Human breast cancer cells generated by oncogenic transformation of primary mammary epithelial cells
Open accessAbstract
A number of genetic mutations have been identified in human breast cancers, yet the specific combinations of mutations required in concert to form breast carcinoma cells remain unknown. One approach to identifying the genetic and biochemical alterations required for this process involves the transformation of primary human mammary epithelial cells (HMECs) to carcinoma cells through the introduction of specific genes. Here we show that introduction of three genes encoding the SV40 large-T antigen, the telomerase catalytic subunit, and an H-Ras oncoprotein into primary HMECs results in cells that form tumors when transplanted subcutaneously or into the mammary glands of immunocompromised mice. The tumorigenicity of these transformed cells was dependent on the level of ras oncogene expression. Interestingly, transformation of HMECs but not two other human cell types was associated with amplifications of the c-myc oncogene, which occurred during the in vitro growth of the cells. Tumors derived from the transformed HMECs were poorly differentiated carcinomas that infiltrated through adjacent tissue. When these cells were injected subcutaneously, tumors formed in only half of the injections and with an average latency of 7.5 weeks. Mixing the epithelial tumor cells with Matrigel or primary human mammary fibroblasts substantially increased the efficiency of tumor formation and decreased the latency of tumor formation, demonstrating a significant influence of the stromal microenvironment on tumorigenicity. Thus, these observations establish an experimental system for elucidating both the genetic and cell biological requirements for the development of breast cancer.
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Introduction of oncogenes and transforming viral oncoproteins into primary rodent cells established that combinations of cancer genes are required.
“In the 1980s, the introduction of oncogenes and transforming viral oncoproteins into primary rodent cells established the requirement of combinations of these cancer genes (95).”
From Telomeres and telomerase in cancer (2010) · cites this paper as [95]
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- Authors
- Elenbaas, B., Spirio, L., Koerner, F., Fleming, M. D., Zimonjic, D. B., Donaher, J. L., Popescu, N. C., Hahn, W. C., & Weinberg, R. A.
- Affiliations
- Brigham and Women's Hospital (US)
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2001-01-01
- Volume
- 15
- Issue
- 1
- Pages
- 50-65
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC312602
- OpenAlex
- W2027345413
- Cited by
- 878
- References
- 54
- Citations by year
- 2026: 9 · 2025: 14 · 2024: 18 · 2023: 32 · 2022: 28 · 2021: 28 · 2020: 27 · 2019: 24 · 2018: 36 · 2017: 36 · 2016: 49 · 2015: 38 · 2014: 39 · 2013: 52 · 2012: 38
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- Leukemia and Lymphoma Society
- Ludwig Institute for Cancer Research
- National Cancer Institute (P01CA080111, 5 P01 CA80111-02)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Health Sciences › Medicine › Pathology and Forensic Medicine › Breast Lesions and Carcinomas
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- breast cancer, oncogenic transformation, mammary epithelial cells, SV40 large T antigen, telomerase catalytic subunit, H-Ras, MYC amplification, tumorigenicity, tumor latency, poorly differentiated carcinoma
- MeSH terms
- Animals, Antigens, Polyomavirus Transforming, Breast, Breast Neoplasms, Cell Division, Cell Transformation, Neoplastic, Epithelial Cells, Female, Humans, Immunologic Deficiency Syndromes, Karyotyping, Genes, ras, Transplantation, Heterologous, Genes, RAG-1, In Situ Hybridization, Fluorescence, Mice, Knockout, Homeodomain Proteins, Telomerase, Mice
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