Early Mammary Development: Growth Hormone and IGF-1

  title={Early Mammary Development: Growth Hormone and IGF-1},
  author={David L. Kleinberg},
  journal={Journal of Mammary Gland Biology and Neoplasia},
  • D. Kleinberg
  • Published 2004
  • Biology
  • Journal of Mammary Gland Biology and Neoplasia
The first step in pubertal mammary development is the appearance of terminal end buds arising from pleuropotent stem cells present in the immature ductal tree of the prepubertal animal. Work from this laboratory indicates that growth hormone is the pituitary hormone responsible for terminal end bud development. Growth hormone likely acts through the production of IGF-1.3 This minireview focuses on the hormonal control of early mammary development with special emphasis on the roles of growth… 

IGF-I: An Essential Factor in Terminal End Bud Formation and Ductal Morphogenesis

The hypothesis that GH acts through locallyproduced IGF-I, which in turn, causes development of terminal end buds (TEBs), the structure that lead the process of mammary gland development during puberty is proven.

Molecular regulators of pubertal mammary gland development

This work reviews the major molecular regulators of pubertal mammary gland development and identifies tissue-specific molecular networks that interpret signals from local cytokines/growth factors in both the epithelial and stromal microenvironments.

The Contribution of Growth Hormone to Mammary Neoplasia

This review will highlight recent evidence linking GH and mammary carcinoma and discuss GH-antagonism as a potential therapeutic approach for treatment of breast cancer.

Establishing a Framework for the Functional Mammary Gland: From Endocrinology to Morphology

Defining the hormonal control of ductal development should facilitate a better understanding of the mechanisms underlying mammary gland tumorigenesis and provide the opportunity to further delineate the regulation ofductal development.

Prolactin and Mammary Gland Development

  • N. Horseman
  • Biology
    Journal of Mammary Gland Biology and Neoplasia
  • 2004
Disruption of the genes for PRLand the PRL receptor, as well as those for transcription factors important in mammary gland regulation(Stat proteins), have provided a new set of animal models with which to study normal mammary glands development and the relationships of PRL to breastcarcinogenesis.

Pubertal Mammary Gland Development: Insights from Mouse Models

During puberty the mammary gland develops from a rudimentary tree to a branched epithelial network of ducts which can support alveolar development and subsequent milk production during pregnancy and

Growth hormone, acting in part through the insulin-like growth factor axis, rescues developmental, but not metabolic, activity in the mammary gland of mice expressing a single allele of the prolactin receptor.

It is suggested that GH can improve mammary development in PRLR(+/-) mice, but that it fails to enhance metabolic activity.

Expression of the insulin-like growth factor binding proteins during postnatal development of the murine mammary gland.

Important functions for the family of IGFBPs during postnatal growth and differentiation of the mammary epithelium are suggested.



Involution of the lactating mammary gland is inhibited by the IGF system in a transgenic mouse model.

It is demonstrated that IGF-I and IGFBP-3 may modulate the involutionary process of the lactating mammary gland by influencing the remodeling of mammary tissue during involution.

Endocrine Influences on the Mammary Gland

The mammary gland is an organ whose morphology and physiology are constantly during the life span of an animal. Therefore, the study of the mammary gland has to be done taking into consideration the

Evidence that the growth hormone receptor mediates differentiation and development of the mammary gland.

It is shown that nonlactogenic rat (r) GH is far more potent than rPRL in inducing rat mammary development, suggesting that GH receptors play a central role in this process.

Non-lactogenic effects of growth hormone on growth and insulin-like growth factor-I messenger ribonucleic acid of rat mammary gland.

It is found that both hGH and rGH were significantly more potent than hPRL and rPRL in stimulating mammary growth in rats, suggesting an independent role for GH in Mammary growth.

Mammary gland development with mammogen I in the castrate and the hypophysectomized rat.

IN 1936, REECE et al. (1) published the first experiments showing that the mammary glands of completely hypophysectomized animals did not respond to administration of ovarian hormones. Gomez and

Primate mammary development. Effects of hypophysectomy, prolactin inhibition, and growth hormone administration.

It is found that physiological or slightly supraphysiological concentrations of hGH in animals with unmeasurable prolactin were incapable of restoring the capacity of E2 to induce full mammary growth and the possibility that heretofore unidentified pituitary substances may be mammogenic.

Mammary Gland Development in the Hypophysectomized Albino Rat.∗

These studies appear to indicate that the development of the mammary gland which normally occurs during the second half of pregnancy can continue in the absence of the pituitary, however, lactation fails within a few hours after parturition.

Mechanism of action of prolactin in the control of mammary gland function.

Progress is highlighted in understanding the mechanism of action of PRL on mammary gland function since large gaps in this understanding remain and areas where research may be fruitful are indicated.

Estradiol enhances the stimulatory effect of insulin-like growth factor-I (IGF-I) on mammary development and growth hormone-induced IGF-I messenger ribonucleic acid.

These studies indicate that IGF-I can have a small independent effect on mammary development, but like GH, E2 is required for a full effect, and that the action of E2 on Mammary development may take place at multiple sites.

Mammary Growth in Hypophysectomized Male Mice Receiving Estrogen and Prolactin.∗

Summary The mammary rudiments grew in hypophysectomized male mice receiving either of 2 purified preparations of prolactin and estrogen. The injection of these preparations of prolactin alone was not