ArticleOncogene1999
p16INK4 mediates contact-inhibition of growth.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 68 citations in OpenAlex.
- Exploring the role of EMT in ovarian cancer progression using a multiscale mathematical model.NPJ systems biology and applications · 2025Article
- HPV16 AND EXPRESSION OF PROTEIN P16INK4A AND E7 ONCOPROTEIN IN COLORECTAL CARCINOMA.Arquivos brasileiros de cirurgia digestiva : ABCD = Brazilian archives of digestive surgery · 2022Article
- Ferroptosis Meets Cell-Cell Contacts.Cells · 2021Review
- Together we stand, apart we fall: how cell-to-cell contact/interplay provides resistance to ferroptosis.Cell death & disease · 2020Review
- Review
- Sleeping Beauty and the Microenvironment Enchantment: Microenvironmental Regulation of the Proliferation-Quiescence Decision in Normal Tissues and in Cancer Development.Frontiers in cell and developmental biology · 2018Review
- CRB3 regulates contact inhibition by activating the Hippo pathway in mammary epithelial cells.Cell death & disease · 2017Article
- p16 protein is upregulated in a stepwise fashion in colorectal adenoma and colorectal carcinoma.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association · 2016Article
- Senescence Mediated by p16Scientific reports · 2016Article
- Treating cancer with selective CDK4/6 inhibitors.Nature reviews. Clinical oncology · 2016Review
- The Hippo-YAP signaling pathway and contact inhibition of growth.Journal of cell science · 2014Article
- Hyaluronan regulates cell behavior: a potential niche matrix for stem cells.Biochemistry research international · 2012Article
- The aryl hydrocarbon receptor (AhR) in the regulation of cell-cell contact and tumor growth.Carcinogenesis · 2010Review
- Aberrant promoter methylation of p16 in colorectal adenocarcinoma in North Indian patients.World journal of gastrointestinal oncology · 2010Article
- Hypersensitivity to contact inhibition provides a clue to cancer resistance of naked mole-rat.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Cell density-dependent inhibition of epidermal growth factor receptor signaling by p38alpha mitogen-activated protein kinase via Sprouty2 downregulation.Molecular and cellular biology · 2009Article
- TCDD deregulates contact inhibition in rat liver oval cells via Ah receptor, JunD and cyclin A.Oncogene · 2008Article
- p38alpha MAPK is required for contact inhibition.Oncogene · 2005Article
- Co-regulation of p16INK4A and migratory genes in culture conditions that lead to premature senescence in human keratinocytes.The Journal of investigative dermatology · 2005Article
- The INK4a/ARF locus and melanoma.Oncogene · 2003Review
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growth of non-transformed cells in vitro is regulated by density-dependent mechanisms via cell-cell contacts, leading to arrest in late G1-phase at confluency (contact-inhibition of growth). In the present study it is shown that this results from p16INK4-mediated dissociation of the complex cdk4-cyclin D1, which is responsible for the inactivation of the gate keeper of G1-S transition, the retinoblastoma protein pRb. As a consequence of the inactivation of cdk4, downstream the activation of cdk2 and hyperphosphorylation and thus inactivation of pRb was impaired. Direct evidence for the central role of p16INK4 in growth control comes from the observation that a competitive inhibitor of p16INK4 repressed contact inhibition of growth. These findings provide an explanation for the high incidence of mutation or loss of INK4 in human tumours.
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.