Abstract
Cell proliferation is normally controlled by the opposing actions of growth stimulators and growth inhibitors. Regulated changes in this balanced system determine the rate of tissue growth during embryogenesis, and later in response to damage or altered functional demand. The negative autocrine hypothesis proposed that any defect in a normal autocrine growth-inhibitory loop could lead to tumor formation in the affected cell type by upsetting this balance [1]. The mechanistic underpinning of this hypothesis lies in the fact that cellular proliferation is a prerequisite for the fixation of deleterious mutations, and thus for tumor promotion and malignant progression [2]. Evidence for the importance of loss of negative regulation in tumorigenesis has been provided by the identification and characterization of ‘tumor suppressor’ genes, exemplified by the retinoblastoma gene, where loss of both alleles leads with high frequency to the development of a particular malignancy [3].
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Wakefield, L.M., Colletta, A.A., McCune, B.K., Sporn, M.B. (1991). Roles for transforming growth factors-β in the genesis, prevention, and treatment of breast cancer. In: Dickson, R.B., Lippman, M.E. (eds) Genes, Oncogenes, and Hormones. Cancer Treatment and Research, vol 61. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3500-3_6
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