Evidence map›Paper›PMID 28283801›Full record

ArticleJournal of neuro-oncology2017

Serum amyloid A1 is upregulated in human glioblastoma.

Franciele Hinterholz Knebel, Miyuki Uno, Thais F Galatro, Luziane Potrich Bellé, Sueli Mieko Oba-Shinjo, Suely Kazue N Marie, Ana Campa

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Journal of neuro-oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Serum amyloid A - a review.Molecular medicine (Cambridge, Mass.) · 2018
    Review
  18. Article
  19. Article
  20. Article
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 1 institution in 1 country.

Franciele Hinterholz KnebelDepartment of Clinical Chemistry, Faculty of Pharmaceutical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil. fhknebel@usp.br.ORCID 0000-0003-2366-9682
Miyuki UnoDepartment of Neurology, School of Medicine, University of São Paulo, São Paulo, São Paulo, Brazil.
Thais F GalatroDepartment of Neurology, School of Medicine, University of São Paulo, São Paulo, São Paulo, Brazil.
Luziane Potrich BelléDepartment of Clinical Chemistry, Faculty of Pharmaceutical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil.
Sueli Mieko Oba-ShinjoDepartment of Neurology, School of Medicine, University of São Paulo, São Paulo, São Paulo, Brazil.
Suely Kazue N MarieDepartment of Neurology, School of Medicine, University of São Paulo, São Paulo, São Paulo, Brazil.
Ana CampaDepartment of Clinical Chemistry, Faculty of Pharmaceutical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil.
Universidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Serum amyloid A1 (SAA1) is a sensitive acute phase reactant primarily produced by the liver in response to acute inflammation. We have recently shown that SAA affects proliferation, migration, and invasion of glioblastoma cell lines, which suggest its participation in the malignant process. Consistently, levels of SAA have been used as a non-invasive biomarker for the prognosis of many cancers. In this study, we aimed to investigate SAA serum levels and expression of SAA genes in human astrocytomas tissues. Serum and tissue samples were obtained from patients with astrocytoma grades I to III and glioblastoma (GBM or grade IV). Levels of circulating SAA were significantly higher in the serum of patients with AGII-IV when compared to non-neoplastic samples derived from non-neoplastic patients (NN) (p > 0.0001). Quantitative real time PCR (qRT-PCR) of 148 astrocytomas samples (grades I-IV) showed that SAA1 mRNA was significantly higher in GBM when compared to AGI-III and NN samples (p < 0.0001). Immunohistochemistry analysis revealed cytoplasmic positivity for SAA in GBM. There was no correlation of SAA1 with clinical end-point of overall survival among GBM patients. However, it was found a positive correlation between SAA1 and genes involved in tumor progression, such as: HIF1A (r = 0.50; p < 0.00001), CD163 (r = 0.52; p < 0.00001), CXCR4 (r = 0.42; p < 0.00001) and CXCR7 (r = 0.33; p = 0.002). In conclusions, we show that astrocytoma patients have increased levels of serum SAA and SAA1 is expressed and secreted in GBM, and its co-expression with tumor-related genes supports its involvement in GBM angiogenesis and progression.

Indexed as

AdultAgedAstrocytomaBiomarkers, TumorBrain NeoplasmsDisease-Free SurvivalFemaleGlioblastomaHumansKaplan-Meier EstimateMaleMiddle AgedSerum Amyloid A ProteinUp-RegulationYoung AdultBiomarkers, TumorSerum Amyloid A ProteinCD163CXCR4CXCR7GlioblastomaHIF1αSerum amyloid A

Identifiers

PMID28283801
OpenAlexW2593201030

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.