ArticleOncogene2006
Loss of one p53 allele results in four-fold reduction of p53 mRNA and protein: a basis for p53 haplo-insufficiency.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 58 citations in OpenAlex.
- Detecting likely germline variants during tumor-based molecular profiling.The Journal of clinical investigation · 2025Review
- Article
- Deletion of 17p in cancers: Guilt by (p53) association.Oncogene · 2025Review
- Single loss of a Trp53 allele triggers an increased oxidative, DNA damage and cytokine inflammatory responses through deregulation of IκBα expression.Cell death & disease · 2021Article
- Article
- A novel mouse model of rhabdomyosarcoma underscores the dichotomy of MDM2-ALT1 function in vivo.Oncogene · 2018Article
- Loss of LZAP inactivates p53 and regulates sensitivity of cells to DNA damage in a p53-dependent manner.Oncogenesis · 2017Article
- Carcinogenic polycyclic aromatic hydrocarbons induce CYP1A1 in human cells via a p53-dependent mechanism.Archives of toxicology · 2016Article
- Expression of vimentin and survivin in clear cell renal cell carcinoma and correlation with p53.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2015Article
- Article
- Integral analysis of p53 and its value as prognostic factor in sporadic colon cancer.BMC cancer · 2013Article
- The molecular mechanism and potential role of heat shock-induced p53 protein accumulation.Molecular and cellular biochemistry · 2013Article
- A deacetylase-deficient SIRT1 variant opposes full-length SIRT1 in regulating tumor suppressor p53 and governs expression of cancer-related genes.Molecular and cellular biology · 2012Article
- A continuum model for tumour suppression.Nature · 2011Review
- Reduction of Pten dose leads to neoplastic development in multiple organs of Pten (shRNA) mice.Cancer biology & therapy · 2010Article
- Article
- Regulation of tumor suppressor p53 at the RNA level.Journal of molecular medicine (Berlin, Germany) · 2010Review
- A new stochastic and state space model of human colon cancer incorporating multiple pathways.Biology direct · 2010Article
- The Arf-inducing transcription factor Dmp1 encodes a transcriptional activator of amphiregulin, thrombospondin-1, JunB and Egr1.International journal of cancer · 2010Article
- Pathways contributing to development of spontaneous mammary tumors in BALB/c-Trp53+/- mice.The American journal of pathology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A haploid genotype may be insufficient to support normal wild-type function. Such haplo-insufficiency has recently been documented for numerous tumour suppressor genes. p53 is a crucial tumour suppressor governing DNA repair, cell cycle arrest and apoptosis via its role as a stress-responsive transcription factor. p53 haplo-insufficiency has been observed in vivo with human familial cancer in Li-Fraumeni Syndrome (LFS) and in mouse p53-knockout models of LFS. The increased tumorigenesis associated with loss of one p53 allele has been attributed to reduced p53-dependent stress responses. However, the underlying biochemical basis for such attenuated responses in p53+/- cells remains unclear. Here we have determined basal p53 messenger RNA (mRNA) and protein levels, and compared the p53 stress response in p53+/+, p53+/- and p53-/- isogenic clones derived from HCT116 cells. Basal expression of p53 in p53+/- cells was 25% relative to p53+/+ cells, and this differential was maintained following oncogenic stress. This deficiency was manifested at both p53 mRNA and protein levels and resulted in attenuated p53 stress responses, in particular for p21waf1 upregulation and survivin downregulation, and reduced G1 arrest and apoptosis. These observations identify a molecular basis for wild-type p53 haplo-insufficiency, which may explain the attenuated tumour-suppressive phenotype observed in cells with a single wild-type p53 allele and in humans with LFS.
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.