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Neil P. Shah

Discontinuation of tyrosine kinase inhibitor (TKI) therapy appears to be safe among adult patients with chronic myeloid leukemia (CML) in the chronic phase who have achieved and maintained a deep molecular response (DMR), according to the updated

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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

, nilotinib, 300 mg daily, had the lowest rates of discontinuation from adverse events or laboratory abnormalities. Are Early Short-Term End Points Good Enough to Recommend Second-Generation TKIs at Diagnosis? Although most patients experience response to

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Irbaz Bin Riaz, Saad Ullah Malik, Muhammad Husnain, Qurat Ul Ain Riaz Sipra, Warda Faridi, Farva R. Gondal, Thanh Ho, Siddhartha Yadav, Zhen Wang, and Manish Kohli

Background: Four large RCTs (ASSURE, S-TARC, PROTECT, ATLAS) tested adjuvant VEGF-TKI therapy in high risk RCC. The results were variable for efficacy and there were concerns for increased toxicity and decline in quality of life (QoL). We performed

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Jerald P. Radich, Michael Deininger, Camille N. Abboud, Jessica K. Altman, Ellin Berman, Ravi Bhatia, Bhavana Bhatnagar, Peter Curtin, Daniel J. DeAngelo, Jason Gotlib, Gabriela Hobbs, Madan Jagasia, Hagop M. Kantarjian, Lori Maness, Leland Metheny, Joseph O. Moore, Arnel Pallera, Philip Pancari, Mrinal Patnaik, Enkhtsetseg Purev, Michal G. Rose, Neil P. Shah, B. Douglas Smith, David S. Snyder, Kendra L. Sweet, Moshe Talpaz, James Thompson, David T. Yang, Kristina M. Gregory, and Hema Sundar

with tyrosine kinase inhibitors (TKIs) in prospective studies, the presence of ACA/Ph + at the time of diagnosis was not associated with worse prognosis. 16 Patients with ACA/Ph + at diagnosis should be watched carefully for evidence of therapy

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Jerald P. Radich

use of tyrosine kinase inhibitors (TKIs), survival in blast crisis has not clearly improved with these targeted agents. Progression to blast crisis in CML is a phenomenon that is still not completely understood. Although definitions of both

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Elizabeth Marrett, Winghan Jacqueline Kwong, Jipan Xie, Ameur Manceur, Selvam Sendhil, Eric Wu, and Raluca Ionescu-Ittu

Background: EGFR-TKI inhibitors are established first line treatments (Tx) for metastatic non-small cell lung cancer (mNSCLC) harboring an EGFR sensitizing mutation. Upon EGFR-TKI resistance, there is little data to support the standard of care in

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Gary R. Hudes, Michael A. Carducci, Toni K. Choueiri, Peg Esper, Eric Jonasch, Rashmi Kumar, Kim A. Margolin, M. Dror Michaelson, Robert J. Motzer, Roberto Pili, Susan Roethke, and Sandy Srinivas

, stimulating multiple downstream signaling pathways and leading to cell growth, proliferation, and angiogenesis. The tyrosine kinase inhibitors (TKIs) block the downstream signaling of the receptor tyrosine kinases. Figure 1 Therapeutic targets in renal cell

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Chunlin Qian, Elizabeth Marrett, Winghan Jacqueline Kwong, and Laura Q.M. Chow

Background: First-line targeted therapy with an EGFR-TKI inhibitor for metastatic non-small cell lung cancer (mNSCLC) harboring a sensitizing EGFR oncogenic driver mutation demonstrated efficacy and improvements in survival in clinical trials and

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Alejandro Garcia-Horton and Jeffrey H. Lipton

The prognosis of chronic myeloid leukemia (CML) has greatly improved since the clinical use of tyrosine kinase inhibitors (TKIs) started with imatinib in the early 2000s. 1 It is now considered a chronic disease, with its incidence being stable

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Jorge Cortes, John M. Goldman, and Timothy Hughes

The treatment landscape for chronic myelogenous leukemia (CML) dramatically changed after the FDA approved the tyrosine kinase inhibitor (TKI) imatinib mesylate (Gleevec, Novartis) in 2001. Imatinib targets BCR-ABL, a fusion protein expressed by