@article {DE CARLO2941, author = {ELISA DE CARLO and MONICA SCHIAPPACASSI and GIACOMO PELIZZARI and TANIA BARESIC and ALESSANDRO DEL CONTE and BRIGIDA STANZIONE and VALENTINA DA ROS and ROBERTO DOLIANA and GUSTAVO BALDASSARRE and ALESSANDRA BEARZ}, title = {Acquired EGFR C797G Mutation Detected by Liquid Biopsy as Resistance Mechanism After Treatment With Osimertinib: A Case Report}, volume = {35}, number = {5}, pages = {2941--2945}, year = {2021}, doi = {10.21873/invivo.12586}, publisher = {International Institute of Anticancer Research}, abstract = {Background: Osimertinib is a third-generation EGFR-tyrosine kinase inhibitor approved for the treatment of T790M-positive non-small-cell lung cancer. More recently, osimertinib demonstrated improved disease control compared to other EGFR-TKIs. Multiple mechanisms of resistance have been described in T790M-positive patients who experienced treatment failure with osimertinib. Case Report: We report the case of a 78-year-old non-smoker woman with stage IV EGFR L858R-positive lung adenocarcinoma presented with T790M mutation after five years of treatment with gefitinib. The patient was started on osimertinib, but after two and a half years of treatment experienced disease progression. The analyses of circulating tumor DNA using next-generation sequencing showed, together with the pre-existing T790M and exon 21 L858R, the presence of the EGFR C797G resistance mutation. Conclusion: Our case report revealed a rare EGFR-dependent acquired resistance mutation to osimertinib in circulating tumor DNA. Liquid biopsy appears to be a promising resource to understand the biology of osimertinib resistance by clonal evolution monitoring and the identification of novel resistance mechanisms.}, issn = {0258-851X}, URL = {https://iv.iiarjournals.org/content/35/5/2941}, eprint = {https://iv.iiarjournals.org/content/35/5/2941.full.pdf}, journal = {In Vivo} }