer-associated thrombosis (2012, result): “In accordance with these results, in vitro pretreatment with imatinib or dasatinib, two abl-specific tyrosine kinase inhibitors (21), had no effect on NET formation (Fig.”
• The biology of CML blast crisis. (2004, background): “For example, the complete cytogenetic response rate (CCyR) for early chronic-phase patients placed on imatinib is approximately 80%; for accelerated phase and blast crisis, the value falls to roughly 40% and 20%, respectively.(4,5)”
• Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer. (2007, neutral): “Bcr-Abl fusion protein (Druker et al., 2001; Mahon et al., 2000).”
• Mechanisms of cancer drug resistance. (2002, background): “This increase in specificity of cancer treatment, from the use of general cytotoxic agents such as nitrogen mustard in the 1940s, to the development of natural-product anticancer drugs in the 1960s such as Vincaalkaloids and anthracyclines, which are more cytotoxic to cancer cells than normal cells,”
• International network of cancer genome projects (2010, methodology): “Key reasons for its formation were: (1) the scope is huge; (2) independent cancer genome initiatives could lead to duplication of effort or incomplete studies; (3) lack of standardization across studies could diminish the opportunities to merge and compare data sets; (4) the spectrum of many cancers”
• Core-binding factors in haematopoiesis and leukaemia (2002, background): “asp?DrugCode=1%2D22096&DrugName=GLEEVEC+ORAL&DrugType=1">Gleevec in BCR–ABL-positive CML patients who have progressed to AM”
• Life Expectancy of Patients With Chronic Myeloid Leukemia Approaches the Life Expectancy of the General Population. (2016, background): “IM treatment significantly increased the survival and quality of life for patients of all ages, particularly those in the chronic phase.(6,7) The improved survival in patients with CML is increasingly prevalent, a trend that is projected to continue during the coming decades.”