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Cancer, 3 patients with newly diagnosed metastatic lung adenocarcinoma are recommended to be tested for mutations in 8 driver genes, including EGFR , ALK , ROS1 , BRAF , RET , MET , NTRK , and KRAS , because FDA-approved therapies are available

References 1 Mendelsohn J . Targeting the epidermal growth factor receptor for cancer therapy . J Clin Oncol 2002 ; 20 : 1s – 13s . 2 Castillo L Etienne-Grimaldi MC Fischel JL . Pharmacological background of EGFR

–epidermal growth factor receptor (EGFR) agents (Cet/Pani) compared with chemotherapy alone in relation to PTL in patients with RAS wt mCRC. Patients and Methods This meta-analysis was reported in accordance with PRISMA guidelines. 20 Study Selection and Data

chemotherapy and targeted agents depending on distinct molecular profiles. Antibodies targeting epidermal growth factor receptor (EGFR), including cetuximab and panitumumab, have shown clinical utility in the late-line setting. 3 , 4 Defining populations most

mutations, and how these data may impact clinical decision-making Identify established predictive markers for cetuximab and panitumumab Discuss the clinical implications of data regarding potential new biomarkers for anti-EGFR therapy Colorectal

Background : Current national guidelines recommend epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) as first-line (1L) for EGFR mutated metastatic non-small cell lung cancer (EGFRm mNSCLC) patients. Depending on the

The identification of molecular targets and the development of agents to treat those targets has changed the paradigm for the management of non–small cell lung cancer (NSCLC). “The progress in NSCLC has been absolutely amazing. EGFR and KRAS

mutation status. 2 , 3 The most frequently altered genes in NSCLC are EGFR (10%–35%), KRAS (25%–30%), FGR (20%), ALK (3%–7%), MET (2%–4%), BRAF (1%–3%), ROS1 (1%–3%), and RET (1%–3%). 2 , 3 For many of the molecular subsets, including

testing of exons 18-21 of the epidermal growth factor receptor ( EGFR) gene performed at an outside institution revealed the presence of both an EGFR L858R missense mutation in exon 21 and a T790M point mutation in exon 20. His local oncologist was

-capture–selected libraries are sequenced to high uniform depth (targeting >500x coverage by non-PCR duplicate read pairs, with >99% exons at coverage >100x) on the Illumina HiSeq2000 sequencing platform. 1 Genomic DNA isolation and EGFR T790M real-time PCR was performed