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Jean L. Grem

status in a Clinical Laboratory Improvement Amendments (CLIA)-accredited laboratory. 12 Retrospective analysis indicates that patients with mutations in the KRAS gene do not benefit from anti-epidermal growth factor receptor (EGFR) antibody therapy

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Bruce Brockstein, Mario Lacouture, and Mark Agulnik

Edited by Kerrin G. Robinson

. Yarden Y . The EGFR family and its ligands in human cancer. Signaling mechanisms and therapeutic opportunities . Eur J Cancer 2001 ; 37 ( Suppl 4 ): S3 – 8 . 17. Schlessinger J . Cell signaling by receptor tyrosine kinases . Cell 2000

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Leora Horn

information, revealing whether the tumor is negative for epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) mutations, for instance. Histology guides treatment choices, and clinical trial data tend to support this approach. For

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Gauri R. Varadhachary

: EGFR, epidermal growth factor receptor; IHC, immunohistochemistry. Several groups have studied the role of immunohistochemistry patterns and decision trees based on immunohistochemistry specificity, sensitivity, and predictive values. These data

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Presented by: Gregory J. Riely

. “There are multiple molecular targets with agents approved for use in the first-line setting, including EGFR , ALK , ROS1 , RET , MET exon 14, and BRAF mutations. Targeted therapies are addressing targets that we’ve not been able to target before

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Paul F. Engstrom

antibody to epidermal growth factor (EGFR), were introduced as single agents in the management of patients with advanced metastatic disease. Randomized studies showed that treatment with at least 3 of these agents could result in higher antitumor response

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Gregory L. Riely

( EGFR )–mutant NSCLC, he emphasized. The 2017 NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for NSCLC recommend biomarker testing for all patients who present with stage IV disease. Molecular testing should be capable of identifying

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Presented by: Jane Yanagawa and Gregory J. Riely

completely resected stage IB–IIIA EGFR -mutation–positive disease (exon 19 del or L858R) were randomly assigned to adjuvant osimertinib or placebo for 3 years. 6 At 2 years, 90% of patients with stage II–IIIA disease who received adjuvant osimertinib were