Case Report
Copyright ©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Oncol. Feb 24, 2025; 16(2): 98812
Published online Feb 24, 2025. doi: 10.5306/wjco.v16.i2.98812
Combined BRAF G469A mutation and echinoderm microtubule associated protein like-4-anaplastic lymphoma kinase rearrangement with resistance: A case report and review of literature
Xuan Guo, Yan Liu, Yu-Ting Wang, Kan Liu, Hui Ding
Xuan Guo, Yan Liu, Yu-Ting Wang, Kan Liu, Hui Ding, Department of Pulmonary and Critical Care Medicine, Yixing People’s Hospital of Jiangsu University, Yixing 214200, Jiangsu Province, China
Co-first authors: Xuan Guo and Yan Liu.
Author contributions: Guo X and Liu Y were actively involved in the conception, they contributed equally to this article, they are the co-first authors of this manuscript; Wang YT and Liu K wrote the manuscript; Ding H designed the project and drafted the manuscript with substantive revision. All authors read and approved the final manuscript.
Supported by the Medical Education Collaborative Innovation Fund of Jiangsu University, No. JDY2022015.
Informed consent statement: This study was approved by the Ethics Committee of Yixing People’s hospital and complied with the ethics standards of the Declaration of Helsinki, and the patient consent to participate in this report.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
CARE Checklist (2016) statement: The authors have read the CARE Checklist (2016), and the manuscript was prepared and revised according to the CARE Checklist (2016).
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Hui Ding, PhD, Department of Pulmonary and Critical Care Medicine, Yixing People’s Hospital of Jiangsu University, No. 1588 Xincheng Road, Yixing 214200, Jiangsu Province, China. dh1350519@163.com
Received: July 6, 2024
Revised: October 13, 2024
Accepted: October 24, 2024
Published online: February 24, 2025
Processing time: 158 Days and 2 Hours
Abstract
BACKGROUND

Through deeper understanding of targetable driver mutations in non-small-cell lung cancer (NSCLC) over the past years, some patients with driver mutations have benefited from the targeted molecular therapies. Although the anaplastic lymphoma kinase and BRAF mutations are not frequent subtypes in NSCLC, the availability of several targeted-drugs has been confirmed through a series of clinical trials. But little is clear about the proper strategy in rare BRAF G469A mutation, not to mention co-exhibition of anaplastic lymphoma kinase and BRAF G469A mutations, which is extremely rare in NSCLC.

CASE SUMMARY

We present a patient to stage IVA lung adenocarcinoma with coexisting echinoderm microtubule associated protein like-4 rearrangement and BRAF G469A mutation. She received several targeted drugs with unintended resistance and suffered from unbearable adverse events.

CONCLUSION

Due to the rarity of co-mutations, the case not only enriches the limited literature on NSCLC harbouring BRAF G469A and echinoderm microtubule associated protein like-4 mutations, but also suggests the efficacy and safety of specific multiple-drug therapy in such patients.

Keywords: Non-small-cell lung cancer; Driver mutation; Rearrangement; Resistance; Case report

Core Tip: We present a non-small-cell lung cancer patient with rarely co-occurring echinoderm microtubule associated protein like-4 rearrangement and BRAF G469A mutation. The patient suffered from anaplastic lymphoma kinase tyrosine kinase inhibitors resistance and adverse events. It’s a question whether the process of reducing dosage of alectinib was easier to cause resistance. Although we were unable to assess the correlation between BRAF G469A mutation and anaplastic lymphoma kinase tyrosine kinase inhibitors resistance, the safety and efficacy of combination therapy to multiple driver oncogenes are important in clinic.