Simultaneous Surgical Treatment for Smile Dysfunction and Lagophthalmos Involving a Dual Latissimus Dorsi Flap

Summary:. Paralytic lagophthalmos and smile dysfunction are serious complications of facial paralysis and various reconstructive procedures have been developed to treat them. Among these procedures, there is no doubt that dynamic procedures are more effective than static ones. The 1-stage simultaneous surgical treatment of these 2 dysfunctions with a dynamic procedure involving a single muscle would be ideal, but no such methods have been reported. In this article, we present a 1-stage method for the simultaneous surgical treatment involving the use of a dual latissimus dorsi muscle flap. In this method, 2 muscle flaps based on the descending and transverse branches of the thoracodorsal vessels are transferred to the face. The descending and transverse branches of the thoracodorsal nerve are sutured to separate branches of the masseteric nerve. Using this method, complete eyelid closure during strong clenching and voluntary smiling during weak clenching without eyelid closure were achieved. Although our method does not result in spontaneous smiling, we believe that it is a good option for some patients with long-standing facial paralysis

High Incidence of C797S Mutation in Patients With Long Treatment History of EGFR Tyrosine Kinase Inhibitors Including Osimertinib

Introduction: Although treatment with osimertinib confers survival benefits in patients with lung cancer with the EGFR T790M mutation, the mechanism of acquired resistance to osimertinib remains poorly understood. We conducted a prospective observational study to identify the mechanism on the basis of repeated tissue biopsies. Methods: Patients with EGFR-mutated advanced lung cancer with a T790M mutation detected on a tissue biopsy underwent a rebiopsy after developing acquired resistance to osimertinib. Nucleic acids extracted from the biopsy samples were subjected to targeted resequencing (Oncomine Comprehensive Assay), and circulating cell-free DNA (ccfDNA) was analyzed by CAncer Personalized Profiling by deep Sequencing (AVENIO ctDNA Surveillance Kit). Results: Between November 2016 and March 2020, a total of 87 patients were screened. Among them, 44 developed acquired resistance. Of these, 19 samples from rebiopsies and 12 from preosimertinib biopsies were able to be analyzed by an Oncomine Comprehensive Assay. A ccfDNA analysis was performed in 16 patients. Regarding the mechanisms of acquired resistance, structural change in EGFR, namely, C797S, G796S, or L792V, was the most frequent alteration, being observed in 57.9% of the cases. MET gain was observed in 31.6% of the cases, and gains in cell cycle genes were observed in 26.3% of the cases. In addition, we identified GAS6 gain and an ATM mutation in a patient with small-cell transformation and a BRAF V600E mutation in a patient with oligoprogressive disease. Conclusions: A repeated tissue biopsy and a ccfDNA analysis were useful in analyzing the mechanisms underlying acquired resistance. A long treatment history of EGFR TKIs may result in a high percentage of EGFR structural change