Case Report: Efficacy of Pyrotinib in ERBB2 Amplification Pulmonary Adenoid Cystic Carcinoma

Zhongben Tang,Gongshun Tang,Jian Zhang,Jian Li,Chen Chen,Jiarong Xiao,Feng Lin,Sini Li,Xiaojun Du

doi:10.3389/fonc.2021.605658

Abstract

Primary pulmonary adenoid cystic carcinomas are salivary tumors that are low-grade malignant and prone to recurrence and metastasis. Surgery is currently the main treatment, but there is no standard with regard to postoperative adjuvant therapy. Adenoid cystic carcinoma is more sensitive to radiotherapy and patients benefit less from chemotherapy, but few studies have focused on targeted therapy, and their conclusions are inconsistent. With respect to primary pulmonary adenoid cystic carcinoma, large-scale studies cannot be conducted due to its low incidence, and studies on the targeted therapy of it are very scarce. A few case reports indicate that targeted therapy can be effective however, suggesting that it may be a good option. The current report is the first on the occurrence of human epidermal growth factor receptor 2 amplification in pulmonary adenoid cystic carcinoma. The patient was treated with pyrotinib for 6 months and achieved stable disease.

Highlights

Adenoid cystic carcinoma (ACC) is a salivary tumor
We describe the effects of targeted therapy in a Primary pulmonary ACC (PPACC) patient with human epidermal growth factor receptor 2 (ERBB2) amplification, and summarize the current research status of PPACC-targeted therapy
ACC is a type of salivary tumor that usually occurs in the salivary gland in the head and neck

Summary

INTRODUCTION

Adenoid cystic carcinoma (ACC) is a salivary tumor. Primary pulmonary ACC (PPACC) is exceptionally rare, and mainly occurs in the trachea or main bronchus. Immunohistochemical results included cytokeratin (+), epithelial membrane antigen (+, part), cytokeratin5/6 (+), P63 (+, part), P40 (+, part), thyroid transcription factor-1 (–), NapsinA (–), CD56 (–), chromogranin A (–), synaptophysin (–), Ki-67 (1%+) During this period, gene detection was performed via nextgeneration sequencing using peripheral blood and paraffin sections of tissues from the left lower pulmonary metastasis using the HapOnco 605 panel (approximately 1.31 Mb in total, covering 464 genes) at another hospital. During the 9-month period from September 2019 to June 2021 (the first 3 months under no treatment and the 6 months under treatment with pyrotinib), the total maximum diameter of the hepatic metastatic tumor only increased by 25%, indicating that targeted therapy greatly reduced the tumor growth rate (Table 1). According to the Response Evaluation Criteria In Solid Tumors, stable disease was achieved

DISCUSSION

Findings

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