ArticleProceedings of the National Academy of Sciences of the United States of America2006
p21 delays tumor onset by preservation of chromosomal stability.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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
64 citing papers in PubMed, 111 citations in OpenAlex.
- The Dual Role of Cellular Senescence in Macrophages: Unveiling the Hidden Driver of Age-Related Inflammation in Kidney Disease.International journal of biological sciences · 2025Review
- Transcriptome-wide analysis of the differences between MCF7 cells cultured in DMEM or αMEM.PloS one · 2024Article
- Mechanisms of chromosomal instability (CIN) tolerance in aggressive tumors: surviving the genomic chaos.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023Review
- Ubiquitin-specific protease 28: the decipherment of its dual roles in cancer development.Experimental hematology & oncology · 2023Review
- Selective ATM inhibition augments radiation-induced inflammatory signaling and cancer cell death.Aging · 2023Article
- Article
- TP53 loss initiates chromosomal instability in fallopian tube epithelial cells.Disease models & mechanisms · 2021Article
- DNA repair pathways and their roles in drug resistance for lung adenocarcinoma.Molecular biology reports · 2021Review
- p53 and Tumor Suppression: It Takes a Network.Trends in cell biology · 2021Review
- The Multifaceted p21 (Cip1/Waf1/Cancers · 2019Review
- The role of p21/CIP1/WAF1 (p21) in the negative regulation of the growth hormone/growth hormone receptor and epidermal growth factor/epidermal growth factor receptor pathways, in growth hormone transduction defect.Annals of pediatric endocrinology & metabolism · 2018Article
- Deconstructing networks of p53-mediated tumor suppression in vivo.Cell death and differentiation · 2018Review
- Endogenous Replication Stress in Mother Cells Leads to Quiescence of Daughter Cells.Cell reports · 2017Article
- ROCK2/rasOncogene · 2017Article
- Pan-cancer analysis distinguishes transcriptional changes of aneuploidy from proliferation.Genome research · 2017Article
- The Regulation of Cellular Functions by the p53 Protein: Cellular Senescence.Cold Spring Harbor perspectives in medicine · 2017Review
- The Role of Aneuploidy in Cancer Evolution.Cold Spring Harbor perspectives in medicine · 2017Review
- Combined loss of PUMA and p21 accelerates c-MYC-driven lymphoma development considerably less than loss of one allele of p53.Oncogene · 2016Article
- Genome Stability Requires p53.Cold Spring Harbor perspectives in medicine · 2016Review
- Tumor-Suppressor Functions of the TP53 Pathway.Cold Spring Harbor perspectives in medicine · 2016Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The p53 protein suppresses tumorigenesis by initiating cellular functions such as cell cycle arrest and apoptosis in response to DNA damage. A p53 mutant, p53R172P, which is deficient for apoptosis but retains a partial cell cycle arrest function, delays tumor onset in mice. Remarkably, lymphomas arising in Trp53(515C/515C) mice (encoding p53R172P) retain stable genomes. Given the dominant role of p21 in p53 cell cycle control, we crossed Trp53(515C/515C) mice onto a p21-null background to determine whether p21 was required for maintaining chromosomal stability and delaying tumor onset. Loss of p21 completely abolished the cell cycle arrest function of p53R172P and accelerated tumor onset in Trp53(515C/515C) mice. Cytogenetic examination of Trp53(515C/515C) p21(-/-) sarcomas and lymphomas revealed aneuploidy and chromosomal aberrations that were absent in Trp53(515C/515C) malignancies. Thus, p21 coupled p53-dependent checkpoint control and preservation of chromosomal stability, and cooperated with apoptosis in suppressing tumor onset in mice.
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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.