# Efficacy of epidermal growth factor receptor-tyrosine kinase inhibitor for lung adenosquamous cell carcinoma harboring EGFR mutation: a retrospective study and pooled analysis

## TL;DR

This study shows that EGFR-TKIs are effective in treating lung adenosquamous cell carcinoma with EGFR mutations, similar to their use in adenocarcinoma.

## Contribution

The study provides pooled evidence and retrospective data on EGFR-TKI efficacy in a rare cancer type with EGFR mutations.

## Key findings

- EGFR-TKIs achieved 54.5% objective response rate and 79.5% disease control rate in treated patients.
- Pooled analysis showed 63.4% ORR and 85.9% DCR for ASC patients with EGFR mutations.
- Erlotinib or gefitinib showed better survival trends than icotinib in treated patients.

## Abstract

To explore the efficacy of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) on lung adenosquamous cell carcinoma (ASC) with EGFR mutation.

Efficacy of EGFR-TKIs in the treatment of advanced or recurrent lung ASC with EGFR mutations was assessed retrospectively in 44 patients. Pooled analysis of 74 patients using EGFR-TKIs, including 30 patients selected from 11 publications, was conducted.

In our retrospective research, patients treated with EGFR-TKI in ASC with EGFR mutations had objective response rate (ORR) of 54.5%, disease control rate (DCR) of 79.5%, median progression free survival (mPFS) of 8.8 months, and median overall survival (mOS) of 19.43 months, respectively. A pooled analysis reveals ORR, DCR, mPFS, and mOS are, respectively, 63.4%, 85.9%, 10.00 months, and 21.37 months for ASC patients. In patients with deletions in exon 19 and exon 21 L858R mutations, mPFS (11.0 versus 10.0 months, P=0.771) and mOS (23.67 versus 20.33 months, P=0.973) were similar. Erlotinib or gefitinib-treated patients had an overall survival trend that was superior to that of icotinib-treated patients.

ASC harboring EGFR mutations can be treated with EGFR-TKI in a similar manner to Adenocarcinoma (ADC) harboring EGFR mutations. There is still a need for further investigation to identify the separate roles of ASC’s two components in treating EGFR.