210P - Digital gene expression profiling to separate malignant pleural mesothelioma from benign reactive mesothelial hyperplasia

Date 15 April 2016
Event European Lung Cancer Conference 2016 (ELCC) 2016
Session Poster lunch
Topics Mesothelioma
Translational Research
Presenter Rossella Bruno
Citation Journal of Thoracic Oncology (2016) 11 (supplement 4): S57-S166. S1556-0864(16)X0004-4
Authors R. Bruno1, G. Alì2, R. Giannini3, M. Lucchi4, F. Melfi5, A. Mussi4, G. Fontanini6
  • 1Department Of Surgical, Medical, Molecular Pathology And Critical Area, Univeristy Degli Studi di Pisa, 56126 - Pisa/IT
  • 2Unit Of Pathological Anatomy, Azienda Ospedaliera Universitaria S.Chiara, Pisa/IT
  • 3Department Of Surgical, Medical, Molecular Pathology And Critical Area, Univeristy Degli Studi di Pisa, Pisa/IT
  • 4Department Of Surgical, Medical, Molecular Pathology And Critical Area, Division Of Thoracic Surgery, Univeristy Degli Studi di Pisa, 56126 - Pisa/IT
  • 5Unit Of Thoracic Surgery, Azienda Ospedaliera Cisanello Pisa, Pisa/IT
  • 6Program Of Pleuropulmonary Pathology, Azienda Ospedaliera Universitaria S.Chiara, Pisa/IT

Abstract

Background

The diagnosis of malignant pleural mesothelioma (MPM) is based on the histological analysis of pleural lesions, however the morphological separation of benign mesothelial hyperplasia (MH) from MPM can be exceedingly difficult. Nowadays the most reliable indicator of malignancy is the mesothelial cells invasion of the chest wall soft tissue or of the underlying lung parenchyma. Several deregulated gene pathways have been described in MPM, we investigated how the over and down expressed genes work together in the differential diagnosis of MPM, by using the NanoString nCounter System ®.

Methods

We designed a custom NanoString Codeset including 113 genes with a crucial role in cancer and 6 reference genes. The gene expression analysis was performed by the nCounter System ®, without any amplification steps, directly on RNA purified from 48 formalin-fixed and paraffin-embedded tissues of epithelioid mesothelioma (32) and MH (16) samples.

Results

A total of 43 genes resulted deregulated in MPM in comparison with MH (Mann–Whitney U test; P 

Conclusions

We analysed a panel of genes some of which known as deregulated in MPM, however none of these genes have yet to be used as a biomarker. To evaluate how transcriptomic data could be applied in the diagnosis of MPM we used an enzyme-free digital count of mRNA molecules to analyse simultaneously all the selected genes and to reduce the potential errors associated with multiple qPCR assays. We identified a specific panel composed of 43 genes, whose expression profile resulted clearly distinct between MPM and MH. Our genes panel may constitute, after further validation on a larger series of samples, a powerful tool to separate MPM from MH, improving the current diagnostic methods.

Clinical trial identification

Legal entity responsible for the study

Azienda Ospedaliero Universitaria Pisana, AOUP, Pisa, Italy.

Funding

Azienda Ospedaliero Universitaria Pisana, AOUP, Pisa, Italy.

Disclosure

All authors have declared no conflicts of interest.