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George D. Demetri, Margaret von Mehren, Cristina R. Antonescu, Ronald P. DeMatteo, Kristen N. Ganjoo, Robert G. Maki, Peter W.T. Pisters, Chandrajit P. Raut, Richard F. Riedel, Scott Schuetze, Hema M. Sundar, Jonathan C. Trent and Jeffrey D. Wayne

117) or platelet-derived growth factor receptor alpha (PDGFRA). The standard of care in the management of patients with GIST rapidly changed after the introduction of tyrosine kinase inhibitors (TKIs), such as imatinib mesylate and sunitinib malate

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Lindsey M. Charo, Adam M. Burgoyne, Paul T. Fanta, Hitendra Patel, Juliann Chmielecki, Jason K. Sicklick and Michael T. McHale

aged <40 years, there are only 2.6 cases per million persons annually. 2 Insertions, deletions, and missense mutations in the KIT and PDGFRA oncogenes cause approximately 85% of GISTs, whereas BRAF V600E missense mutations lead to approximately 1

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Khalid Mamlouk, Zach Crouch, Philina Lee, Clive Mendonca, Maria Gumina and Brian Rubin

Background: In the United States, 3,000–4,000 cases of GIST occur each year. Approximately 80% of newly diagnosed GIST harbor mutations in KIT and up to 10% harbor mutations in PDGFRA, including an activation loop mutation at amino acid 842 that is

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George D. Demetri, Robert S. Benjamin, Charles D. Blanke, Jean-Yves Blay, Paolo Casali, Haesun Choi, Christopher L. Corless, Maria Debiec-Rychter, Ronald P. DeMatteo, David S. Ettinger, George A. Fisher, Christopher D. M. Fletcher, Alessandro Gronchi, Peter Hohenberger, Miranda Hughes, Heikki Joensuu, Ian Judson, Axel Le Cesne, Robert G. Maki, Michael Morse, Alberto S. Pappo, Peter W. T. Pisters, Chandrajit P. Raut, Peter Reichardt, Douglas S. Tyler, Annick D. Van den Abbeele, Margaret von Mehren, Jeffrey D. Wayne and John Zalcberg

Such “mini-GISTs” are immunopositive for KIT and often contain an oncogenic mutation in the KIT or plateletderived growth factor receptor alpha ( PDGFRA) gene. 8 These findings suggest that most small GISTs do not progress rapidly into large

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John F. de Groot, Erik P. Sulman and Kenneth D. Aldape

(n = 52), and 2 additional subtypes: neural and classical. For the subset of 116 cases with both mutation and copy number data, correlations to TP53, IDH1, PDGFRA, EGFR, NF1 , and CDKN2A were reported. (A, B, C, D) Kaplan-Meier graphs showing the

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Maha Alkhuziem, Adam M. Burgoyne, Paul T. Fanta, Chih-Min Tang and Jason K. Sicklick

imatinib), which inhibits the KIT oncoprotein. 2 Many clinicians and scientists thought the disease was cured. However, the story was not complete. A few years later, we learned that GISTs could also be caused by PDGFRA mutations. 3 Before next

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of mutations ( VEGFR1-3 , PDGFR-A , PDGFR-B , and FGFR1-3 ) will have clinically meaningful benefits with nintedanib in terms of response rate (RR) and progression-free survival (PFS). Furthermore, this investigation plans to perform exome

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propose that patients who are molecularly selected for treatment based on the presence of mutations (VEGFR1-3, PDGFR-A, PDGFR-B, and FGFR1-3) will have clinically meaningful benefits with nintedanib in terms of response rate and progression-free survival

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–small cell lung cancer (NSCLC). We propose that patients who are molecularly selected for treatment with nintedanib based on the presence of mutations ( VEGFR1–3, PDGFR-A, PDGFR-B , and FGFR1–3 ) will have clinically meaningful benefits in terms of response

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Soft Tissue Sarcoma, Version 2.2012

Featured Updates to the NCCN Guidelines

Margaret von Mehren, Robert S. Benjamin, Marilyn M. Bui, Ephraim S. Casper, Ernest U. Conrad III, Thomas F. DeLaney, Kristen N. Ganjoo, Suzanne George, Ricardo Gonzalez, Martin J. Heslin, John M. Kane III, Joel Mayerson, Sean V. McGarry, Christian Meyer, Richard J. O'Donnell, Benjamin Paz, John D. Pfeifer, Raphael E. Pollock, R. Lor Randall, Richard F. Riedel, Scott Schuetze, Karen D. Schupak, Herbert S. Schwartz, Sridhar Shankar, Brian A. Van Tine, Jeffrey Wayne, Hema Sundar and Nicole R. McMillian

-derived growth factor receptor alpha (PDG-FRA). 1 – 3 Most GISTs (80%) are KIT-positive, and 5% to 10% have mutations in the PDGFRA gene and express little or no KIT. Approximately 10% to 15% of GISTs have no detectable KIT or PDGFRA mutations (wild