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erlotinib and crizotinib for epidermal growth factor receptor ( EGFR )-mutated and anaplastic lymphoma kinase ( ALK )-rearranged NSCLC, respectively. This article focuses on the first-line treatment of NSCLC with no identifiable mutations with FDA

primary (CK7+, CK20-, TTF1+). The patient's tumor was negative for both KRAS and epidermal growth factor receptor (EGFR)–activating mutations. PET/CT showed the FDG-avid mass in the right upper lobe of the lung, and metastases to the bone, liver, and

; DC, dendritic cell; EGFR, epidermal growth factor receptor; GM-CSF, granulocyte-macrophage colony-stimulation factor; HER2, human epidermal growth factor receptor-2; IL, interleukin; PD-1, programmed death-1; VEGF, vascular endothelial growth factor

rates of epidermal growth factor receptor (EGFR) amplification and chromosome 10 loss. 12 , 16 , 17 Based on an examination of microarray studies from several independent studies, followed by validation in formalin-fixed paraffin-embedded (FFPE) samples

Background: Targeted therapies for non-small lung cancer (NSCLC) have vastly improved survival and other outcomes for patients whose tumors have genetic mutations such as ALK, BRAF, EGFR, and ROS1. Identification of genetic mutations often

, several studies have shown that HER2 amplification is implicated in the resistance to EGFR-targeted therapies. 1 , 4 , 9 , 10 Multiple studies have provided scientific evidence to support HER2-directed therapies in CRC. 3 , 8 These studies interrogated

policies that addressed single-gene ctDNA testing (eg, EGFR , ALK , BRAF ) that did not include a provision for ctDNA-based panel testing ( supplemental eAppendix 3 ). Private Payers We searched the Canary Insights Database with the terms “liquid biopsy

, cyclophosphamide/bortezomib/dexamethasone; Dara, daratumumab; DL co , diffusing capacity of the lung for carbon monoxide; EF, ejection fraction; eGFR, estimated glomerular filtration rate; GI, gastrointestinal; LMDex, lenalidomide/ melphalan/dexamethasone; NT

stage IV diagnosis, 87.2% with nonsquamous histology, 36.1% with bone metastasis, 29.4% with brain metastasis, 43.2% with 0–1 performance status, and 21.6% with a known EGFR or ALK mutation. A total of 233 pts had been tested for PD-L1 (78

recurrence risk within 10 years among node-negative, estrogen receptor-positive patients. 8 , 9 A second example is testing for somatic mutations in the EGFR gene to predict response to tyrosine kinase inhibitors, such as gefitinib in first-line therapy or