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Jerald P. Radich and Vivian Oehler

Tyrosine kinase inhibitors (TKIs) are now standard up-front therapy for chronic myeloid leukemia (CML). Patients with newly diagnosed chronic-phase CML treated with the TKI imatinib mesylate typically experience a complete cytogenetic remission. Outcomes for patients with advanced-phase disease are distinctly worse. Unfortunately, a small proportion of chronic-phase patients experience relapse during this therapy, and most with advanced-phase disease develop resistance to imatinib mesylate after months of therapy. Hematopoietic cell transplantation remains the only curative approach for CML and can salvage patients with advanced-phase disease. Therefore, physicians must carefully monitor patients with chronic-phase CML treated with TKIs so that they can undergo hematopoietic cell transplant (or treatment with another TKI or experimental therapy) before frank progression occurs. Fortunately, monitoring CML using cytogenetic and molecular methods (i.e., quantitative polymerase chain reaction) effectively defines end points that correlate highly with outcome.

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Patrick A. Brown and Joseph C. Alvarnas

with ALL but in fewer than 5% of childhood patients. Importantly, the addition of BCR-ABL tyrosine kinase inhibitors (TKIs) to chemotherapy for Ph+ ALL appears to markedly improve responses. Notwithstanding these clear differences in disease biology in

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Jean McDougall, Scott D. Ramsey and Jerald Radich

Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment of chronic myelogenous leukemia (CML). Current guidelines do not specify which of the 3 TKIs approved for the first-line treatment of chronic phase CML are preferred, and no

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Arnel Pallera, Jessica K. Altman, Ellin Berman, Camille N. Abboud, Bhavana Bhatnagar, Peter Curtin, Daniel J. DeAngelo, Jason Gotlib, R. Tanner Hagelstrom, Gabriela Hobbs, Madan Jagasia, Hagop M. Kantarjian, Patricia Kropf, Leland Metheny, Joseph O. Moore, Evelena Ontiveros, Enkhtsetseg Purev, Albert Quiery, Vishnu V.B. Reddy, Michal G. Rose, Neil P. Shah, B. Douglas Smith, David S. Snyder, Kendra L. Sweet, Raoul Tibes, David T. Yang, Kristina Gregory, Hema Sundar, Michael Deininger and Jerald P. Radich

. Management of Chronic Myeloid Leukemia During Pregnancy Tyrosine kinase inhibitor (TKI) therapy with small molecule inhibitors of BCR-ABL tyrosine kinase (imatinib, dasatinib, and nilotinib) is the standard first-line therapy for patients with newly

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Kevin S. Scher, Juan-Sebastian Saldivar, Michael Fishbein, Alberto Marchevsky and Karen L. Reckamp

/print certificate. Release date: September 19, 2013; Expiration date: September 19, 2014. Learning Objectives Upon completion of this activity, participants will be able to: Explain a potential resistance mechanism to EGFR-TKI therapy when used to

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Elias Jabbour, Michael S. Mathisen and Susan O’Brien

. Small molecule tyrosine kinase inhibitors (TKIs) were developed to exploit the presence of the aberrantly expressed BCR-ABL protein in CML cells. This “targeted” approach was found to dramatically alter the natural history of the disease, improving 10

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maximum tolerated dose of combination afatinib and necitumumab therapy in patients with EGFR mutation–positive NSCLC that has progressed after first- and third-generation EGFR tyrosine kinase inhibitors (TKIs) Determine efficacy and safety profile of

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Karen L. Reckamp

, the recommendation is to consider testing for the same 4 mutations in a subset of patients and to perform PD-L1 testing in all patients. EGFR Mutations It has been established that EGFR tyrosine kinase inhibitors (TKIs) work well for patients

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Matthew Zibelman and Elizabeth R. Plimack

for treatment of patients with mRCC who had progressed after prior treatment with a tyrosine kinase inhibitor (TKI) by demonstrating improved OS versus everolimus in a phase III trial (CheckMate 025). 8 Although the overall response rate (ORR) for

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Toni K. Choueiri

tumor, targeting the vascular endothelial growth factor (VEGF) receptor is a rational treatment approach. Upstream of VEGF, the mTOR pathway is important in cell metabolism and proliferation. The anti-VEGF tyrosine kinase inhibitors (TKIs) and mTOR