Researchers at Georgetown University and the University of Nebraska have developed a humanized mouse model expressing the human prolactin gene, to better study ER+ breast cancer. Current models do not properly represent the hormonal environment seen in patients. Furthermore, mouse prolactin fails to activate human prolactin receptors in xenograft experiments, ultimately selecting for prolactin-independent tumor growth and differentiation.
This model overcomes these limitations by replacing the mouse prolactin gene, with a knock-in of human prolactin, therefore mimicking the hormonal environment of breast cancer patients. Crossing these mice with immunodeficient strains, allows for human cell transplantation and engraftments to reliably study ER+ breast cancer.
BACKGROUND
High levels of circulating prolactin have been associated with an increased risk of breast cancer. Together with ER and PR, prolactin plays a crucial role in breast development, influencing both mammary cell proliferation and differentiation. Although prolactin receptors are expressed in the majority of breast cancers, current mouse models fail to account for the hormonal environment seen in patients. In these models, human prolactin is not sufficient to activate mouse prolactin receptors, while mouse prolactin acts as an antagonist to the human prolactin receptor. The NSG-Pro mouse overcomes these issues by expressing the human prolactin gene allowing for physiological levels of circulating human prolactin, and therefore more reliable assessments of disease progression and drug response.
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OTC Contact: Tracy L. Bruehs, J.D., M.S., Director – tlb23@georgetown.edu for more information or assistance with ordering through Jackson Labs (https://www.jax.org/strain/036917)
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