The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
In vitro establishment is not a sufficient prerequisite for transformation by activated ras oncogenes
Abstract
Activated ras genes transform REF52 cells only at low frequencies and adenovirus early region 1A collaborates with ras oncogenes to convert REF52 cells to a tumorigenic phenotype. While failure to transform did not result from an absence of ras gene expression, E1A appeared to enhance expression of transfected ras genes by approximately tenfold. However, enhanced ras expression alone does not account for collaboration by E1A since overexpression of T24 Ha-ras p21 induced morphological crisis and cell growth arrest rather than stable transformation. These results indicate that E1A contributes complementing biochemical activities that enable ras genes to transform REF52 and suggest that the role of E1A in primary cell transformation may extend beyond facilitating in vitro establishment.
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“REF52 cells are immortal fibroblasts but are similar to primary cells in that they display a high degree of growth control and require coexpression of a cooperating oncogene for transformation by ras (Franza et al. 1986).”
From Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a (1997) · cites this paper as Franza et al. 1986
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Cites
Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes
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Research works printed but not linked: 1
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Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218
The essence of senescence: Figure 1.
Kuilman, T., Michaloglou, C., Mooi, W. J., & Peeper, D. S. (2010) · Genes & Development · doi:10.1101/gad.1971610 · Cited by 2,038
Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization
Zindy, F., Eischen, C. M., Randle, D. H., Kamijo, T., Cleveland, J. L., Sherr, C. J., & Roussel, M. F. (1998) · Genes & Development · doi:10.1101/gad.12.15.2424 · Cited by 1,245
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ERK implication in cell cycle regulation
Chambard, J., LeFloch, R., Pouysségur, J., & Lenormand, P. (2006) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2006.11.010 · Cited by 749
Metadata
- Authors
- Franza, B. R., Maruyama, K., Garrels, J. I., & Ruley, H. E.
- Affiliations
- Cold Spring Harbor Laboratory (US)
- Massachusetts Institute of Technology (US)
- ORCID
- Maruyama, Kazuo
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1986-02
- Volume
- 44
- Issue
- 3
- Pages
- 409-418
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2158195967
- Cited by
- 166
- References
- 43
- Citations by year
- 2024: 4 · 2023: 3 · 2022: 1 · 2021: 2 · 2019: 1 · 2017: 1 · 2016: 3 · 2014: 2 · 2013: 3 · 2012: 2
- FWCI
- 5.77
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Cancer Society
- National Cancer Institute
- Cancer Research Institute
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and Retrovirus Studies
- Keywords
- oncogenic Ras, adenovirus E1A, cell transformation, growth arrest, tumorigenicity, oncogene cooperation, in vitro establishment
- MeSH terms
- Adenoviridae, Cell Line, Cell Transformation, Neoplastic, Enhancer Elements, Genetic, Genes, Viral, Neoplasm Proteins, Oncogenes, Transfection, Proto-Oncogene Proteins p21(ras)
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