Titlebook: Mammary Tumor Cell Cycle, Differentiation, and Metastasis; Advances in Cellular Robert B. Dickson,Marc E. Lippman Book 1996 Kluwer Academic

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Antiprogestin-progesterone interactions. Until today the available treatment strategies for hormone-dependent breast cancer have mainly been based on estrogen-ablative principles, and improvements in the therapy for breast cancer are still sorely needed. A totally different strategy utilizes progesterone antagonists: This class of compou

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Antiestrogen-estrogen receptor interactions phase. Conversely, estrogen antagonists that inhibit cell proliferation reduce the proportion of cells in S phase [1]. The precise role of estrogen in cell growth and proliferation is poorly understood. Initially it was proposed that estrogens stimulate proliferation indirectly by increasing the pr

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Differentiation antigens in stromal and epithelial cells of the breastdes) that are not found anywhere else in the body suggests that there may be functionally distinct fibroblasts associated with the intralobular stroma. The heterogeneity of benign and malignant breast diseases also indicates that the different types of lesions may reflect origins from cells that hav

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Cell motility in breast canceravior. The earliest stage of tumor formation is proliferation. Through genetic mutations, a cell or group of cells becomes refractory to normal growth regulation. The resultant mass of cells exerts pressure on surrounding tissue but does not cross tissue boundaries. Noninvasive tumors have been term

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Cathepsins D and B in breast cancers [1,2]. Examples of cathepsins are found in three classes of proteases, for example, cathepsin D is an aspartic protease, cathepsin B a cysteine protease, and cathepsin G is a serine protease. Although several cathepsins have collagenolytic activity, there are no cathepsins among the metalloproteas