ArticleMolecular and cellular biology2003
Dissecting the contribution of p16(INK4A) and the Rb family to the Ras transformed phenotype.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed.
- HDAC3 Regulates the Transition to the Homeostatic Myelinating Schwann Cell State.Cell reports · 2018Article
- Clinical correlation of molecular (VEGF, FGF, PDGF, c-Myc, c-Kit, Ras, p53) expression in juvenile nasopharyngeal angiofibroma.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2018Article
- Association between melanocytic nevi and risk of breast diseases: The French E3N prospective cohort.PLoS medicine · 2014Article
- A genetic screen for anchorage-independent proliferation in mammalian cells identifies a membrane-bound neuregulin.PloS one · 2010Article
- Loss of anchorage in checkpoint-deficient cells increases genomic instability and promotes oncogenic transformation.Journal of cell science · 2009Article
- NF1 loss disrupts Schwann cell-axonal interactions: a novel role for semaphorin 4F.Genes & development · 2008Article
- Critical and distinct roles of p16 and telomerase in regulating the proliferative life span of normal human prostate epithelial progenitor cells.The Journal of biological chemistry · 2008Article
- The retinoblastoma protein is required for Ras-induced oncogenic transformation.Molecular and cellular biology · 2006Article
- Surprising dependency for retinoblastoma protein in ras-mediated tumorigenesis.Molecular and cellular biology · 2006Review
- The Ras/Raf/ERK signalling pathway drives Schwann cell dedifferentiation.The EMBO journal · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although oncogenic Ras commonly contributes to the development of cancer, in normal primary cells it induces cell cycle arrest rather than transformation. Here we analyze the additional genetic changes required for Ras to promote cell cycle progression rather than arrest. We show that loss of p53 is sufficient for oncogenic Ras to stimulate proliferation in the absence of extrinsic mitogens in attached cells. However, surprisingly, we find that p53 loss is not sufficient for Ras to overcome anchorage dependence or contact inhibition. In contrast, expression of simian virus 40 (SV40) large T antigen (LT) allows Ras to overcome these additional cell cycle controls. Mutational analysis of SV40 LT shows that this action of SV40 LT depends on its ability to inactivate the retinoblastoma (Rb) family of proteins, in concert with the loss of p53. Importantly, we show that inactivation of the Rb family of proteins can be mimicked by loss of the cyclin-dependent kinase inhibitor p16(INK4A). p16(INK4A) is commonly lost in human tumors, but its contribution to the transformed phenotype is unknown. We demonstrate here a role for p16(INK4A) in the loss of cell cycle controls required for tumorigenesis and show how accumulating genetic changes cooperate and contribute to the transformed phenotype.
Indexed as
Identifiers
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.