ArticleOncogene2000
Activation of the insulin-like growth factor II transcription by aflatoxin B1 induced p53 mutant 249 is caused by activation of transcription complexes; implications for a gain-of-function during the formation of hepatocellular carcinoma.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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
33 citing papers in PubMed, 92 citations in OpenAlex.
- HBx-Associated Reactivation of the IGF2 Locus in Chronic HBV Infection and HBV-Related Hepatocarcinogenesis: Evidence Boundaries and Biomarker Implications.Biomedicines · 2026Review
- Aflatoxin B1 and food safety: Mechanisms of action associated to Hepatocellular Carcinoma.Archives of microbiology · 2026Review
- Cooperation Between Aflatoxin-Induced p53 Aberrations and Hepatitis B Virus in Hepatocellular Carcinoma.Journal of xenobiotics · 2025Review
- It takes a team: a gain-of-function story of p53-R249S.Journal of molecular cell biology · 2019Review
- Transcriptional Regulation by Wild-Type and Cancer-Related Mutant Forms of p53.Cold Spring Harbor perspectives in medicine · 2017Review
- Roles of p53 in extrinsic factor-induced liver carcinogenesis.Hepatoma research · 2017Article
- Emerging Non-Canonical Functions and Regulation by p53: p53 and Stemness.International journal of molecular sciences · 2016Review
- Cellular Adaptation to VEGF-Targeted Antiangiogenic Therapy Induces Evasive Resistance by Overproduction of Alternative Endothelial Cell Growth Factors in Renal Cell Carcinoma.Neoplasia (New York, N.Y.) · 2015Article
- Targeting the insulin-like growth factor pathway in hepatocellular carcinoma.World journal of hepatology · 2014Review
- The GH-IGF-SST system in hepatocellular carcinoma: biological and molecular pathogenetic mechanisms and therapeutic targets.Infectious agents and cancer · 2014Review
- Current understanding of the role and targeting of tumor suppressor p53 in glioblastoma multiforme.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Review
- Article
- Igf2 pathway dependency of the Trp53 developmental and tumour phenotypes.EMBO molecular medicine · 2012Article
- Mutant p53: one name, many proteins.Genes & development · 2012Review
- Aflatoxin B1 up-regulates insulin receptor substrate 2 and stimulates hepatoma cell migration.PloS one · 2012Article
- Targeting insulin-like growth factor axis in hepatocellular carcinoma.Journal of hematology & oncology · 2011Review
- Mutant p53 gain-of-function in cancer.Cold Spring Harbor perspectives in biology · 2010Review
- When mutants gain new powers: news from the mutant p53 field.Nature reviews. Cancer · 2009Review
- Reactivation of the insulin-like growth factor-II signaling pathway in human hepatocellular carcinoma.World journal of gastroenterology · 2008Review
- Mutant p53: an oncogenic transcription factor.Oncogene · 2007Review
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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aflatoxin B1 (AFB1) induced mutation of the p53 gene at codon 249 (p53mt249) is critical during the formation of hepatocellular carcinoma (HCC) following hepatitis B virus (HBV) infection. p53mt249 markedly increases insulin-like growth factor II (IGF-II) transcription largely from promoter 4, accumulating the fetal form of IGF-II. Modulation of the transcription factor binding to IGF-II P4 by wild-type p53 and p53mt249 was identified. Wild-type p53 inhibited binding of transcription factors Sp1 and TBP on the P4 promoter, while p53mt249 enhanced the formation of transcriptional complexes through enhanced DNA-protein (Sp1 or TBP) and protein-protein (Sp1 and TBP) interactions. p53mt249 stimulates transcription factor Sp1 phosphorylation which might be a cause of increased transcription factor binding on the P4 promoter while wild-type p53 does not. Transfection of hepatocytes with p53mt249 impaired induction of apoptosis by the HBV-X protein and TNF-alpha. Therefore, the blocking of apoptosis through enhanced production of IGF-II should provide a favorable opportunity for the selection of transformed hepatocytes. These results explain the molecular basis for the genesis of HCC by p53mt249 which was found to be induced by a potent mutagen, AFB1.
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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.