Transcriptionnal signature of Non Small Cell Lung Carcinomas with FHITlow/pHER2high phenotype

The tumor suppressor fragile histidine triad (FHIT) is frequently lost in NSCLC. We recently showed that FHIT controls HER2 receptor activity in lung tumor cells and that tumor cells from NSCLC patients harboring an FHITlow/pHER2high phenotype are sensitive to anti-HER2 drugs. Here, we sought to identify the transcriptomic signature of this phenotype and to evaluate its clinical significance. We performed an RNA sequencing analysis on tumor cells isolated from NSCLC displaying or not an FHITlow/pHER2high status and a functional analysis of differentially regulated genes. Overall design: Comparative gene expression profiling analysis of RNA-seq data for FHITlow/pHER2high and other tumors