ReviewAging2010
How to become immortal: let MEFs count the ways.
Review in Aging, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 45 citations in OpenAlex.
- Frequent expression of aberrant chimeric Cdkn2a transcripts in mouse models of muscular dystrophy.Scientific reports · 2026Article
- Tfcp2l1 as a central integrator of hypoxia, dedifferentiation, and tumor progression.Journal of experimental & clinical cancer research : CR · 2025Review
- Molecular and cell phenotype programs in oral epithelial cells directed by co-exposure to arsenic and smokeless tobacco.bioRxiv : the preprint server for biology · 2024Article
- Sustained activation of NF-κB through constitutively active IKKβ leads to senescence bypass in murine dermal fibroblasts.Cell cycle (Georgetown, Tex.) · 2024Article
- Loss of fragile WWOX gene leads to senescence escape and genome instability.Cellular and molecular life sciences : CMLS · 2023Article
- Article
- The role of oxidative stress in intervertebral disc cellular senescence.Frontiers in endocrinology · 2022Review
- Spontaneous and photosensitization-induced mutations in primary mouse cells transitioning through senescence and immortalization.The Journal of biological chemistry · 2020Article
- Experimental identification of cancer driver alterations in the era of pan-cancer genomics.Cancer science · 2019Review
- Mutation Analysis in Cultured Cells of Transgenic Rodents.International journal of molecular sciences · 2018Article
- Cryopreservation of Primary Mouse Neurons: The Benefit of Neurostore Cryoprotective Medium.Frontiers in cellular neuroscience · 2018Article
- Runx3 plays a critical role in restriction-point and defense against cellular transformation.Oncogene · 2017Article
- Modeling cancer driver events in vitro using barrier bypass-clonal expansion assays and massively parallel sequencing.Oncogene · 2017Article
- Article
- Nutlin-3a selects for cells harbouring TP53 mutations.International journal of cancer · 2017Article
- Senescence in the aging process.F1000Research · 2017Review
- Mice deficient in poly(C)-binding protein 4 are susceptible to spontaneous tumors through increased expression of ZFP871 that targets p53 for degradation.Genes & development · 2016Article
- Fibroblast sources: Where can we get them?Cytotechnology · 2016Article
- p73: a Positive or Negative Regulator of Angiogenesis, or Both?Molecular and cellular biology · 2015Review
- Freshly frozen E18 rat cortical cells can generate functional neural networks after standard cryopreservation and thawing procedures.Cytotechnology · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding the molecular mechanisms and biological consequences of genetic changes occurring during bypass of cellular senescence spans a broad area of medical research from the cancer field to regenerative medicine. Senescence escape and immortalisation have been intensively studied in murine embryonic fibroblasts as a model system, and are known to occur when the p53/ARF tumour suppressor pathway is disrupted. We showed recently that murine fibroblasts with a humanised p53 gene (Hupki cells, from a human p53 knock-in mouse model) first senesce, and then become immortalised in the same way as their homologues with normal murine p53. In both cell types, immortalised cultures frequently sustain either a p53 gene mutation matching a human tumour mutation and resulting in loss of p53 transcriptional transactivation, or a biallelic deletion at the p19/ARF locus. Whilst these genetic events were not unexpected, we were surprised to find that a significant proportion of immortalised cell cultures apparently had neither a p53 mutation nor loss of p19/ARF. Here we consider various routes to p53/ARF disruption in senescence bypass, and dysfunction of other tumour suppressor networks that may contribute to release from tenacious cell cycle arrest in senescent cultures.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.