Anti-cancer therapy operates on the assumption that the genetic pathways disrupted during tumorigenesis are distinct from those that mediate drug sensitivity. The main objective of this therapy is to present tumor cells with obstacles unrelated to the process of cellular transformation or to exploit vulnerabilities created by tumor development, such as uncontrolled DNA synthesis, checkpoint abnormalities, or an addiction to an oncogenic signal. Cytotoxic therapies, for example, rely on the introduction of DNA damage or the inhibition of chromosome segregation. These lesions, when introduced at high levels, elicit a DNA damage response presumably distinct from any encountered during the early stages of tumor development.
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Hemann, M.T., Lowe, S.W. (2007). P53 Links Tumor Development to Cancer Therapy. In: Hainaut, P., Wiman, K.G. (eds) 25 Years of p53 Research. Springer, Dordrecht. https://doi.org/10.1007/978-1-4020-2922-6_15
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