Evidence map›Paper›PMID 26011625›Full record

ArticleCancer science2015

Differential reactivation of fetal/neonatal genes in mouse liver tumors induced in cirrhotic and non-cirrhotic conditions.

Xi Chen, Masahiro Yamamoto, Kiyonaga Fujii, Yasuharu Nagahama, Takako Ooshio, Bing Xin, Yoko Okada, Hiroyuki Furukawa, Yuji Nishikawa

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.1field-weighted citation impact, top 9% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 49 citations in OpenAlex.

  1. Trial
  2. Trefoil Factor-3 Is a Hypoxia-Triggered Pro-Tumorigenic Factor in Hepatoblastoma.Liver international : official journal of the International Association for the Study of the Liver · 2026
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  20. Lgr5Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Xi ChenDivision of Tumor Pathology, Department of Pathology, Asahikawa Medical University, Asahikawa, Japan.
Masahiro YamamotoDivision of Tumor Pathology, Department of Pathology, Asahikawa Medical University, Asahikawa, Japan.
Kiyonaga FujiiDivision of Tumor Pathology, Department of Pathology, Asahikawa Medical University, Asahikawa, Japan.
Yasuharu NagahamaDivision of Tumor Pathology, Department of Pathology, Asahikawa Medical University, Asahikawa, Japan.
Takako OoshioDivision of Tumor Pathology, Department of Pathology, Asahikawa Medical University, Asahikawa, Japan.
Bing XinDivision of Tumor Pathology, Department of Pathology, Asahikawa Medical University, Asahikawa, Japan.
Yoko OkadaDivision of Tumor Pathology, Department of Pathology, Asahikawa Medical University, Asahikawa, Japan.
Hiroyuki FurukawaDivision of Gastroenterological and General Surgery, Department of Surgery, Asahikawa Medical University, Asahikawa, Japan.
Yuji NishikawaDivision of Tumor Pathology, Department of Pathology, Asahikawa Medical University, Asahikawa, Japan.
Asahikawa Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma develops in either chronically injured or seemingly intact livers. To explore the tumorigenic mechanisms underlying these different conditions, we compared the mRNA expression profiles of mouse hepatocellular tumors induced by the repeated injection of CCl4 or a single diethylnitrosamine (DEN) injection using a cDNA microarray. We identified tumor-associated genes that were expressed differentially in the cirrhotic CCl4 model (H19, Igf2, Cbr3, and Krt20) and the non-cirrhotic DEN model (Tff3, Akr1c18, Gpc3, Afp, and Abcd2) as well as genes that were expressed comparably in both models (Ly6d, Slpi, Spink3, Scd2, and Cpe). The levels and patterns of mRNA expression of these genes were validated by quantitative RT-PCR analyses. Most of these genes were highly expressed in mouse livers during the fetal/neonatal periods. We also examined the mRNA expression of these genes in mouse tumors induced by thioacetamide, another cirrhotic inducer, and those that developed spontaneously in non-cirrhotic livers and found that they shared a similar expression profile as that observed in CCl4 -induced and DEN-induced tumors, respectively. There was a close relationship between the expression levels of Igf2 and H19 mRNA, which were activated in the cirrhotic models. Our results show that mouse liver tumors reactivate fetal/neonatal genes, some of which are specific to cirrhotic or non-cirrhotic modes of pathogenesis.

Indexed as

AnimalsCarcinoma, HepatocellularDisease Models, AnimalGene Expression Regulation, NeoplasticHumansImmunohistochemistryIn Situ HybridizationLiver CirrhosisLiver NeoplasmsMaleMiceMice, Inbred C3HMice, Inbred C57BLOligonucleotide Array Sequence AnalysisPolymerase Chain ReactionHepatocellular carcinomainsulin-like growth factor 2liver cirrhosismRNA expressiontrefoil factor 3

Identifiers

PMID26011625
PMCPMC4556385
OpenAlexW1492511624

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.