A New Concept of Breast Cancer Growth Regulation and its Potential Clinical Applications
Major changes in our conceptual thinking about the regulation of growth of human breast cancer have occurred in the past decade. In the early 1970s our understanding of the mechanisms regulating breast cancer cell proliferation was simplistic. The pituitary hormone prolactin was thought to be important due to its critical involvement in normal breast differentiation and function and because it has a pivotal role in rodent breast cancer (Welsch and Nagasawa, 1977). However, the importance of this hormone in human breast cancer remains to be defined. The female sex steroid hormone estrogen, on the other hand, was known to be an important growth factor since the observation that about one-third of patients with breast cancer would have temporary tumor regression following treatments designed either to lower the serum estrogen level or to block its effects. Later estrogens and antiestrogens also were reported to have direct effects on proliferation of cultured human breast cancer cells (Lippman et al., 1977). At this time cumulative data suggested that the mechanisms of estrogen action on cells involved the binding of estrogen to the estrogen receptor protein followed by the tight coupling of the receptor-hormone complex to DNA resulting in alterations of specific gene transcription and protein synthesis. Exactly how estrogens increased cell proliferation was not known. Nevertheless, knowledge of these simple biochemical pathways had important clinical implications that eventually led to the use of estrogen receptor assays for predicting response to endocrine therapy and for predicting the clinical course of patients with early stage disease.
KeywordsBreast Cancer Breast Cancer Cell Breast Cancer Cell Line Human Breast Cancer Cell Human Breast Cancer Cell Line
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