Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia.

By Brian J. Druker, F. Guilhot, S. O’Brien, I. Gathmann, H. Kantarjian, N. Gattermann, M. Deininger, R. Silver, J. Goldman, R. Stone and 22 more. New England Journal of Medicine, 2006

3,470 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/dc557d82cba8d57bd573f334465789667d41e96d

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. Brian J. Druker
2. Michael R. Stratton
3. J. Melo
4. Zhesheng Chen
5. C. Ashby
6. J. Cortes
7. Jorge Soares
8. George A. Calin

In Hematology

1. Brian J. Druker
2. J. Melo
3. Michael R. Stratton
4. J. Cortes
5. J. Goldman
6. C. Ashby
7. Zhesheng Chen
8. J. Apperley

In Rheumatology

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

Citations in the corpus

• Dasatinib or imatinib in newly diagnosed chronic-phase chronic myeloid leukemia: 2-year follow-up from a randomized phase 3 trial (DASISION). (2012, background): “Death on study treatment or within 30 days of last dose 7 (3) 4 (2)”
• Chronic myeloid leukemia: an update of concepts and management recommendations of European LeukemiaNet. (2009, result): “At 12 months, a CCgR yielded superior results compared with a PCgR for 5-year PFS and OS,(35,39,118) and a PCgR was always better than a less than PCgR.(35,117) After 18 months of imatinib therapy, the PFS (99%) and the OS (98%) of CCgRs were always superior to those of PCgRs (87% and 76%, respectiv”
• Cancer stem cells: impact, heterogeneity, and uncertainty. (2012, background): “Cancer Cell 2 These clinical observations appear to be explained by the persistence of rare imatinib-resistant CML stem cells (Chu et al., 2011; Graham et al., 2002; Holtz et al., 2002).”
• Ponatinib in Refractory Philadelphia Chromosome–Positive Leukemias (2012, neutral): “Withdrawal of consent 2 (3) 1 (2) 1 (11) 0 0 0 0”
• Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia. (2007, background): “In a recent update of the IRIS study, the projected overall survival rate of these patients was 89% by 60 months and freedom from progression to accelerated phase (AP) or blast crisis (BC) was 93%.(1) Patients achieving a 3-log reduction of BCR-”
• Systematic identification of genomic markers of drug sensitivity in cancer cells (2012, background): “Insets (1) and (2) are magnified views of selected highly significant associations; the drug name, therapeutically relevant target(s) (in superscript) and cancer gene (in brackets) are given for each.”
• European LeukemiaNet recommendations for the management of chronic myeloid leukemia: 2013. (2013, background): “It is recommended that in practice outside of clinical trials, the firstline treatment of CP CML can be any of the 3 TKIs that have been approved for this indication and are available nearly worldwide, namely imatinib (400mg once daily), nilotinib (300mg twice daily), and dasatinib (100 mg once dail”
• Targeting the cancer kinome through polypharmacology (2010, neutral): “…have revolutionized the treatment of a select group of diseases, such as chronic myeloid leukaemia (CML) and gastrointestinal stromal tumours (GIST), which are driven by a single oncogenic kinase; for these conditions, kinase inhibitors have achieved multi-year increases in survival 5–7 .”
• AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance. (2009, background): “The exemplar of targeted therapy in CML is the BCR-ABL inhibitor imatinib (Gleevec; STI571), a safe and effective first-line therapy for most patients diagnosed with chronic phase disease (Druker et al., 2006).”