Evidence map›Paper›PMID 22879388›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2012

EWS-FLI-1-targeted cytotoxic T-cell killing of multiple tumor types belonging to the Ewing sarcoma family of tumors.

Christopher H Evans, Fangjun Liu, Ryan M Porter, Regina P O'Sullivan, Taha Merghoub, Elaine P Lunsford, Kyle Robichaud, Frans Van Valen, Stephen L Lessnick, Mark C Gebhardt and 1 more

Abstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

28 citing papers in PubMed, 47 citations in OpenAlex.

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  9. Role of immunotherapy in Ewing sarcoma.Journal for immunotherapy of cancer · 2020
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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

11 authors at 3 institutions in 1 country.

Christopher H EvansBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Fangjun Liu
Ryan M Porter
Regina P O'Sullivan
Taha Merghoub
Elaine P Lunsford
Kyle Robichaud
Frans Van Valen
Stephen L Lessnick
Mark C Gebhardt
James W Wells
Huntsman Cancer Institute · USMemorial Sloan Kettering Cancer Center · USBeth Israel Deaconess Medical Center · US

Funding

Healing of Segmental Defects of Bone by Gene TransferR01AR050243 · NIAMS · MAYO CLINIC ROCHESTER · PI EVANS, CHRISTOPHER HOWARD · 2003 to 2014
$6.0M
NIAMS NIH HHS R01 AR050243
6 · The paper itself

Abstract

purposeThe Ewing sarcoma family of tumors (ESFT) comprises a group of aggressive, malignant bone, and soft tissue tumors that predominantly affect children and young adults. These tumors frequently share expression of the EWS-FLI-1 translocation, which is central to tumor survival but not present in healthy cells. In this study, we examined EWS-FLI-1 antigens for their capacity to induce immunity against a range of ESFT types.

designComputer prediction analysis of peptide binding, HLA-A2.1 stabilization assays, and induction of cytotoxic T-lymphocytes (CTL) in immunized HLA-A2.1 transgenic mice were used to assess the immunogenicity of native and modified peptides derived from the fusion region of EWS-FLI-1 type 1. CTL-killing of multiple ESFT family members in vitro, and control of established xenografts in vivo, was assessed. We also examined whether these peptides could induce human CTLs in vitro.

resultsEWS-FLI-1 type 1 peptides were unable to stabilize cell surface HLA-A2.1 and induced weak CTL activity against Ewing sarcoma cells. In contrast, peptides with modified anchor residues induced potent CTL killing of Ewing sarcoma cells presenting endogenous (native) peptides. The adoptive transfer of CTL specific for the modified peptide YLNPSVDSV resulted in enhanced survival of mice with established Ewing sarcoma xenografts. YLNPSVDSV-specific CTL displayed potent killing of multiple ESFT types in vitro: Ewing sarcoma, pPNET, Askin's Tumor, and Biphenotypic sarcoma. Stimulation of human peripheral blood mononuclear cells with YLNPSVDSV peptide resulted in potent CTL-killing.

conclusionsThese data show that YLNPSVDSV peptide is a promising antigen for ESFT immunotherapy and warrants further clinical development.

Indexed as

ImmunotherapyOncogene Proteins, FusionSarcoma, EwingT-Lymphocytes, CytotoxicAdultAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHLA-A2 AntigenHumansLeukocytes, MononuclearMiceMice, TransgenicPeptidesSignal TransductionXenograft Model Antitumor AssaysEWS-FUS protein, humanHLA-A2 AntigenOncogene Proteins, FusionPeptides

Identifiers

PMID22879388
PMCPMC3463738
OpenAlexW2162301936

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Registered trials

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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.