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Preclinical models of breast cancer: B6BC, a transplantable hormone receptor-positive C57BL/6 mouse cell line

Genes & Immunity volume 25, pages 172–174 (2024)Cite this article

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A Correction to this article was published on 20 February 2024

This article has been updated

Preclinical animal models are essential tools to develop and evaluate new anticancer treatments, notably immunotherapies, in which the complex interactions between cancer cells and the immune system need to be recapitulated. Consequently, the degree to which the preclinical model mimics certain disease aspects likely conditions its clinical translatability. In the context of breast cancer (BC), representative models should mimic key disease features such as the hormone receptor and ERBB2 status, as well as the composition of the tumor immune infiltrate. However, such information is generally limited notably for transplantable mouse cancer cell lines, which tend to be poorly characterized with respect to their histopathological subtype and to the tumor microenvironment that they generate, especially if they fail to strive after injection into syngeneic hosts [1].

Despite the fact that hormone receptor-positive BC (which express estrogen receptor, ER, and/or progesterone receptor, PR) are among the most common woman cancers, there have been no hormone receptor-positive cell lines that could be transplanted into immunocompetent C57BL/6 mice, the most frequently used inbred mouse strain [2]. To fill this gap, we established the first ER+ mammary carcinoma cell line transplantable into syngeneic C57BL/6 females, called B6BC cells. Such B6BC cells were generated from a tumor of a hormone-dependent carcinogen-induced BC model in C57BL/6 females [3]. We extensively characterized the cancer cell-intrinsic and tumor-infiltrating immune cell properties of B6BC cell-derived tumors, while comparing them to tumors arising from several other commonly used cell lines in the setting of non-resected advanced disease, as well as to the original tumor they derived from [3, 4]. In this Spotlight we focus on the comparison of ER+ B6BC tumors inoculated into C57BL/6 mice with ER+ TS/A tumors developing in BALB/C females and ER- E0771 (also spelled EO771) from C57BL/6 mice (Table 1).

Table 1 Comparison of three mouse mammary carcinoma cell lines.
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References

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Acknowledgements

GK is supported by the Ligue contre le Cancer (équipe labellisée); Agence National de la Recherche (ANR) – Projets blancs; AMMICa US23/CNRS UMS3655; Association pour la recherche sur le cancer (ARC); Cancéropôle Ile-de-France; Fondation pour la Recherche Médicale (FRM); a donation by Elior; Equipex Onco-Pheno-Screen; European Joint Programme on Rare Diseases (EJPRD); European Research Council Advanced Investigator Award (ERC-2021- ADG, ICD-Cancer, Grant No. 101052444), European Union Horizon 2020 Projects Oncobiome, Prevalung (grant No. 101095604) and Crimson; Fondation Carrefour; Institut National du Cancer (INCa); Institut Universitaire de France; LabEx Immuno-Oncology (ANR-18-IDEX-0001); a Cancer Research ASPIRE Award from the Mark Foundation; the RHU Immunolife; Seerave Foundation; SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE); and SIRIC Cancer Research and Personalized Medicine (CARPEM). This study contributes to the IdEx Université de Paris ANR-18-IDEX-0001.

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Authors and Affiliations

  1. Centre de Recherche des Cordeliers, Équipe labellisée par la Ligue contre le cancer, Inserm U1138, Université Paris Cité, Sorbonne Université, Institut Universitaire de France, Paris, France

    Maria Perez-Lanzon, Maria Chiara Maiuri & Guido Kroemer

  2. Metabolomics and Cell Biology Platforms, UMS AMICCa, Gustave Roussy, Villejuif, France

    Maria Perez-Lanzon, Maria Chiara Maiuri & Guido Kroemer

  3. Department of Molecular Medicine and Medical Biotechnologies, University of Napoli Federico II, Napoli, Italy

    Maria Chiara Maiuri

  4. Departamento de Bioquimica y Biologia Molecular, Instituto Universitario de Oncologia (IUOPA), Universidad de Oviedo, Oviedo, Spain

    Carlos Lopez-Otin

  5. Institut du Cancer Paris CARPEM, Hôpital Européen Georges Pompidou, France-HP, Paris, France

    Guido Kroemer

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  1. Maria Perez-Lanzon
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  2. Maria Chiara Maiuri
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  3. Carlos Lopez-Otin
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  4. Guido Kroemer
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Contributions

M.P.-L. designed the table. M.P.-L., M.C.M., C.L.-O. and G.K. conceived, wrote and revised the manuscript.

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Correspondence to Maria Chiara Maiuri or Guido Kroemer.

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Competing interests

GK has been holding research contracts with Daiichi Sankyo, Eleor, Kaleido, Lytix Pharma, PharmaMar, Osasuna Therapeutics, Samsara Therapeutics, Sanofi, Tollys, and Vascage. GK is on the Board of Directors of the Bristol Myers Squibb Foundation France. GK is a scientific co-founder of everImmune, Osasuna Therapeutics, Samsara Therapeutics and Therafast Bio. GK is in the scientific advisory boards of Hevolution, Institut Servier, Longevity Vision Funds and Rejuveron Life Sciences. GK is the inventor of patents covering therapeutic targeting of aging, cancer, cystic fibrosis and metabolic disorders. GK’s wife, Laurence Zitvogel, has held research contracts with Glaxo Smyth Kline, Incyte, Lytix, Kaleido, Innovate Pharma, Daiichi Sankyo, Pilege, Merus, Transgene, 9 m, Tusk and Roche, was on the on the Board of Directors of Transgene, is a cofounder of everImmune, and holds patents covering the treatment of cancer and the therapeutic manipulation of the microbiota. GK’s brother, Romano Kroemer, was an employee of Sanofi and now consults for Boehringer-Ingelheim. The funders had no role in the design of the study; in the writing of the manuscript, or in the decision to publish the results.

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Perez-Lanzon, M., Maiuri, M.C., Lopez-Otin, C. et al. Preclinical models of breast cancer: B6BC, a transplantable hormone receptor-positive C57BL/6 mouse cell line. Genes Immun 25, 172–174 (2024). https://doi.org/10.1038/s41435-023-00241-8

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