Abstract

Objectives. There have been advances in the identification and understanding of molecular subsets of lung cancer, defined by specific oncogenic aberrations. A number of actionable genetic alterations have been identified, such as the epidermal growth factor receptor (EGFR) mutation. We aimed to establish the reasons why patients were not undergoing EGFR mutation testing at the time of histological diagnosis. Methods. The records of 70 patients with advanced adenocarcinoma of the lung managed through a single multidisciplinary team at a single institution were reviewed. Data were collected on method of tumour sample collection, whether this was sent for EGFR testing, and the result. Results. Seventy patients were identified. In 21/25 (84%) cases, cytological sampling was sufficient for EGFR mutation analysis, compared with 40/45 (89%) cases with histological sampling. EGFR mutation testing was not carried out in 22/70 (31.4%) patients. There was insufficient tumour sample for EGFR testing in 9/22 (40.9%) patients. Other reasons for not testing included poor patient fitness and problems in the diagnostic pathway. Conclusions. In this series, cytological tumour sampling was not the predominant reason why cancers failed to have EGFR mutation status established.

Highlights

  • Lung cancer represents a significant health problem

  • Oral tyrosine kinase inhibitors (TKIs) have been shown to prolong progression-free survival in patients with advanced NSCLC harbouring a sensitising epidermal growth factor receptor (EGFR) mutation compared with doublet chemotherapy in a number of clinical trials [3,4,5]

  • As well as investigating other reasons why patients’ tumour samples were not tested, we looked at the records of 70 consecutive patients with advanced adenocarcinoma of the lung managed through a single multidisciplinary team (MDT) in SE Wales

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Summary

Introduction

Lung cancer represents a significant health problem. In Europe in 2012, there were an estimated 410,000 new cases diagnosed, and most patients present with advanced stage, incurable disease [1].In recent years, there have been advances in the identification and understanding of molecular subsets of lung cancer, defined by specific oncogenic aberrations [2]. Oral tyrosine kinase inhibitors (TKIs) have been shown to prolong progression-free survival in patients with advanced NSCLC harbouring a sensitising EGFR mutation compared with doublet chemotherapy in a number of clinical trials [3,4,5]. Recent analysis of data from the LUX-LUNG 3 and LUX-LUNG 6 trials has shown that in patients with exon deletions (the commonest sensitising EGFR mutation), afatinib significantly prolongs overall survival in the firstline setting in stage IIIB-IV NSCLC when compared with doublet chemotherapy [3, 4]. Several other genetic alterations have been identified These include ROS1, AKT, BRAF, FGFR, MET, MEK1, PTEN RET, PIK3CA, KRAS, and HER2 [2]. It is imperative that adequate samples are acquired for molecular

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