Evidence map›Paper›PMID 19195051›Full record

ReviewWorld journal of gastroenterology2009

Dysregulation of apoptosis in hepatocellular carcinoma cells.

Isabel Fabregat

Open access · bronzeAbstract readEditorialReview
In one paragraph

Review in World journal of gastroenterology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed
11.1field-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.

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

128 citing papers in PubMed, 270 citations in OpenAlex.

  1. Trial
  2. Article
  3. Molecular and clinical oncology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
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  11. Article
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  13. Review
  14. Anti-carcinogenic effects and mechanisms of actions ofAmerican journal of cancer research · 2024
    Article
  15. Article
  16. Article
  17. Components of the JNK-MAPK pathway play distinct roles in hepatocellular carcinoma.Journal of cancer research and clinical oncology · 2023
    Article
  18. Article
  19. Article
  20. Review

68 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

1 author at 1 institution in 2 countries.

Isabel Fabregat
Institut d'Investigació Biomédica de Bellvitge · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a major health problem, being the sixth most common cancer world-wide. Dysregulation of the balance between proliferation and cell death represents a pro-tumorigenic principle in human hepatocarcinogenesis. This review updates the recent relevant contributions reporting molecular alterations for HCC that induce an imbalance in the regulation of apoptosis. Alterations in the expression and/or activation of p53 are frequent in HCC cells, which confer on them resistance to chemotherapeutic drugs. Many HCCs are also insensitive to apoptosis induced either by death receptor ligands, such as FasL or TRAIL, or by transforming growth factor-beta (TGF-beta). Although the expression of some pro-apoptotic genes is decreased, the balance between death and survival is dysregulated in HCC mainly due to overactivation of anti-apoptotic pathways. Indeed, some molecules involved in counteracting apoptosis, such as Bcl-X(L), Mcl-1, c-IAP1, XIAP or survivin are over-expressed in HCC cells. Furthermore, some growth factors that mediate cell survival are up-regulated in HCC, as well as the molecules involved in the machinery responsible for cleavage of their pro-forms to an active peptide. The expression and/or activation of the JAK/STAT, PI3K/AKT and RAS/ERKs pathways are enhanced in many HCC cells, conferring on them resistance to apoptotic stimuli. Finally, recent evidence indicates that inflammatory processes, as well as the epithelial-mesenchymal transitions that occur in HCC cells to facilitate their dissemination, are related to cell survival. Therefore, therapeutic strategies to selectively inhibit anti-apoptotic signals in liver tumor cells have the potential to provide powerful tools to treat HCC.

Indexed as

Aflatoxin B1AnimalsApoptosisCarcinoma, HepatocellularCell DeathCell DivisionCell SurvivalGene Expression Regulation, NeoplasticHumansInflammationKineticsLiver NeoplasmsMiceMice, TransgenicReceptors, Death DomainTransforming Growth Factor betaAflatoxin B1Receptors, Death DomainTransforming Growth Factor betaTumor Suppressor Protein p53

Identifiers

PMID19195051
PMCPMC2653340
OpenAlexW2161818053

What OpenQuestion holds

Textmetadata
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.