Titlebook: Genes, Oncogenes, and Hormones; Advances in Cellular Robert B. Dickson,Marc E. Lippman Book 1992 Springer Science+Business Media New York 1

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https://doi.org/10.1007/978-94-009-3261-6.]. An independent line of evidence for the role of recessive genetic mutations in tumor development has come from the study of familial pediatric tumors. It had been postulated that two mutational events are required for the development of retinoblastoma [.]. In hereditary retinoblastoma, since the

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Left Ventricular Contactile Reserve], as well as in c-.B activation by promoter insertion during retroviral leukemogenesis [.]. The transforming gene of the feline sarcoma virus SM-FeSV represents another growth factor receptor tyrosine kinase, the CSF-1 receptor [.]. Oncogenic conversion by a retrovirus in this case (v-.) involves m

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https://doi.org/10.1007/978-3-642-61956-4e the growth of both normal mammary and tumor cells remain elusive. It has been proposed that the escape from estrogen-dependent growth of HBC cells is due, at least in part, to alterations in their autocrine and/or paracrine growth mechanisms [.–.]. Consequently, disordered secretion of growth fact

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Antony J. O’sullivan,Robert D. Burgoynery importance. In postmenopausal breast cancer, when blood levels of estrogen and progesterone are extremely low, breast tumors appear to arise under control of other factors, among which are estrogen synthesized peripherally by aromatase and sulfatase mechanisms. Likely candidates for additional fa

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