Evidence map›Paper›PMID 24020493›Full record

ArticleJournal of experimental & clinical cancer research : CR2013

Cause-specific telomere factors deregulation in hepatocellular carcinoma.

Manale El Idrissi, Valérie Hervieu, Philippe Merle, Franck Mortreux, Eric Wattel

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.8field-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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Significance ofCancers · 2021
    Article
  5. Emerging roles of telomeric chromatin alterations in cancer.Journal of experimental & clinical cancer research : CR · 2019
    Review
  6. Review
  7. Article
  8. Article
  9. Genetic alterations in hepatocellular carcinoma: An update.World journal of gastroenterology · 2016
    Review
  10. Review
  11. Article
  12. Telomeres, NAFLD and Chronic Liver Disease.International journal of molecular sciences · 2016
    Review
  13. A 41-gene signature derived from breast cancer stem cells as a predictor of survival.Journal of experimental & clinical cancer research : CR · 2014
    Article
  14. Review
  15. Review
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

5 authors at 4 institutions in 1 country.

Manale El IdrissiUMR5239 Oncovirologie et Biothérapies, Faculté de Médecine Lyon Sud, ENS - HCL, Université Lyon 1, CNRS, Pierre Bénite, France. eric.wattel@ens-lyon.fr.
Valérie Hervieu
Philippe Merle
Franck Mortreux
Eric Wattel
Université Claude Bernard Lyon 1 · FRCentre de Recherche en Cancérologie de Lyon · FRCentre National de la Recherche Scientifique · FRHôpital Lyon Sud · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAmong the numerous genetic defects associated with hepatocarcinogenesis, telomere abnormalities appear to play a role both in tumor promotion and maintenance. Telomeres, the chromosome extremities, are protected by specific proteins, the shelterin complex and by additional factors. Besides telomerase dysregulation, expression changes of these telomere factors have been observed in cancers.

methodsHere, we tested the hypothesis that such dysregulation might occur in hepatocellular carcinoma (HCC) with specific patterns depending on the cause of HCC. We compared telomere length, telomerase activity (TA), hTERT and telomere genes expression using PCR and Western-blot analyses between non-cirrhotic liver, peritumoral cirrhotic tissue (40 samples) and cancerous tissue (40 samples) derived from 40 patients with HBV-, HCV-, or alcohol-related HCC.

resultsAlterations in TA, hTERT expression and telomere length between non-cirrhotic, cirrhotic, and tumor samples were not significantly influenced by the cause of HCC. In contrast, the expression pattern of hTR, shelterin, and non-shelterin telomere protective factors clearly distinguished the 3 causes of cirrhosis and HCC. For patients with HBV diseased liver, when compared with non-cirrhotic liver, the cirrhotic tissue underexpressed all shelterin and all but HMRE11A and RAD50 non-shelterin telomere factors. For HCV the expression level of POT1, RAP1, Ku80, and RAD50 was higher in cirrhotic than in non-cirrhotic liver samples without evidence for significant transcriptional change for the remaining genes. For alcohol-related liver diseases, the expression level of POT1, RAP1, TIN2, hMRE11A, hMRE11B, Ku70, Ku80, RAD50, TANK1, and PINX1 was higher in cirrhotic than in non-cirrhotic liver samples. For the 3 causes of HCC, there was no significant change in shelterin and non-shelterin gene expression between cirrhosis and HCC samples.

conclusionsThese results validate our hypotheses and demonstrate that cirrhosis and HCC add-up numerous telomere dysfunctions including numerous cause-specific changes that appear to occur early during the course of the disease.

Indexed as

AdultAgedCarcinoma, HepatocellularFemaleHepacivirusHepatitis BHepatitis B virusHepatitis CHumansImmunohistochemistryLiver NeoplasmsMaleMiddle AgedRNATelomeraseTelomereRNATelomerasetelomerase RNA

Identifiers

PMID24020493
PMCPMC3850108
OpenAlexW2162878476

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.