ArticleCancer research2022
p53 Activation Paradoxically Causes Liver Cancer.
Article in Cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 9 citations in OpenAlex.
- Broussoflavonol B induces S-phase arrest and apoptosis in pancreatic cancer cells by modulating the cell cycle checkpoint through inhibition of the AURKA/PLK1 pathway.Cancer cell international · 2025Article
- p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis.Cancer research communications · 2023Article
- Tissue specificity and spatio-temporal dynamics of the p53 transcriptional program.Cell death and differentiation · 2023Review
- Could senescence phenotypes strike the balance to promote tumor dormancy?Cancer metastasis reviews · 2023Review
- Comprehensive analysis of the correlation of the pan-cancer gene HAUS5 with prognosis and immune infiltration in liver cancer.Scientific reports · 2023Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of p53 regulates a transcriptional program that can cause cell cycle arrest, senescence, apoptosis, and ferroptosis, which are potent tumor suppressive mechanisms. Unexpectedly, Makino and colleagues show in this issue of Cancer Research that the constitutive activation of p53 in murine hepatocytes leads to tumor development. Detailed analyses indicate that p53 activation leads to loss of hepatocytes, increased expression of chemokines and humoral factors, and expansion of the hepatic progenitor cell population. These progenitor cells are highly proliferative, show chromosomal instability, and eventually transform. In chronic liver disease in humans, activation of p53 is associated with increased liver cancer development. This study highlights the complexity and non-cell autonomous nature of the physiologic p53 response. See related article by Makino et al., p. 2860.
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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.