Evidence map›Paper›PMID 23758232›Full record

ArticleThe New England journal of medicine2013

Oncofetal gene SALL4 in aggressive hepatocellular carcinoma.

Kol Jia Yong, Chong Gao, Joline S J Lim, Benedict Yan, Henry Yang, Todor Dimitrov, Akira Kawasaki, Chee Wee Ong, Kwong-Fai Wong, Sanghoon Lee and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in The New England journal of medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 3 pooled it
14.5field-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

133 citing papers in PubMed, 3 syntheses or guidelines pooled it, 260 citations in OpenAlex.

  1. Pooled it
  2. Higher expression of SALL4 predicts poor cancer prognosis: A meta-analysis.Cancer biomarkers : section A of Disease markers · 2017
    Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Oncofetal MCB1 Is a Functional Biomarker for HCC Personalized Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. mJournal of hepatocellular carcinoma · 2024
    Article
  18. Mechanisms of angiogenesis in tumour.Frontiers in oncology · 2024
    Review
  19. Article
  20. Article

73 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 7 institutions in 4 countries.

Kol Jia YongCancer Science Institute of Singapore, the National University of Singapore Graduate School for Integrative Sciences and Engineering, Singapore.
Chong Gao
Joline S J Lim
Benedict Yan
Henry Yang
Todor Dimitrov
Akira Kawasaki
Chee Wee Ong
Kwong-Fai Wong
Sanghoon Lee
Sharada Ravikumar
Supriya Srivastava
Xi Tian
Ronnie T Poon
Sheung Tat Fan
John M Luk
Yock Young Dan
Manuel Salto-Tellez
Li Chai
Daniel G Tenen
National University Cancer Institute, Singapore · SGBrigham and Women's Hospital · USNational University of Singapore · SGQueen Mary Hospital · CNHarvard Stem Cell Institute · USNational University Health System · SGQueen's University Belfast · GB

Funding

TYROSINE KINASE ONCOGENESIS IN MYELOID LEUKEMIAP01CA066996 · NCI · DANA-FARBER CANCER INSTITUTE · PI SCOTT A ARMSTRONG · 1996 to 2026
$52.5M
Transcription regulation in hematopoiesisP01HL095489 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI PARK, SHINYOUNG · 2010 to 2020
$20.1M
Hematopoietic stem cell commitmentP01DK080665 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TENEN, DANIEL G · 2008 to 2012
$7.3M
ROLE OF C/EBPalpha AND MYELOPOIESISR01HL056745 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TENEN, DANIEL G · 1996 to 2010
$3.7M
SELF-RENEWAL IN LEUKEMIC STEM CELLSR01HL092437 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI CHAI, LI · 2008 to 2012
$2.4M
Molecular biology of myeloid differentiationR01HL112719 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TENEN, DANIEL G · 2012 to 2015
$2.2M
Distinct acute myeloid leukemia subclasses with CEBPA mutationsR01CA118316 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TENEN, DANIEL G · 2007 to 2011
$2.0M
NCI NIH HHS P01 CA066996NCI NIH HHS R01 CA118316NHLBI NIH HHS P01 HL095489NHLBI NIH HHS P01HL095489NHLBI NIH HHS R01 HL056745NHLBI NIH HHS R01 HL092437NHLBI NIH HHS R01HL092437NHLBI NIH HHS R01 HL112719NIDDK NIH HHS P01 DK080665NIDDK NIH HHS P01DK080665
6 · The paper itself

Abstract

backgroundHepatocellular carcinoma is the third leading cause of cancer-related deaths worldwide. In the heterogeneous group of hepatocellular carcinomas, those with characteristics of embryonic stem-cell and progenitor-cell gene expression are associated with the worst prognosis. The oncofetal gene SALL4, a marker of a subtype of hepatocellular carcinoma with progenitor-like features, is associated with a poor prognosis and is a potential target for treatment.

methodsWe screened specimens obtained from patients with primary hepatocellular carcinoma for the expression of SALL4 and carried out a clinicopathological analysis. Loss-of-function studies were then performed to evaluate the role of SALL4 in hepatocarcinogenesis and its potential as a molecular target for therapy. To assess the therapeutic effects of a peptide that targets SALL4, we used in vitro functional and in vivo xenograft assays.

resultsSALL4 is an oncofetal protein that is expressed in the human fetal liver and silenced in the adult liver, but it is reexpressed in a subgroup of patients who have hepatocellular carcinoma and an unfavorable prognosis. Gene-expression analysis showed the enrichment of progenitor-like gene signatures with overexpression of proliferative and metastatic genes in SALL4-positive hepatocellular carcinomas. Loss-of-function studies confirmed the critical role of SALL4 in cell survival and tumorigenicity. Blocking SALL4-corepressor interactions released suppression of PTEN (the phosphatase and tensin homologue protein) and inhibited tumor formation in xenograft models in vivo.

conclusionsSALL4 is a marker for a progenitor subclass of hepatocellular carcinoma with an aggressive phenotype. The absence of SALL4 expression in the healthy adult liver enhances the potential of SALL4 as a treatment target in hepatocellular carcinoma. (Funded by the Singapore National Medical Research Council and others.).

Indexed as

AdultAnimalsBiomarkers, TumorCarcinoma, HepatocellularGene ExpressionGene Expression Regulation, NeoplasticHumansLiverLiver NeoplasmsMetabolic Networks and PathwaysMiceMice, Inbred StrainsPrognosisPTEN PhosphohydrolaseTranscription FactorsTransplantation, HeterologousBiomarkers, TumorPTEN PhosphohydrolasePTEN protein, humanSALL4 protein, humanTranscription Factors

Identifiers

PMID23758232
PMCPMC3781214
OpenAlexW2051298779

What OpenQuestion holds

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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.