The concept that hormones influence tumor growth originated in 1889 with the proposal of Albert Schinzinger who suggested that breast cancer is related to the ovaries. Several years later, Sir George Beatson observed that remission of disseminated breast cancer could be achieved in premenopausal patients by performing bilateral oophorectomy. As a result of the contri butions of Hedley Atkins, Charles Huggins and others, additive and ablative hormonal therapies have been widely used for the treatment of advanced breast cancers for several decades. Model systems to study the effects of hormones…mehr
The concept that hormones influence tumor growth originated in 1889 with the proposal of Albert Schinzinger who suggested that breast cancer is related to the ovaries. Several years later, Sir George Beatson observed that remission of disseminated breast cancer could be achieved in premenopausal patients by performing bilateral oophorectomy. As a result of the contri butions of Hedley Atkins, Charles Huggins and others, additive and ablative hormonal therapies have been widely used for the treatment of advanced breast cancers for several decades. Model systems to study the effects of hormones on growth and regression of breast tumors have been available for many years; however, the complexities of the hormonal environment have rendered in vivo studies difficult in man and experimental animals. Recently, the availability of long-term cultures of breast cancer cells has stimulated many investigators to use these cell lines to unravel the mechanisms of hormone action. Because of theextreme diversity and complexity of advances regarding the endocrinology of the breast and breast cancers, a multi-authored review was deemed necessary. It has been gratifying to receive contributions from many noted scholars. In Volume I of this monograph, the influence of steroid hormones and their antagonists upon normal and neoplastic tissues of the mammary gland are presented. In Volume II, the effects of peptide and other hormones are reviewed.
1 Role of Prolactin or Placental Lactogen in Mammary Tumor Development in Experimental Animals.- Prolactin or placental lactogen and mammary tumor development.- A mechanism of role of prolactin in mammary tumor development.- Factors which modulate mammary tumor development and prolactin secretion.- Role of prolactin in mammary tumor virus production.- Strain-difference in circulating levels of prolactin or placental lactogen and mammary gland susceptibility to it.- Future prospects.- References.- 2 Prolactin and Prolactin Receptors in Tumor Development, Growth and Cellular Functions.- Models of hormone-dependent mammary cancer.- Hormonal regulation of PRL receptors in normal tissue.- Hormonal regulation of receptors in mammary tumors.- Prolactin and human breast cancer.- Summary and conclusions.- References.- 3 Studies of Prolactin Receptors and the Possible Proliferative Role of Prolactin and Other Pituitary Factors in Human Breast Tumor Cells.- References.- Acknowledgement.- 4 Mode of Action of Prolactin on Normal and Neoplastic Mammary Tissues.- Prolactin receptors.- Internalization of prolactin.- Actions of prolactin at the plasma membrane.- Sodium-potassium hypothesis.- Calcium ions.- Polyamines, prostaglandins and cyclic nucleotides.- Phospholipase A2.- Prostaglandins (PG).- Cyclic nucleotides.- Polyamines.- Actions of prolactin on the proliferation of mammary cells.- References.- 5 Growth Factors for Hormone-Sensitive Tumor Cells.- Effects of known growth factors on mammary tumor cell proliferation.- Effects of estrogens on growth factor activities for estrogen-responsive tumor cells.- Platelet derived growth factors.- Pituitary derived mammary cell growth factors.- Summary of new approaches to growth factor involvement in mammary tumor growth in vivo.- References.- 6 Primary and Permissive Actions of Insulin in Breast Cancer.- I. Direct actions of insulin on experimental mammary tumors.- II. Facilitative effects of insulin on mammary tumors.- III. Estrogen-insulin interactions.- IV. Insulin and human breast cancer.- V. Conclusions.- Acknowledgement.- References.- 7 Effect of Thyroid Hormones on Mammary Tumor Induction and Growth.- Epidemiologic and clinical studies.- Animal studies.- Possible mechanisms.- References.- 8 Mode of Cyclic Amp Action in Growth Control.- Normal and neoplastic growth of the mammary gland.- Mechanism of mammary tumor regression.- Cyclic nucleotides in transformation.- Cyclic AMP in reversion of malignancy.- Conclusion.- Acknowledgement.- References.- 9 Prostaglandins, Fatty Acids and Phospholipids in Normal and Neoplastic Breast Tissues.- Content of fatty acids and phospholipids.- Metabolism of phospholipids.- Effects of dietary lipids.- Effects of dietary carbohydrates.- Lipid inducers of cell transformation.- Fatty acid synthesis.- Phospholipases and prostaglandins.- Acknowledgement.- References.- 10 Polyamines in Normal and Neoplastic Growth of Mammary Gland.- Developmental changes in the synthesis and accumulation of polyamines in mammary gland.- The functions of polyamines during mammary cell proliferation.- The role of polyamines in the differentiation of mammary gland.- Polyamine transport.- Concluding remark.- References.- 11 Hormone Regulation of Casein Gene Expression in Normal and Neoplastic Cells in Murine Mammary Glands.- I. Introduction.- II. General macromolecular activity.- III. Direct measure of casein mRNA.- IV. Purification of casein mRNA and synthesis of complementary DNA.- V. Quantitative measurement of casein gene expression by the cDNAcsn.- VI. Hormonal modulation of casein genetranscription.- VII. Casein gene expression in mammary tissue in vitro.- VIII. Casein gene expression in a two-step culture model of the whole mammary organ.- IX. Simultaneous occurrence of morphogenesis and casein gene expression.- X. Glucocorticoid is obligatory to casein gene expression.- XI. Negative influence of progesterone on casein gene expression.- XII. Cloning of cDNAcsn.- XIII. Mammary neoplasia and casein gene expression.- XIV. Summary and comments.- Acknowledgements.- References.
1 Role of Prolactin or Placental Lactogen in Mammary Tumor Development in Experimental Animals.- Prolactin or placental lactogen and mammary tumor development.- A mechanism of role of prolactin in mammary tumor development.- Factors which modulate mammary tumor development and prolactin secretion.- Role of prolactin in mammary tumor virus production.- Strain-difference in circulating levels of prolactin or placental lactogen and mammary gland susceptibility to it.- Future prospects.- References.- 2 Prolactin and Prolactin Receptors in Tumor Development, Growth and Cellular Functions.- Models of hormone-dependent mammary cancer.- Hormonal regulation of PRL receptors in normal tissue.- Hormonal regulation of receptors in mammary tumors.- Prolactin and human breast cancer.- Summary and conclusions.- References.- 3 Studies of Prolactin Receptors and the Possible Proliferative Role of Prolactin and Other Pituitary Factors in Human Breast Tumor Cells.- References.- Acknowledgement.- 4 Mode of Action of Prolactin on Normal and Neoplastic Mammary Tissues.- Prolactin receptors.- Internalization of prolactin.- Actions of prolactin at the plasma membrane.- Sodium-potassium hypothesis.- Calcium ions.- Polyamines, prostaglandins and cyclic nucleotides.- Phospholipase A2.- Prostaglandins (PG).- Cyclic nucleotides.- Polyamines.- Actions of prolactin on the proliferation of mammary cells.- References.- 5 Growth Factors for Hormone-Sensitive Tumor Cells.- Effects of known growth factors on mammary tumor cell proliferation.- Effects of estrogens on growth factor activities for estrogen-responsive tumor cells.- Platelet derived growth factors.- Pituitary derived mammary cell growth factors.- Summary of new approaches to growth factor involvement in mammary tumor growth in vivo.- References.- 6 Primary and Permissive Actions of Insulin in Breast Cancer.- I. Direct actions of insulin on experimental mammary tumors.- II. Facilitative effects of insulin on mammary tumors.- III. Estrogen-insulin interactions.- IV. Insulin and human breast cancer.- V. Conclusions.- Acknowledgement.- References.- 7 Effect of Thyroid Hormones on Mammary Tumor Induction and Growth.- Epidemiologic and clinical studies.- Animal studies.- Possible mechanisms.- References.- 8 Mode of Cyclic Amp Action in Growth Control.- Normal and neoplastic growth of the mammary gland.- Mechanism of mammary tumor regression.- Cyclic nucleotides in transformation.- Cyclic AMP in reversion of malignancy.- Conclusion.- Acknowledgement.- References.- 9 Prostaglandins, Fatty Acids and Phospholipids in Normal and Neoplastic Breast Tissues.- Content of fatty acids and phospholipids.- Metabolism of phospholipids.- Effects of dietary lipids.- Effects of dietary carbohydrates.- Lipid inducers of cell transformation.- Fatty acid synthesis.- Phospholipases and prostaglandins.- Acknowledgement.- References.- 10 Polyamines in Normal and Neoplastic Growth of Mammary Gland.- Developmental changes in the synthesis and accumulation of polyamines in mammary gland.- The functions of polyamines during mammary cell proliferation.- The role of polyamines in the differentiation of mammary gland.- Polyamine transport.- Concluding remark.- References.- 11 Hormone Regulation of Casein Gene Expression in Normal and Neoplastic Cells in Murine Mammary Glands.- I. Introduction.- II. General macromolecular activity.- III. Direct measure of casein mRNA.- IV. Purification of casein mRNA and synthesis of complementary DNA.- V. Quantitative measurement of casein gene expression by the cDNAcsn.- VI. Hormonal modulation of casein genetranscription.- VII. Casein gene expression in mammary tissue in vitro.- VIII. Casein gene expression in a two-step culture model of the whole mammary organ.- IX. Simultaneous occurrence of morphogenesis and casein gene expression.- X. Glucocorticoid is obligatory to casein gene expression.- XI. Negative influence of progesterone on casein gene expression.- XII. Cloning of cDNAcsn.- XIII. Mammary neoplasia and casein gene expression.- XIV. Summary and comments.- Acknowledgements.- References.
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