The 1999 James Ewing Lecture: in pursuit of molecules of oncogenesis and neoplastic therapy.
Breast cancer is a progressive, phenotypic, genetic and epigenetic alteration, induced by various stimulants of which the principal steroid hormone, estrogen, initiates and promotes neoplastic transformation of normal ductal mammary epithelium to acquire distinct biochemical and molecular characteristics. The molecular events that characterize oncogenesis with dysregulated physiologic states represent an area of intense translational research. The progress of the last century suggests that the targeted responses initiated by this steroid hormone can be attenuated and modified with anti-estrogen therapies or through applied intervention with selective estrogen receptor modulation. New pharmacological, genetic, and biological agents will undoubtedly afford clinical investigators of the next millennium the opportunity to provide major impact on the disease progression of this neoplasm, through these targeted endocrine responses for estrogen.
Bland
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Department of Surgery, Brown University School of Medicine, Providence, Rhode Island, USA.
D000970:Antineoplastic Agents / Q000627:therapeutic use*; D018931:Antineoplastic Agents, Hormonal / Q000627:therapeutic use; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000209:etiology* / Q000235:genetics; D020847:Estrogen Receptor Modulators / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D009376:Neoplasms, Hormone-Dependent / Q000188:drug therapy*; D011494:Protein Kinases / Q000378:metabolism
D000970:Antineoplastic Agents; D018931:Antineoplastic Agents, Hormonal; D020847:Estrogen Receptor Modulators; D011494:Protein Kinases