Its molecular mechanisms involve, among others, the inhibition of p53, extracellular-signal-regulated kinase/mitogen-activated protein kinase and AKT/protein kinase B activation, and sustained hypoxia-inducible factor 1-α activation, all of which promote tumor cell proliferation, cell survival and tumor-associated neoangiogenesis (16,28–32). Here, TP53 is linked to neoplasm.