© 1990 Oxford University Press
other |
Effect of human chlorionic gonadoropin on mammary gland differentiation and carcinogenesis
Department of of Pathology, Michigan Cancer Foundation 110 East Warren Avenue, Detroit, MI 48201, USA
The observation that mammary carcinogenesis is inhibited in rats which completed a pregnancy prior to exposure to the chemical carcinogen 7,12-dimethylbenz[a]anthracene (DMBA) led us to determine whether the protective effect of pregnancy could be mimicked by treatment with the placental hormone chorionic gonadotropin (hCG). We also studied the effect of this treatment on mammary gland structure and differentiation, and determined whether hCG exerts toxic or collateral effects on body weight and endocrine organs. The systemic effect of hCG on body wt and endocrine organs and mammary gland was studied in outbred virgin Sprague-Dawley rats which at the age of 50 days started receiving 100 IU hCG i.p. daily for 21 days. The animals were subdivided into nine groups of five animals each; one group was killed on the first day of and the others at 5, 10, 15 and 21 days of injection and 5,10,15 and 21 days post injection. The effect of the hormonal treatment on the estrous cycle was determined by studying the vaginal smears taken during and after the injection period. The following parameters were determined: body wt, weight and morphology of pituitary gland, adrenals, ovaries and uterine horns. Mammary glands were processed for histology, autoradiography for determination of DNA labeling index (DNA-LI) and whole mount preparation for morphometric studies. The effect of hCG on mammary carcinogenesis was studied in two groups of virgin rats; group I, which at the age of 50 days started receiving a daily i.p. injection of 100 IU hCG for 21 days; 21 days after the last injection they were given 8 mg DMBA/100 g body wt. Group II animals received DMBA only. hCG treated animals gained weight as a function of age at the same rate as controls. Treatment did not modify the weight of adrenal glands. The weight of ovaries, uterus and pituitary gland were transitorily increased by the 15th day of treatment, but had returned to the same values of controls by the time of DMBA administration. Treatment stimulated mammary gland differentiation, measured as a progressive reduction in number of terminal end buds and increase in the number of alveolar buds and lobules. The DNA-LI was significantly depressed in all terminal structures in the glands of treated animals. In group I animate hCG treatment decreased incidence of adenocarcinomas to 6.15 from 43.87percnt; in group II animals. It was concluded that hCG at the dose used was not toxic to the animals, as evidenced by the lack of effect on body wt and no residual effect on weight of internal organs, and it stimulated gland differentiation, significantly protecting the mammary gland from DMBA-induced carcinogenesis.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  N. A. Rahman and C.V. Rao Recent progress in luteinizing hormone/human chorionic gonadotrophin hormone research Mol. Hum. Reprod., November 1, 2009; 15(11): 703 - 711. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Chen, M. G. Kibriya, F. Jasmine, R. M. Santella, R. T. Senie, and H. Ahsan Do Placental Genes Affect Maternal Breast Cancer? Association between Offspring's CGB5 and CSH1 Gene Variants and Maternal Breast Cancer Risk Cancer Res., December 1, 2008; 68(23): 9729 - 9734. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. B. Michels, F. Xue, G. A. Colditz, and W. C. Willett Induced and Spontaneous Abortion and Incidence of Breast Cancer Among Young Women: A Prospective Cohort Study Arch Intern Med, April 23, 2007; 167(8): 814 - 820. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. A. Arslan, A. Zeleniuch-Jacquotte, A. Lukanova, Y. Afanasyeva, J. Katz, M. Levitz, G. Del Priore, and P. Toniolo Effects of Parity on Pregnancy Hormonal Profiles Across Ethnic Groups with a Diverse Incidence of Breast Cancer. Cancer Epidemiol. Biomarkers Prev., November 1, 2006; 15(11): 2123 - 2130. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. K. Ong, C. Y. Ng, C. Leong, C. P. Ng, C. S. Ong, T. T. T. Nguyen, and H. Huynh Structural Characterization of Three Novel Rat OKL38 Transcripts, Their Tissue Distributions, and Their Regulation by Human Chorionic Gonadotropin Endocrinology, October 1, 2004; 145(10): 4763 - 4774. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. L. Milliken, R. K. Ameduri, M. D. Landis, A. Behrooz, F. W. Abdul-Karim, and R. A. Keri Ovarian Hyperstimulation by LH Leads to Mammary Gland Hyperplasia and Cancer Predisposition in Transgenic Mice Endocrinology, September 1, 2002; 143(9): 3671 - 3680. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. A. Lamartiniere, J. Wang, M. Smith-Johnson, and I.-E. Eltoum Daidzein: Bioavailability, Potential for Reproductive Toxicity, and Breast Cancer Chemoprevention in Female Rats Toxicol. Sci., February 1, 2002; 65(2): 228 - 238. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. R. Ginger, M. F. Gonzalez-Rimbau, J. P. Gay, and J. M. Rosen Persistent Changes in Gene Expression Induced by Estrogen and Progesterone in the Rat Mammary Gland Mol. Endocrinol., November 1, 2001; 15(11): 1993 - 2009. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Sivaraman, O. M. Conneely, D. Medina, and B. W. O'Malley p53 is a potential mediator of pregnancy and hormone-induced resistance to mammary carcinogenesis PNAS, October 12, 2001; (2001) 221459098. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Kuperwasser, J. Pinkas, G. D. Hurlbut, S. P. Naber, and D. J. Jerry Cytoplasmic Sequestration and Functional Repression of p53 in the Mammary Epithelium Is Reversed by Hormonal Treatment Cancer Res., May 1, 2000; 60(10): 2723 - 2729. [Abstract] [Full Text]
|
|
|
|
 |
|
 J. C.L. Tou and L. U. Thompson Exposure to flaxseed or its lignan component during different developmental stages influences rat mammary gland structures Carcinogenesis, September 1, 1999; 20(9): 1831 - 1835. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Sivaraman, O. M. Conneely, D. Medina, and B. W. O'Malley p53 is a potential mediator of pregnancy and hormone-induced resistance to mammary carcinogenesis PNAS, October 23, 2001; 98(22): 12379 - 12384. [Abstract] [Full Text] [PDF]
|
|