Effect of the tyrosine kinase inhibitor STI571 in a patient with a metastatic gastrointestinal stromal tumor.

By Heikki Joensuu, P. Roberts, M. Sarlomo‐Rikala, Leif C. Andersson, P. Tervahartiala, David A. Tuveson, S. Silberman, R. Capdeville, S. Dimitrijević, Brian J. Druker and 1 more. New England Journal of Medicine, 2001

2,075 citations recorded by the source corpus.

Subfields: Gastroenterology, Hematology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/398f057b79cd11e54ab2fd1ea73b17e994d8c3ff

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Gastroenterology

1. Christopher Corless
2. M. Heinrich
3. Heikki Joensuu
4. J. Fletcher
5. C. Fletcher

In Hematology

1. M. Heinrich
2. Brian J. Druker
3. P. Cohen
4. Christopher Corless
5. Derek C. Radisky
6. Mina J. Bissell
7. T. Jacks
8. P. Jänne

In Pulmonary and Respiratory Medicine

1. Heikki Joensuu
2. Christopher Corless
3. M. Heinrich
4. Brian J. Druker
5. P. Jänne

Citations in the corpus

• Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumor. (2003, background): “Subsequent treatment of a patient with metastatic GIST resulted in marked clinical, radiologic, and pathologic improvement.(17) The clinical activity of imatinib for unresectable, metastatic GISTs has been documented in two clinical studies.”
• Integrated PET/CT: current applications and future directions. (2006, background): “Unlike contrast-enhanced CT, FDG PET is able to show early effects in patients undergoing treatment with imatinib mesylate (Gleevec; Novartis, Basel, Switzerland) (36).”
• Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors. (2002, methodology): “In both preclinical experiments 13 and a previous case study, 14 inhibition by imatinib had considerable antiproliferative and proapoptotic effects on gastrointestinal stromal tumor cells.”
• The discovery of receptor tyrosine kinases: targets for cancer therapy (2004, background): “As KIT is thought to have an important role in the pathogenesis of gastrointestinal stromal tumours (GISTs), clinical studies with imatinib were successfully extended to this tumour typ”
• Drug-induced death signaling strategy rapidly predicts cancer response to chemotherapy (2015, positive): “, 2011), or cKITmutations to guide treatment with imatinib in GIST (Joensuu et al., 2001).”
• Putting tumours in context (2001, background): “cgi?l=25">ABL kinase activity in chronic myelogenous leukaemia cells) indicates that this might be a valid approac”
• A quantitative analysis of kinase inhibitor selectivity (2008, background): “For example, the discovery that imatinib inhibits KIT in addition to ABL1 and the PDGF receptors first suggested the use of imatinib for the treatment of gastrointestinal stromal tumor”
• Consensus meeting for the management of gastrointestinal stromal tumors. Report of the GIST Consensus Conference of 20-21 March 2004, under the auspices of ESMO. (2005, methodology): “Hence, clinical practice has been generally based on the analysis of retrospective series of patients and prospective series with limited follow-up, given that the first treatment with imatinib in a GIST patient was in 2000 [13].”
• Correlation of computed tomography and positron emission tomography in patients with metastatic gastrointestinal stromal tumor treated at a single institution with imatinib mesylate: proposal of new computed tomography response criteria. (2007, background): “imatinib (Gleevec; Novartis, Basel, Switzerland), a tyrosine kinase inhibitor, was reported.(2) Imatinib, a”
• STI571 inactivation of the gastrointestinal stromal tumor c-KIT oncoprotein: biological and clinical implications (2001, background): “A recently published single patient case report demonstrated a response to STI571 in GIST (Joensuu et al., 2001).”
• Molecular correlates of imatinib resistance in gastrointestinal stromal tumors. (2006, methodology): “Conclusion Different molecular mechanisms are responsible for primary and secondary imatinib resistance in GISTs.”
• Gastrointestinal stromal tumours: origin and molecular oncology (2011, methodology): “With the knowledge that imatinib inhibits KIT signalling, imatinib was first used clinically to treat a 50-year-old female with metastatic GIST, and a dramatic response was see”