Evidence map›Paper›PMID 28160555›Full record

SynthesisOncotarget2017

Oncofetal gene SALL4 and prognosis in cancer: A systematic review with meta-analysis.

Lorenzo Nicolè, Tiziana Sanavia, Nicola Veronese, Rocco Cappellesso, Claudio Luchini, Paolo Dabrilli, Ambrogio Fassina

Open access · diamondAbstract readMeta-AnalysisSystematic Review
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

26 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Alectinib and SALL4-Targeted Fatty Acid Oxidation: A Strategy to Combat Oxaliplatin Resistance in Gastric Cancer.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025
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  9. Review
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  13. Pluripotency Stemness and Cancer: More Questions than Answers.Advances in experimental medicine and biology · 2022
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
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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

7 authors at 4 institutions in 2 countries.

Lorenzo NicolèDepartment of Medicine, Surgical Pathology & Cytopathology Unit, University of Padova, Padova, Italy.
Tiziana SanaviaDepartment of Biomedical Informatics, Harvard Medical School, Boston, MA, USA.
Nicola VeroneseNational Research Council, Neuroscience Institute, Aging Branch, Padova, Italy.
Rocco CappellessoDepartment of Medicine, Surgical Pathology & Cytopathology Unit, University of Padova, Padova, Italy.
Claudio LuchiniDepartment of Pathology and Diagnostics, University and Hospital Trust of Verona, Verona, Italy.
Paolo DabrilliDepartment of Medicine, Surgical Pathology & Cytopathology Unit, University of Padova, Padova, Italy.
Ambrogio FassinaDepartment of Medicine, Surgical Pathology & Cytopathology Unit, University of Padova, Padova, Italy.
University of Padua · ITHarvard University · USNeuroscience Institute · ITOspedale Santa Chiara · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Spalt-Like Transcription Factor 4 (SALL4) oncogene plays a central function in embryo-fetal development and is absent in differentiated tissues. Evidence suggests that it can be reactivated in several cancers worsening the prognosis. We aimed at investigating the risk associated with SALL4 reactivation for all-cause mortality and recurrence in cancer using the current literature. A PubMed and SCOPUS search until 1st September 2016 was performed, focusing on perspective studies reporting prognostic parameters in cancer data. In addition, 17 datasets of different cancer types from The Cancer Genome Atlas were considered. A total of 9,947 participants across 40 cohorts, followed-up for about 5 years on average, were analyzed comparing patients showing SALL4 presence (SALL4+, n = 1,811) or absence (SALL4-, n = 8,136). All data were summarised using risk ratios (RRs) for the number of deaths/recurrences and hazard ratios (HRs) for the time-dependent risk related to SALL4+, adjusted for potential confounders. SALL4+ significantly increased overall mortality (RR = 1.34, 95% confidence intervals (CI)=1.21-1.48, p<0.0001, I2=66%; HR=1.4; 95%CI: 1.19-1.65; p<0.0001; I2=63%) and recurrence of disease (RR = 1.25, 95% CI = 1.1-1.42, p=0.0006, I2=62%); HR=1.52; 95% CI: 1.22-1.89, p=0.0002; I2=69%) compared to SALL4-. Moreover, SALL4 remained significantly associated with poor prognosis even using HRs adjusted for potential confounders (overall mortality: HR=1.4; 95%CI: 1.19-1.65; p<0.0001; I2=63%; recurrence of disease: HR=1.52; 95% CI: 1.22-1.89, p=0.0002; I2=69%). These results suggest that SALL4 expression increases both mortality and recurrence of cancer, confirming this gene as an important prognostic marker and a potential target for personalized medicine.

Indexed as

HumansNeoplasmsPrognosisTranscription FactorsSALL4 protein, humanTranscription Factorscancermeta-analysisprognosisSALL4targeted therapy

Identifiers

PMID28160555
PMCPMC5410278
OpenAlexW2583443690

What OpenQuestion holds

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LicenceCC BY
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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.