Titlebook: Hormonal Carcinogenesis II; Proceedings of the S J. Jonathan Li (Professor of Pharmacology, Toxicol Conference proceedings 1996 Springer-Ve

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Introductionage at menopause, menstrual characteristics, nulliparity, age at first full-term pregnancy, number of live births, and lactation. A woman’s family history of breast cancer has also been known for quite some time to affect breast cancer risk strongly (2).

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Breast Susceptibility to Carcinogenesist is not fully developed at birth (1, 2). No other organ presents such dramatic changes in size, shape and function as does the breast during growth, puberty, pregnancy and lactation (2–4). It is agreed that the developmental phase of the human breast starts as early as the stage of nipple epitheliu

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Hormones, Growth Factors, and Gene Expression in Preneoplasias of the Mouse Mammary Gland mice, the intermediate stages are well-defined and their biological properties extensively studied (2, 4). These intermediate stages are visualized as ductal or alveolar hyperplasias, both of which contain cells with an enhanced probability for tumor formation (2, 4, 5). These cell populations, ter

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Pathogenesis of Ductal and Lobular Progestin-Induced Mammary Carcinomas in BALB/c Micese to 80% and a mean latency of around 13 months (1). These tumors were mostly ductal, progestin-dependent (PD) adenocarcinomas with high levels of estrogen and progesterone receptors (ER and PR) (2). We later found that progesterone (P) also induced mammary carcinomas, but this time the tumors were

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