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Hillary Johnson-Jahangir, William Sherman and Désirée Ratner

, with en face margin evaluation performed using complete circumferential peripheral and deep margin assessment. 9 – 14 However, in surgically difficult cases, complete excision may result in cosmetic deformity or functional disability. Using imatinib

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David D. Stenehjem, Frederick Albright, Kuan-Ling Kuo, Karina Raimundo, Hillevi Bauer, Paul J. Shami, Michael W. Deininger, Lei Chen and Diana I. Brixner

Imatinib became the front-line treatment for patients with chronic-phase chronic myelogenous leukemia (CP-CML) based on results from the International Randomized Study of Interferon and STI571 (IRIS), which compared imatinib versus interferon

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Michael Deininger

References 1 Hughes TP Kaeda J Branford S . Frequency of major molecular responses to imatinib or interferon alfa plus cytarabine in newly diagnosed chronic myeloid leukemia . N Engl J Med 2003 ; 349 : 1423 – 1432 . 2

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Jane Apperley

target of the TKI; imatinib inhibits not only Abl but also c-kit, platelet-derived growth factor receptors α and β (PDGFR-α/β), ARG, and c-FMS. Dasatinib, a second-generation TKI, also inhibits Src and related proteins. Several of these proteins are known

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Susan O'Brien, Ellin Berman, Joseph O. Moore, Javier Pinilla-Ibarz, Jerald P. Radich, Paul J. Shami, B. Douglas Smith, David S. Snyder, Hema M. Sundar, Moshe Talpaz and Meir Wetzler

years, and eventually leads to terminal blast-phase disease, with death occurring from bleeding and infectious complications. 3 First-Line Treatment: Imatinib Versus Second-Generation Tyrosine Kinase Inhibitors Imatinib Imatinib is a selective inhibitor

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Lucas Vieira dos Santos, João Paulo Lima, Kathia Cristina Abdalla, Arinilda Campos Bragagnoli, Florinda Almeida Santos, Alexandre dos Anjos Jácome and Fabiano Elias Porto

imatinib Distinguish between the signs and symptoms of bone pain associated with imatinib therapy versus bone metastasis in patients with GISTs Background Gastrointestinal stromal tumors (GISTs) are the most common nonepithelial cancers of the

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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

for GISTs rapidly changed after the introduction of effective molecularly targeted therapy (such as imatinib and sunitinib). Because of these changes, the NCCN organized a multidisciplinary panel composed of experts in medical oncology, molecular

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M. Zach Koontz, Brendan M. Visser and Pamela L. Kunz

consideration of neoadjuvant imatinib with the hope of shrinking the tumor enough to facilitate duodenectomy rather than requiring a Whipple pancreaticoduodenectomy. Her past medical and surgical history was significant for a complicated appendectomy requiring

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Joshua B. Brown, Reetesh K. Pai, Melissa A. Burgess, Jennifer Chennat and Amer H. Zureikat

. Imatinib mesylate, a tyrosine kinase inhibitor, has shown efficacy in advanced and metastatic GIST. 2 More recently, imatinib has been used in the neoadjuvant setting in an effort to downstage tumors, with studies showing its ability to reduce the

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James Perkins, Patrick Boland, Steven J. Cohen, Anthony J. Olszanski, Yan Zhou, Paul Engstrom and Igor Astsaturov

for NET Describe the rationale for the use of imatinib in the treatment of patients with NET with activating KIT mutations Evaluate the data supporting the hypothesis that NET and GIST arise from a common precursor Neuroendocrine tumors (NET