Using such modified fibroblasts which were kept in-culture, our study shows that both Ras hyper-activation and p53 down-regulation were required together in order to induce the expression of the cancer-related chemokine cluster; however, when such cells were exposed to the tumor microenvironment in vivo, the inflammatory milieu had a more powerful driving force towards a higher tumor-promoting phenotype than the genetic modifications, as manifested in this case by elevated levels of the cancer-related chemokine cluster. This evidence concerns the gene TP53 and neoplasm.