They include (i) shared signatures with highly cycling and proliferative cells as well as with embryonic stem cells, an observation similar to that of aggressive lung tumours [16], (ii) an upregulation of signatures corresponding to poorly differentiated tumours as well as of genes involved in epithelial mesenchymal transition (EMT) and (iii) an upregulation of genes involved in various oncogenic signatures, including HRAS, TNFA/NFKB and EGF-associated signatures (Supplementary Fig. S9A, B). This evidence concerns the gene HRAS and neoplasm.