Thus, with the present work, we sought to review current knowledge on somatic profiles in the setting of bronchial cancer (for targetable mutations such as EGFR, ALK, BRAF and HER2, as well as some non-targetable mutations such as TP53, and KRAS) and their associations with environmental risk factors for the malignancy.
As a part of our continuous search for oncogenic viruses in bronchial cancer, we extended our HPV studies to analyse also SV40, BKV, JCV and HCMV sequences in bronchial cancer and related these data with p53 codon 72 polymorphism.
p21 TA levels vary considerably among BC patients which may be attributable to 1) genetic alterations in Rb and p53 and 2) variation in TA levels of upstream transcription factors E2F1 and p73.
In conclusion, this work is one first attempt to examine if the deregulation of the p53/MDM2 autoregulatory feedback loop is due to novel properties of certain p53 mutants in the specific environment of a subset of bronchogenic carcinomas.