Cyclin D1 provides a link between development and oncogenesis in the retina and breast
Open accessAbstract
Mice lacking cyclin D1 have been generated by gene targeting in embryonic stem cells. Cyclin D1-deficient animals develop to term but show reduced body size, reduced viability, and symptoms of neurological impairment. Their retinas display a striking reduction in cell number due to proliferative failure during embryonic development. In situ hybridization studies of normal mouse embryos revealed an extremely high level of cyclin D1 in the retina, suggesting a special dependence of this tissue on cyclin D1. In adult mutant females, the breast epithelial compartment fails to undergo the massive proliferative changes associated with pregnancy despite normal levels of ovarian steroid hormones. Thus, steroid-induced proliferation of mammary epithelium during pregnancy may be driven through cyclin D1.
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Other D type cyclins can functionally replace cyclin D1 in most tissues.
“From experiments with cyclin D1 KO mice, it is known that other D type cyclins can functionally replace cyclin D1 in most tissues.17,18”
From Interleukin 6 Is Important for Survival After Partial Hepatectomy in Mice (2003) · cites this paper as [17]
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- Authors
- Sicinski, P., Donaher, J. L., Parker, S. B., Li, T., Fazeli, A., Gardner, H., Haslam, S. Z., Bronson, R. T., Elledge, S. J., & Weinberg, R. A.
- Affiliations
- Whitehead Institute for Biomedical Research (US)
- Massachusetts Eye and Ear Infirmary (US)
- Michigan State University (US)
- Tufts University (US)
- Howard Hughes Medical Institute (US)
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1995-08
- Volume
- 82
- Issue
- 4
- Pages
- 621-630
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2058705034
- Cited by
- 1,021
- References
- 1
- Citations by year
- 2026: 5 · 2025: 12 · 2024: 6 · 2023: 17 · 2022: 10 · 2021: 8 · 2020: 16 · 2019: 10 · 2018: 16 · 2017: 19 · 2016: 22 · 2015: 10 · 2014: 19 · 2013: 26 · 2012: 29
- FWCI
- 23.64
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- National Institutes of Health (5r35ca039826-10)
- National Institute on Aging (AG11085, R01AG011085)
- National Cancer Institute (R35-CA39826)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- cyclin D1, retinal development, retinal cell proliferation, embryonic development, breast epithelium, ovarian steroids, carcinogenesis, neurological deficit
- MeSH terms
- Animals, Cell Differentiation, Cell Division, Female, Male, Mammary Glands, Animal, Mice, Mutant Strains, Neoplasms, Experimental, Phenotype, Pregnancy, Receptors, Estrogen, Retina, Stem Cells, Steroids, Oncogene Proteins, Cyclins, Gene Targeting, Gene Expression Regulation, Developmental, Cyclin D1, Mice
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