Evidence map›Paper›PMID 26536864›Full record

ReviewMolecular cancer2015

The H19 Long non-coding RNA in cancer initiation, progression and metastasis - a proposed unifying theory.

Eli Raveh, Imad J Matouk, Michal Gilon, Abraham Hochberg

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04767750 (Role of LncRNA H19 in The Regulation of IGF-1R Expression), which is not on this map. Cited by 313 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
313citing papers in PubMed, 1 pooled it
18.6field-weighted citation impact, top 1% 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.

NCT04767750 completednot on this mapstarted 2020, after this paper: background citation

Role of LncRNA H19 in The Regulation of IGF-1R Expression: A Possible Association Between Type 2 Diabetes and Hepatocellular Carcinoma

TypeobservationalSponsorMansoura UniversityRan2020 to 2022Enrolled101ConditionsHepatocellular Carcinoma, Type 2 Diabetes, CancerArmsBlood sample collection
3 · Its place in the literature

Who cites it

313 citing papers in PubMed, 1 synthesis or guideline pooled it, 547 citations in OpenAlex.

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  11. Simulated burn pit smoke condensates cause sustained impact on human airway epithelial cells.Toxicological sciences : an official journal of the Society of Toxicology · 2025
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253 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Eli RavehThe Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, Faculty of Sciences, The Edmond J. Safra Campus, The Hebrew University of Jerusalem, Jerusalem, 91904, Israel. Eli.Raveh@mail.huji.ac.il.
Imad J MatoukThe Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, Faculty of Sciences, The Edmond J. Safra Campus, The Hebrew University of Jerusalem, Jerusalem, 91904, Israel. imad.matouq@mail.huji.ac.il.
Michal GilonThe Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, Faculty of Sciences, The Edmond J. Safra Campus, The Hebrew University of Jerusalem, Jerusalem, 91904, Israel. Michal.Gilon@mail.huji.ac.il.
Abraham HochbergThe Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, Faculty of Sciences, The Edmond J. Safra Campus, The Hebrew University of Jerusalem, Jerusalem, 91904, Israel. hochberg@cc.huji.ac.il.
Hebrew University of Jerusalem · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The imprinted oncofetal long non-coding RNA (lncRNA) H19 is expressed in the embryo, down-regulated at birth and then reappears in tumors. Its role in tumor initiation and progression has long been a subject of controversy, although accumulating data suggest that H19 is one of the major genes in cancer. It is actively involved in all stages of tumorigenesis and is expressed in almost every human cancer. In this review we delineate the various functions of H19 during the different stages in the complex process of tumor progression. H19 up-regulation allows cells to enter a "selfish" survival mode in response to stress conditions, such as destabilization of the genome and hypoxia, by accelerating their proliferation rate and increasing overall cellular resistance to stress. This response is tightly correlated with nullification, dysfunction or significant down-regulation of the master tumor suppressor gene P53. The growing evidence of H19's involvement in both proliferation and differentiation processes, together with its involvement in epithelial to mesenchymal transition (EMT) and also mesenchymal to epithelial transition (MET), has led us to conclude that some of the recent disputes and discrepancies arising from current research findings can be resolved from a viewpoint supporting the oncogenic properties of H19. According to a holistic approach, the versatile, seemingly contradictory functions of H19 are essential to, and differentially harnessed by, the tumor cell depending on its context within the process of tumor progression.

Indexed as

AnimalsDisease ProgressionEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGenomic InstabilityHumansRNA, Long NoncodingH19 long non-coding RNARNA, Long Noncoding

Identifiers

PMID26536864
PMCPMC4632688
OpenAlexW2168089202

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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.