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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Michael Cecchini, Jeffrey Sklar, and Jill Lacy
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(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
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
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
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
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
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
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
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
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
