ArticleOncogene2000
The consequence of p53 overexpression for liver tumor development and the response of transformed murine hepatocytes to genotoxic agents.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- The Role of Chronic Liver Diseases in the Emergence and Recurrence of Hepatocellular Carcinoma: An Omics Perspective.Frontiers in medicine · 2022Review
- Mulberry fruits extracts induce apoptosis and autophagy of liver cancer cell and prevent hepatocarcinogenesis in vivo.Journal of food and drug analysis · 2020Article
- Correlating Anticancer Drug Delivery Efficiency with Vascular Permeability of Renal Clearable Versus Non-renal Clearable Nanocarriers.Angewandte Chemie (International ed. in English) · 2019Article
- Tuning the In Vivo Transport of Anticancer Drugs Using Renal-Clearable Gold Nanoparticles.Angewandte Chemie (International ed. in English) · 2019Article
- p53 as a Dichotomous Regulator of Liver Disease: The Dose Makes the Medicine.International journal of molecular sciences · 2018Review
- Article
- Functional annotation of novel lineage-specific genes using co-expression and promoter analysis.BMC genomics · 2010Article
- 20 years studying p53 functions in genetically engineered mice.Nature reviews. Cancer · 2009Review
- The expression of TA and DeltaNp63 are regulated by different mechanisms in liver cells.Oncogene · 2005Article
- Cell death by mitotic catastrophe: a molecular definition.Oncogene · 2004Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To analyse the effect of p53 on liver tumor development, we generated transgenic mice overexpressing wild-type p53 in the liver and crossed them with transgenic mice in which the expression of the SV40 large T antigen (TAg) induces hepatic tumors. Remarkably, whereas preneoplastic TAg liver exhibited anisocaryosis and anisocytosis, TAg/p53 liver never presented any dysplastic cells. Moreover, whereas expression of p53 did not affect hepatic development, its constitutive expression in tumorigenic livers resulted in a significantly enhanced apoptosis once nodules had appeared. In contrast, p53 overexpression did not modify the elevated proliferation of TAg-transformed hepatocytes and had no effect on hepatocarcinoma progression. In vitro analysis of primary hepatocytes exposed to various genotoxic agents showed that p53 failed to sensitize normal or TAg-transformed hepatocytes to apoptosis, except when high doses of doxorubicin, UV-B and UV-C radiation were used. Our results confirmed that the hepatocyte cell type is very resistant to genotoxic agents and showed that constitutive expression of p53 failed to improve their responsiveness. In addition, our results showed that suppression of dysplastic cells, probably by restoring normal cytokinesis and karyokinesis, and enhancement of apoptosis by means of p53 overexpression were insufficient to counteract or delay the TAg-induced liver tumoral progression. Oncogene (2000) 19, 3498 - 3507
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