Evidence map›Paper›PMID 25071022›Full record

ArticleOncotarget2014

FAS/FASL are dysregulated in chordoma and their loss-of-function impairs zebrafish notochord formation.

Luca Ferrari, Anna Pistocchi, Laura Libera, Nicola Boari, Pietro Mortini, Gianfranco Bellipanni, Antonio Giordano, Franco Cotelli, Paola Riva

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Fish TNF and TNF receptors.Science China. Life sciences · 2021
    Review
  3. Article
  4. Article
  5. Article
  6. 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

9 authors at 3 institutions in 2 countries.

Luca FerrariDipartimento di Biotecnologie Mediche e Medicina Traslazionale, Università Degli Studi di Milano, Via Viotti 3/5 20133 Milan, Italy; These authors contribute equally in this study.
Anna PistocchiDipartimento di Biotecnologie Mediche e Medicina Traslazionale, Università Degli Studi di Milano, Via Viotti 3/5 20133 Milan, Italy; Dipartimento di Bioscienze, Università Degli Studi di Milano, Via Celoria 26 20133 Milan, Italy; These authors contribute equally in this study.
Laura LiberaDipartimento di Biotecnologie Mediche e Medicina Traslazionale, Università Degli Studi di Milano, Via Viotti 3/5 20133 Milan, Italy.
Nicola BoariDipartimento di Neurochirurgia, Università Vita-Salute IRCCS Ospedale San Raffaele, Via Olgettina 60, 20132 Milan, Italy.
Pietro MortiniDipartimento di Neurochirurgia, Università Vita-Salute IRCCS Ospedale San Raffaele, Via Olgettina 60, 20132 Milan, Italy.
Gianfranco BellipanniDepartment of Biology, College of Science and Technology, Temple University, Philadelphia, Pennsylvania 19122, USA; Sbarro Institute for Cancer Research and Molecular Medicine, College of Science and Technology, Temple University, Philadelphia, Pennsylvania 19122, USA.
Antonio GiordanoDepartment of Biology, College of Science and Technology, Temple University, Philadelphia, Pennsylvania 19122, USA; Sbarro Institute for Cancer Research and Molecular Medicine, College of Science and Technology, Temple University, Philadelphia, Pennsylvania 19122, USA.
Franco CotelliDipartimento di Bioscienze, Università Degli Studi di Milano, Via Celoria 26 20133 Milan, Italy.
Paola RivaDipartimento di Biotecnologie Mediche e Medicina Traslazionale, Università Degli Studi di Milano, Via Viotti 3/5 20133 Milan, Italy.
University of Milan · ITIRCCS Ospedale San Raffaele · ITTemple University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chordoma is a rare malignant tumor that recapitulates the notochord phenotype and is thought to derive from notochord remnants not correctly regressed during development. Apoptosis is necessary for the proper notochord development in vertebrates, and the apoptotic pathway mediated by Fas and Fasl has been demonstrated to be involved in notochord cells regression. This study was conducted to investigate the expression of FAS/FASL pathway in a cohort of skull base chordomas and to analyze the role of fas/fasl homologs in zebrafish notochord formation. FAS/FASL expression was found to be dysregulated in chordoma leading to inactivation of the downstream Caspases in the samples analyzed. Both fas and fasl were specifically expressed in zebrafish notochord sorted cells. fas and fasl loss-of-function mainly resulted in larvae with notochord multi-cell-layer jumps organization, larger vacuolated notochord cells, defects in the peri-notochordal sheath structure and in vertebral mineralization. Interestingly, we observed the persistent expression of ntla and col2a1a, the zebrafish homologs of the human T gene and COL2A1 respectively, which are specifically up-regulated in chordoma. These results demonstrate for the first time the dysregulation of FAS/FASL in chordoma and their role in notochord formation in the zebrafish model, suggesting their possible implication in chordoma onset.

Indexed as

AdultAgedAnimalsCell DifferentiationChordomaFas Ligand Proteinfas ReceptorFemaleHumansMaleMiddle AgedNotochordYoung AdultZebrafishFas Ligand Proteinfas Receptor

Identifiers

PMID25071022
PMCPMC4170636
OpenAlexW1542291851

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.