Abstract
The development of cancer results from the cumulative acquisition of somatic and/or germline mutations in regulatory genes that control various aspects of cellular proliferation, differentiation, apoptosis, and DNA repair (1–6). Gain or loss of function in protooncogenes or tumor suppressor genes accounts for the majority of these genetic defects (6–8). Generally, gain of function is observed in dominantly transforming oncogenes, which can occur by point mutations, gene amplification, chromosomal translocation, or insertional mutagenesis (6,9,10). Conversely, loss of function, because of the inactivation of tumor suppressor genes, can occur by point mutations or a loss of heterozygosity (LOH) in one allele (11,12). Changes in the expression of these genes can also contribute to the pathogenesis of cancer, and may be caused by environmental stimuli such as viruses, radiation, carcinogens, hormones, and growth factors (GFs) (6–10).
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Salomon, D.S., Bianco, C., De Santis, M., Martinez-Lacaci, I., Wechselberger, C., Ebert, A.D. (2000). Epidermal Growth Factor-Related Peptides in Endocrine Neoplasias. In: Ethier, S.P. (eds) Endocrine Oncology. Contemporary Endocrinology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-223-4_9
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