EGFR A289V

Hence, we hypothesize that GBM tumors harboring EGFR missense mutations (G598V, A289V) influence stem cell properties via multiple pathways to evade therapeutic effects and inhibiting these different signaling pathways will decrease therapeutic resistance in GBM. Understanding the mechanism of these EGFR mutations may lead to improved therapeutic strategies for GBM patients.

This analysis describes the largest EGFR ECD mutational landscape of advanced NSCLC patients detected via ctDNA. EGFR ECD mutations in NSCLC do not appear to be mutually exclusive with other oncogenic driver mutations, and further evaluation of biological and clinical relevance is warranted.

EGFR amplification was the most common mutation type. There were 122 SNV and Indel subtypes altogether and occurred throughout almost the entire exon region, in which exon7 contained maximum 21 different subtypes and the p.A289V was the main type. The distribution of subtypes in ECD were much more than in ICD.

The majority of patients 24/30 (80%) were treated with concurrent Temozolomide (TMZ)/radiation and adjuvant TMZ... We show that mutation dynamics in GBM differ between patients, and frequencies of driver mutations vary during the tumor progression. It was possibly to identify the same mutation during treatment in the same patient. These observations can be used to design future targeted trials and potentially be used for evaluation of treatment response in the individual patient.