ArticleOncogene1999
Identification of a gene at 16q24.3 that restores cellular senescence in immortal mammary tumor cells.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 28 citations in OpenAlex.
- Alternative Promoters ofGenes · 2022Article
- Chromosome 6 encoded RNaseT2 protein is a cell growth regulator.Journal of cellular and molecular medicine · 2010Article
- Extra copies of chromosomes 16 and X in invasive breast carcinomas are related to aggressive phenotype and poor prognosis.Journal of clinical pathology · 2007Article
- Functional identification of a BAC clone from 16q24 carrying a senescence gene SEN16 for breast cancer cells.Oncogene · 2005Article
- Identification of a YAC from 16q24 carrying a senescence gene for breast cancer cells.Oncogene · 2000Article
- Isoforms of Ionotropic Glutamate Receptor GRIK2 Induce Senescence of Carcinoma Cells.Cancer genomics & proteomicsArticle
- Monochromosomal Hybrids and Chromosome Transfer: A Functional Approach for Gene Identification.Cancer genomics & proteomicsReview
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have mapped a cellular senescence gene, SEN16, within a genetic distance of 3 - 7 cM, at 16q24.3. Microcell mediated transfer of a normal human chromosome 16, 16q22-qter or 16q23-qter restored cellular senescence in four immortal cell lines, derived from human and rat mammary tumors. The resumption of indefinite cell proliferation, concordant with the segregation of the donor chromosome, confirmed the presence of a senescence gene at 16q23-qter. While microcell hybrids were maintained in selection medium to retain the donor chromosome, sporadic immortal revertant clones arose among senescent cells. Reversion to immortal growth could occur due to inactivation of the senescence gene either by a mutation or a deletion. The analysis for chromosome 16 specific DNA markers, in revertant clones of senescent microcell hybrids, revealed a consensus deletion, spanning a genetic interval of approximately 3 - 7 cM at 16q24.3.
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