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Jane Apperley

T he use of tyrosine kinase inhibitors (TKIs) in the management of chronic myelogenous leukemia (CML) has changed the natural course of the disease to such an extent that considerations regarding quality of life have become almost as important as

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Céline Mascaux, Ming-Sound Tsao and Fred R. Hirsch

kinase activity. Its overexpression was found to be involved in the pathogenesis of various tumors, and therefore an attractive target for cancer therapy. Consequently, monoclonal antibodies and small molecule tyrosine kinases inhibitors (TKIs) were

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Robert I. Haddad

(TKIs) can be used. The Role for TKIs The vascular endothelial growth factor (VEGF) pathway is important in thyroid cancer, and various tyrosine kinases are activated in the disease. Thus, there is a therapeutic role for multikinase inhibitors

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David S. Ettinger, Douglas E. Wood, Dara L. Aisner, Wallace Akerley, Jessica Bauman, Lucian R. Chirieac, Thomas A. D'Amico, Malcolm M. DeCamp, Thomas J. Dilling, Michael Dobelbower, Robert C. Doebele, Ramaswamy Govindan, Matthew A. Gubens, Mark Hennon, Leora Horn, Ritsuko Komaki, Rudy P. Lackner, Michael Lanuti, Ticiana A. Leal, Leah J. Leisch, Rogerio Lilenbaum, Jules Lin, Billy W. Loo Jr, Renato Martins, Gregory A. Otterson, Karen Reckamp, Gregory J. Riely, Steven E. Schild, Theresa A. Shapiro, James Stevenson, Scott J. Swanson, Kurt Tauer, Stephen C. Yang, Kristina Gregory and Miranda Hughes

in exon 21 (L858R in 40%). Both mutations result in activation of the tyrosine kinase domain, and both are associated with sensitivity to the small molecule tyrosine kinase inhibitors (TKIs), such as erlotinib, gefitinib, and afatinib (see “EGFR TKIs

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Wallace Akerley

inhibitors (TKIs) are approved to treat EGFR -biomarker–defined NSCLC. Among those with mutations, 90% will have a deletion in exon 19 or L858R in exon 21 of EGFR , Dr. Akerley said. In the early days when EGFR was not yet recognized as the biomarker

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Charu Aggarwal, Neeta Somaiah and George R. Simon

EGFR . Because response rates for EGFR–tyrosine kinase inhibitors (TKIs) are so low in patients with EGFR wild-type mutations, progression-free and overall survivals would have to be the appropriate end points to discern these differences. The

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Ammar Sukari, Misako Nagasaka and Erin Wakeling

was started on osimertinib and achieved a partial response within 2 months of starting this new third-generation EGFR tyrosine kinase inhibitor (TKI). Because NGS showed multiple lesions with T790M, the possibility of a germline mutation was suspected

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NCCN Guidelines Insights: Kidney Cancer, Version 2.2020

Featured Updates to the NCCN Guidelines

Robert J. Motzer, Eric Jonasch, M. Dror Michaelson, Lakshminarayanan Nandagopal, John L. Gore, Saby George, Ajjai Alva, Naomi Haas, Michael R. Harrison, Elizabeth R. Plimack, Jeffrey Sosman, Neeraj Agarwal, Sam Bhayani, Toni K. Choueiri, Brian A. Costello, Ithaar H. Derweesh, Thomas H. Gallagher, Steven L. Hancock, Christos Kyriakopoulos, Chad LaGrange, Elaine T. Lam, Clayton Lau, Bryan Lewis, Brandon Manley, Brittany McCreery, Andrew McDonald, Amir Mortazavi, Phillip M. Pierorazio, Lee Ponsky, Bruce G. Redman, Bradley Somer, Geoffrey Wile, Mary A. Dwyer, CGC, Lydia J. Hammond and Griselda Zuccarino-Catania

and the results from trials with novel immunotherapy combinations 9 , 33 (with either other immunotherapies or a tyrosine kinase inhibitor [TKI]) on first-line treatment options for advanced or relapsed stage IV clear cell renal cell carcinoma (ccRCC

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Eric Jonasch

also second-line options. Nivolumab was approved in November 2015 for patients in whom tyrosine kinase inhibitors (TKIs) failed. Approval was based on a study of 821 patients randomized to receive nivolumab versus everolimus with a primary end point

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Fiona Tsui-Fen Cheng, Fu Ou-Yang, Nina Lapke, Kai-Che Tung, Yen-Kung Chen, Yuh-Yu Chou and Shu-Jen Chen

(TKI) pazopanib, which is indicated for the treatment of renal cell carcinoma and soft tissue sarcoma. This case report shows that pazopanib induced an encouraging clinical response in a patient with breast cancer and FGFR1 amplification. Importantly