For decades now, it is well established that mutated TP53 frequently prevents tumor cells from undergoing apoptosis, even in the presence of marked DNA damage33,34; consequently, this may contribute to explain not only the lower response here observed to radiochemotherapy among cases which carry del(17p) in their ancestral tumor clone, but also the occurrence of both cytogenetic and clinical progression after therapy in a subset of these cases. This evidence concerns the gene TP53 and neoplasm.