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Michael Cecchini, Jeffrey Sklar, and Jill Lacy

pancreaticoduodenectomy was sent to Foundation Medicine (Cambridge, MA) for genomic analysis, which revealed an activating mutation in exon 19 (L747_P753>S) of EGFR with a mutation allele frequency (MAF) of 16%. Mutations were also detected in CDKN2A (splice site 144

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Shankar Sellappan, Adele Blackler, Wei-Li Liao, Emily O'Day, Peng Xu, Sheeno Thyparambil, Fabiola Cecchi, Todd Hembrough, and Daniel V.T. Catenacci

(10.15/2.15 mean copy number/cell = 4.72 ratio). By next-generation sequencing (NGS), this biopsy demonstrated 9 copies of HER2 . The HER2, EGFR, and HER3 protein levels were also assessed by targeted mass spectrometry 5 ; the HER2 protein expression

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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

Background: Mutations in the epidermal growth factor receptor (EGFR) gene have been identified in 10%–50% of patients with non-small cell lung cancer (NSCLC). Exon 20 insertion mutations represent about 2%–10% of this group. Reports of real world

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Emil Lou, Donna D'Souza, and Andrew C. Nelson

mutations do not benefit from treatment with epidermal growth factor receptor (EGFR) inhibitors. 4 During this time, there have been investigations examining whether this is broadly and universally true across all forms of KRAS mutations, or whether any

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Luxi Chen, John Davelaar, Srinivas Gaddam, Kambiz Kosari, Nicholas Nissen, George Chaux, Christopher Lee, Eric Vail, Andrew Hendifar, Jun Gong, Karen Reckamp, and Arsen Osipov

/irinotecan/oxaliplatin) as neoadjuvant therapy, NGS of the pancreatic tissue revealed EGFR (OMIM #131550) S768I and G719C gain of function (GoF) mutations. The S768I and G719C mutations are located in exons 20 and 18, respectively, within the tyrosine kinase domain of the

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Kristen Keon Ciombor and Tanios Bekaii-Saab

treatment options for mCRC Appraise the recent clinical trial results of anti-EGFR and anti-VEGF therapies for determining optimal drug combinations and treatment sequences for mCRC Describe the 2 proven examples of genetic alterations leading to

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Angela M. Davies, Philip C. Mack, Primo N. Lara Jr., Derick H. Lau, Kathleen Danenberg, Paul H. Gumerlock, and David R. Gandara

; 7 : 1850 – 1855 . 32 Perez-Soler R Chachoua A Huberman M . A phase II trial of the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor OSI-774, following platinum based chemotherapy, inpatients with advanced, EGFR

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Lyndsay J. Willmott, Daniele A. Sumner, and Bradley J. Monk

Clinical Oncology. All rights reserved. Endothelial Growth Factor Receptor–Targeted Therapy Endothelial growth factor receptor (EGFR) is a 170 kDa transmembrane glycoprotein that promotes cell growth in various normal and transformed tissues

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Balazs Halmos, Maximilian J. Hochmair, Alessandro Morabito, Desiree Hao, Cheng-Ta Yang, Ross A. Soo, James C-H Yang, Rasim Gucalp, Lara Wang, Angela Märten, and Tanja Cufer

Background: EGFR TKIs have shown first-line efficacy in EGFR m+ NSCLC but acquired resistance is inevitable; with afatinib, this is predominantly through the emergence of T790M. Therefore, a key consideration when assessing therapeutic choices is

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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) ( identifiers: NCT01670877 and NCT01953926). This