ReviewJournal of gastroenterology and hepatology2012
Cancer stem cells generated by alcohol, diabetes, and hepatitis C virus.
Review in Journal of gastroenterology and hepatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 43 citations in OpenAlex.
- The regulatory effect of the YY1/miR‑HCC2/BAMBI axis on the stemness of liver cancer cells.International journal of oncology · 2023Article
- Mouse Models of Hepatocellular Carcinoma: Classification, Advancement, and Application.Frontiers in oncology · 2022Review
- Review
- Reenvisioning Traditional to Regenerative Therapeutic Advances in Managing Nonalcoholic Fatty Liver Disease in Diabetes Mellitus.Journal of diabetes research · 2021Review
- Correlating Transcriptional Networks to Papillary Renal Cell Carcinoma Survival: A Large-Scale Coexpression Analysis and Clinical Validation.Oncology research · 2020Article
- The Cancer Stem Cell in Hepatocellular Carcinoma.Cancers · 2020Review
- Unveiling new disease, pathway, and gene associations via multi-scale neural network.PloS one · 2020Article
- Stem cells under the influence of alcohol: effects of ethanol consumption on stem/progenitor cells.Cellular and molecular life sciences : CMLS · 2019Review
- Baicalein Targets GTPase-Mediated Autophagy to Eliminate Liver Tumor-Initiating Stem Cell-Like Cells Resistant to mTORC1 Inhibition.Hepatology (Baltimore, Md.) · 2018Article
- Alcohol and Cancer Stem Cells.Cancers · 2017Review
- Bile acids promote diethylnitrosamine-induced hepatocellular carcinoma via increased inflammatory signaling.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Innate immunity and hepatocarcinoma: Can toll-like receptors open the door to oncogenesis?World journal of hepatology · 2016Review
- Significance of hepatitis virus infection in the oncogenic initiation of hepatocellular carcinoma.World journal of gastroenterology · 2016Review
- Digital quantitation of HCC-associated stem cell markers and protein quality control factors using tissue arrays of human liver sections.Experimental and molecular pathology · 2014Article
- TLR3/4 signaling is mediated via the NFκB-CXCR4/7 pathway in human alcoholic hepatitis and non-alcoholic steatohepatitis which formed Mallory-Denk bodies.Experimental and molecular pathology · 2014Article
- High expression of peroxiredoxin 4 affects the survival time of colorectal cancer patients, but is not an independent unfavorable prognostic factor.Molecular and clinical oncology · 2014Article
- SALL4 immunoreactivity predicts prognosis in Western hepatocellular carcinoma patients but is a rare event: a study of 236 cases.The American journal of surgical pathology · 2014Article
- Human viral oncogenesis: a cancer hallmarks analysis.Cell host & microbe · 2014Review
- The liver is populated by a broad spectrum of markers for macrophages. In alcoholic hepatitis the macrophages are M1 and M2.Experimental and molecular pathology · 2014Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Cancer stem cells (tumor-initiating stem-like cells: TISCs) are resistant to chemotherapy and are associated with metastatic hepatocellular carcinoma (HCC), which is commonly observed in hepatitis C virus (HCV)-infected patients with obesity or alcohol abuse. However, it is unknown whether the TLR4-NANOG pathway serves as a universal oncogenic signaling in the genesis of TISCs and HCC. We aimed to determine whether Tlr4 is a putative proto-oncogene for TISCs in liver oncogenesis due to different etiologies and how Tlr4 is regulated at the transcriptional and epigenetic levels. CD133+/CD49f+ TISCs were isolated using FACS from HCC developed in HCV Core Tg mice fed alcohol, diethylnitrosamine-treated mice, and alcoholic patients with or without HCV infection. CD133+/CD49f+ cells isolated from the animal models and patients are tumorigenic both in vitro and in a xenograft model, and Tlr4 or Nanog silencing with shRNA attenuates their tumor initiating property. Functional oncogene screening of a cDNA library identified the organ size control pathway targets Yap1 and AKT activator Igf2bp3 as NANOG-dependent genes that inhibit transforming growth factor-β signaling in TISCs. Tlr4 expression is higher in TISCs compared with CD133-/CD49f+ cells. Taken together, Tlr4 may be a universal proto-oncogene responsible for the genesis of TLR4-NANOG dependent TISCs, and this pathway serves as a novel therapeutic target for HCC.
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.