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HER2-Mutated Breast Cancer Responds to Treatment With Single-Agent Neratinib, a Second-Generation HER2/EGFR Tyrosine Kinase Inhibitor

Noa Efrat Ben-Baruch, Ron Bose, Shyam M. Kavuri, Cynthia X. Ma, and Matthew J. Ellis

metastatic breast cancer for HER2 mutations, and treating patients with HER2-positive breast cancer with the second-generation HER2/EGFR tyrosine kinase inhibitor neratinib (HKI-272) ( ClinicalTrials.gov identifiers: NCT01670877 and NCT01953926). This

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Treatment Trends and Clinical Outcomes of Left-Sided RAS/RAF Wild-Type Metastatic Colorectal Cancer in the United States

Christopher Nevala-Plagemann, Siddharth Iyengar, Andrew D. Trunk, Lisa Pappas, Benjamin Haaland, and Ignacio Garrido-Laguna

VEGF, and the anti-EGFR antibodies cetuximab and panitumumab. 2 – 4 All 3 of these agents are now approved for use in the first-line setting in patients with RAS / RAF WT mCRC. 5 – 7 Increased use of these agents has likely led to improvement in

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Targeted Agents: Management of Dermatologic Toxicities

Barbara Burtness

Head and Neck Cancers Program, Smilow Cancer Hospital at Yale-New Haven. Dr. Burtness is a member of the NCCN Guidelines Panel for Head and Neck Cancers and the NCCN Task Force on Management of Dermatologic and Other Toxicities Associated with EGFR

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NCCN Guidelines Updates: Management of Metastatic Colorectal Cancer

Wells A. Messersmith

-approved drugs for use in colorectal cancer. Abbreviations: EGFR, epidermal growth factor receptor; TAS-102, trifluridine-tipiracil; VEGF, vascular endothelial growth factor. a VEGFR, BRAF, and others. The issue of cost remains a major concern in the treatment of

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HSR21-063: Treatment Patterns Among Patients With EGFR Mutated Metastatic NSCLC Who Have Discontinued EGFR-TKI and Platinum-Based Chemotherapy Regimens

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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Targeted Therapy for Patients With Metastatic Non–Small Cell Lung Cancer

Karen L. Reckamp

Conference. 1 The list of mutations with approved targeted therapies includes EGFR mutations (present in 30%–40% of Asians 2 and 10%–20% of Caucasians), 3 ALK rearrangements (present in up to 7%), ROS1 rearrangements (1.7%), and BRAF mutations

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Anti-EGFR Therapy in Right-Sided Metastatic Colorectal Cancer: Right or Wrong?

Benjamin A. Weinberg

chemotherapy, biologic agents are an important component of the arsenal against metastatic CRC (mCRC). Use of cetuximab and panitumumab, which are monoclonal antibodies targeting the epidermal growth factor receptor (EGFR), has evolved substantially over the

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HSR22-154: Treatment Patterns Following Osimertinib Discontinuation in Patients With EGFR Mutated Metastatic NSCLC

Elizabeth Marrett, Winghan Jacqueline Kwong, Jinlin Song, Ameur M. Manceur, Selvam Sendhil, and Eric Wu

Background : Osimertinib is a third generation EGFR-TKI increasingly used as first-line treatment (Tx) for metastatic non-small cell lung cancer (mNSCLC) harboring an EGFR sensitizing mutation. This study characterized the subsequent line of

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CGE23-069: Evaluation of Patients With Multiple EGFR Genomic Tests in the Metastatic NSCLC Setting

Lincy Lal, Anna O Williford, Dana E Milne, and Mark S Walker

Background: Few studies have evaluated EGFR status concordance of multiple genomic tests using real-world data (RWD). Results of metastatic Non–Small Cell Lung Cancer (NSCLC) patients with multiple EGFR genomic tests within the ConcertAI Genome

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Molecular Biomarkers in Gastric Cancer

Elena Elimova, Roopma Wadhwa, Hironori Shiozaki, Kazuki Sudo, Jeannelyn S. Estrella, Brian D. Badgwell, Prajnan Das, Aurelio Matamoros Jr, Shumei Song, and Jaffer A. Ajani

the crosstalk with epidermal growth factor receptor (EGFR) and G-protein–coupled receptor (GPCR) signaling. Two kinase cascades participate in this pathway and are formed: MST1/2 and LATS1/2. The activation of these kinases leads to phosphorylation of