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Merav Bar and Jerald Radich

Tyrosine Kinase Inhibitor Therapy for Chronic Myeloid Leukemia, 2012 Before the introduction of the tyrosine kinase inhibitors (TKIs), allogeneic hematopoietic cell transplantation (HCT) was the only “curative” approach for chronic myeloid

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Jerald P. Radich

(TKI) imatinib is well-known. The embarrassment of riches in CML continues, with the emergence of both second- and third-generation TKIs; however, not every patient with CML tolerates therapy, has a response to initial treatment, or avoids relapse. Thus

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Barbara Burtness, Milan Anadkat, Surendra Basti, Miranda Hughes, Mario E. Lacouture, Joan S. McClure, Patricia L. Myskowski, Jennifer Paul, Clifford S. Perlis, Leonard Saltz and Sharon Spencer

This NCCN Task Force Report describes the management of dermatologic and ocular toxicities that occur in patients treated with epidermal growth factor receptor (EGFR) inhibitors. Task force members are from NCCN member institutions and include oncologists, dermatologists, an ophthalmologist, and a mid-level oncology provider. This report describes commonly used therapies that the task force agreed are appropriate standards of care for dermatologic and ophthalmologic toxicities associated with EGFR inhibitors, which generally are supported only by anecdotal evidence. Few recommendations are evidence based; however, some commonly used therapies have data supporting their use. Conclusions from completed clinical trials are generally limited by the small numbers of patients enrolled. The information in this report is based on available published data on treating toxicities associated with EGFR inhibitors, data from treatment of clinically similar toxicities from different etiologies, and expert opinion among the NCCN Task Force members.

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Susan O’Brien, Jerald P. Radich, Camille N. Abboud, Mojtaba Akhtari, Jessica K. Altman, Ellin Berman, Daniel J. DeAngelo, Michael Deininger, Steven Devine, Amir T. Fathi, Jason Gotlib, Madan Jagasia, Patricia Kropf, Joseph O. Moore, Arnel Pallera, Javier Pinilla-Ibarz, Vishnu VB. Reddy, Neil P. Shah, B. Douglas Smith, David S. Snyder, Meir Wetzler, Kristina Gregory and Hema Sundar

.2014 Version 1.2014 © National Comprehensive Cancer Network, Inc. 2013, All rights reserved. The NCCN Guidelines® and this illustration may not be reproduced in any form without the express written permission of NCCN®. Tyrosine kinase inhibitor (TKI

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Susan O’Brien, Jerald P. Radich, Camille N. Abboud, Mojtaba Akhtari, Jessica K. Altman, Ellin Berman, Peter Curtin, Daniel J. DeAngelo, Michael Deininger, Steven Devine, Amir T. Fathi, Jason Gotlib, Madan Jagasia, Patricia Kropf, Joseph O. Moore, Arnel Pallera, Vishnu VB. Reddy, Neil P. Shah, B. Douglas Smith, David S. Snyder, Meir Wetzler, Kristina Gregory and Hema Sundar

therapy, and clonal evolution). It should be noted that clinical trials of tyrosine kinase inhibitors (TKIs) have largely reported efficacy data using the modified MD Anderson Cancer Center accelerated phase criteria (15% and <30% peripheral blood or bone

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Stephen Harnicar

has not been determined. In addition to high-dose imatinib, patients now have more options for front-line therapy with the introduction of the second-generation tyrosine kinase inhibitors (TKIs). Originally approved for imatinib failure or

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Maral DerSarkissian, Shuanglian Li, Aaron Galaznik, Rachel Bhak, Iryna Bocharova, Thomas Kulalert, Huamao M. Lin, Hui Huang and Mei Sheng Duh

chemotherapy, approximately 20% of both TN and RR patient groups had exposure to various EGFR TKIs. Overall, median rwOS was low at 14.6 months for TN patients, and 10.1 months for RR patients. Conclusion: Real world survival of patients with EGFR exon 20

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Paul J. Shami

occupied a substantial portion of the medical literature over the past 10 years because of the development of highly successful tyrosine kinase inhibitors (TKIs) that have changed the treatment paradigm. In fact, attempts to follow a similar strategy for

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Michael Cecchini, Jeffrey Sklar and Jill Lacy

790M -mediated resistance to a first-generation tyrosine kinase inhibitor (TKI). The course described here supports the conclusions that activating EGFR mutations in PDAC respond to EGFR TKIs, and resistance to therapy may be due to similar

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Scott M. Lindhorst, Richard D. Lopez and Ronald D. Sanders

/print certificate. Release date: July 12, 2013; Expiration date: July 12, 2014 Learning Objectives Upon completion of this activity, participants will be able to: Compare and contrast response rates to TKI therapy for patients who present with CML in