Emergence of the Dedifferentiated Phenotype in Hepatocyte-Derived Tumors in Mice: Roles of Oncogene-Induced Epigenetic Alterations
Watanabe K., Yamamoto M., Xin B., Ooshio T., Goto M., Fujii K.
Animal Study, published in Hepatol Commun (2019) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Hepatol Commun (2019)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 31061957
- PMCID
- PMC6492474
- DOI
- 10.1002/hep4.1327
- Citations
- 11
Abstract (original English)
Hepatocellular carcinoma often reactivates the genes that are transiently expressed in fetal or neonatal livers. However, the mechanism of their activation has not been elucidated. To explore how oncogenic signaling pathways could be involved in the process, we examined the expression of fetal/neonatal genes in liver tumors induced by the introduction of myristoylated v-akt murine thymoma viral oncogene (AKT), HRas proto-oncogene, guanosine triphosphatase (HRAS V12 ), and MYC proto-oncogene, bHLH transcription factor (Myc), in various combinations, into mouse hepatocytes in vivo . Distinct sets of fetal/neonatal genes were activated in HRAS- and HRAS/Myc-induced tumors: aldo-keto reductase family 1, member C18 ( Akr1c18 ), glypican 3 ( Gpc3 ), carboxypeptidase E ( Cpe ), adenosine triphosphate-binding cassette, subfamily D, member 2 ( Abcd2 ), and trefoil factor 3 ( Tff3 ) in the former; insulin-like growth factor 2 messenger RNA binding protein 3 ( Igf2bp3 ), alpha fetoprotein ( Afp ), Igf2 , and H19, imprinted maternally expressed transcript ( H19 ) in the latter. Interestingly, HRAS/Myc-induced tumors comprised small cells with a high nuclear/cytoplasmic ratio and messenger RNA (mRNA) expression of delta-like noncanonical Notch ligand 1 ( Dlk1 ), Nanog homeobox ( Nanog ), and sex determining region Y-box 2 ( Sox2 ). Both HRAS- and HRAS/Myc-induced tumors showed decreased DNA
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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