Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2024 Jun 24;29(1):12.
doi: 10.1007/s10911-024-09566-0.

Rat Models of Hormone Receptor-Positive Breast Cancer

Raquel Nicotra #  1   2 , Catrin Lutz #  3   4 , Hendrik A Messal  5   6 , Jos Jonkers  7   8
Affiliations
Review

Rat Models of Hormone Receptor-Positive Breast Cancer

Raquel Nicotra et al. J Mammary Gland Biol Neoplasia. .

Abstract

Hormone receptor-positive (HR+) breast cancer (BC) is the most common type of breast cancer among women worldwide, accounting for 70-80% of all invasive cases. Patients with HR+ BC are commonly treated with endocrine therapy, but intrinsic or acquired resistance is a frequent problem, making HR+ BC a focal point of intense research. Despite this, the malignancy still lacks adequate in vitro and in vivo models for the study of its initiation and progression as well as response and resistance to endocrine therapy. No mouse models that fully mimic the human disease are available, however rat mammary tumor models pose a promising alternative to overcome this limitation. Compared to mice, rats are more similar to humans in terms of mammary gland architecture, ductal origin of neoplastic lesions and hormone dependency status. Moreover, rats can develop spontaneous or induced mammary tumors that resemble human HR+ BC. To date, six different types of rat models of HR+ BC have been established. These include the spontaneous, carcinogen-induced, transplantation, hormone-induced, radiation-induced and genetically engineered rat mammary tumor models. Each model has distinct advantages, disadvantages and utility for studying HR+ BC. This review provides a comprehensive overview of all published models to date.

Keywords: Breast cancer (BC); Hormone receptor (HR); Mammary tumor; Rat model.

PubMed Disclaimer

Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Comparison of rats and mice in the context of HR+ BC research, in terms of modeling of functional ER signaling and generated resources
Fig. 2
Fig. 2
Comparison of human, rat and mouse in regards to their biology, mammary gland architecture and tumor features in the context of HR+ BC
Fig. 3
Fig. 3
Overview of different rat tumor induction models, clockwise, in order of emergence, and their utility for BC research
Fig. 4
Fig. 4
Notable advances in the generation of rat models of HR+ BC over the past 113 years. Colors represent the different tumor induction models
Fig. 5
Fig. 5
Experimental advantages and limitations as well as unique clinical relevance and utilization potential of the different rat models of HR+ BC
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

References

    1. DeSantis CE et al. Breast cancer statistics, 2019 CA: A Cancer Journal for Clinicians, 2019. 69(6): pp. 438–451. - PubMed
    1. Sung H, et al. Global Cancer statistics 2020: GLOBOCAN estimates of incidence and Mortality Worldwide for 36 cancers in 185 countries. Cancer J Clin. 2021;71(3):209–49. doi: 10.3322/caac.21660. - DOI - PubMed
    1. Perou CM, et al. Molecular portraits of human breast tumours. Nature. 2000;406(6797):747–52. doi: 10.1038/35021093. - DOI - PubMed
    1. Nolan E, Lindeman GJ, Visvader JE. Deciphering breast cancer: from biology to the clinic. Cell. 2023;186(8):1708–28. doi: 10.1016/j.cell.2023.01.040. - DOI - PubMed
    1. Goldhirsch A, et al. Personalizing the treatment of women with early breast cancer: highlights of the St Gallen International Expert Consensus on the primary therapy of early breast Cancer 2013. Ann Oncol. 2013;24(9):2206–23. doi: 10.1093/annonc/mdt303. - DOI - PMC - PubMed

Substances