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Part of the book series: Cancer Treatment and Research ((CTAR,volume 71))

Abstract

Cancer originates from cells that have acquired a succession of genetic changes that progressively enable them to proliferate outside the constraints of normal growth control. The earliest changes are considered to impinge on very few or even single cells, providing them with a growth advantage that facilitates their clonal expansion, and leads to the production of a significant population of cells that can act as a target for secondary mutations. Thus genetic alterations that have been envisaged may result in the inappropriate induction of potent cell signaling molecules that function as growth factors and/or promote neovascularization, the loss of functions that normally inhibit cell proliferation, and the induction of enzymes that can affect tissue remodeling. The basis for this conceptual framework, and the identification of candidate gene products involved in neoplastic transformation, has arisen in large part from the study of tumors in animal systems.

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Dickson, C., Fantl, V. (1994). Fgf-3, an oncogene in murine breast cancer. In: Dickson, R.B., Lippman, M.E. (eds) Mammary Tumorigenesis and Malignant Progression. Cancer Treatment and Research, vol 71. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2592-9_18

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  • DOI: https://doi.org/10.1007/978-1-4615-2592-9_18

  • Publisher Name: Springer, Boston, MA

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