Notably, knock-in mice harboring different p53 mutations exhibit non-identical tumor phenotypes: p53R270H/+ mice, corresponding to the human p53R273H DNA contact hotspot mutation, show increased incidence of carcinomas and B cell lymphomas compared to p53+/− mice, while p53R172H/+ mice, corresponding to the human p53R175H structural hotspot mutation, frequently develop osteosarcomas18. This evidence concerns the gene TP53 and carcinoma.