Evidence map›Paper›PMID 24130880›Full record

ArticlePloS one2013

Targeting c-MYC with T-cells.

Florian Helm, Thomas Kammertoens, Frank M Lehmann, Andrea Wilke, Heiko Bruns, Josef Mautner, Georg W Bornkamm, Armin Gerbitz

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Strategies to Inhibit Myc and Their Clinical Applicability.Frontiers in cell and developmental biology · 2017
    Review
  4. Review
  5. 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

8 authors at 3 institutions in 1 country.

Florian HelmDepartment of Immunology, Charité Berlin, Berlin, Germany.
Thomas Kammertoens
Frank M Lehmann
Andrea Wilke
Heiko Bruns
Josef Mautner
Georg W Bornkamm
Armin Gerbitz
Charité - Universitätsmedizin Berlin · DEHelmholtz Zentrum München · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over-expression of the proto-oncogene c-MYC is frequently observed in a variety of tumors and is a hallmark of Burkitt´s lymphoma. The fact that many tumors are oncogene-addicted to c-MYC, renders c-MYC a powerful target for anti-tumor therapy. Using a xenogenic vaccination strategy by immunizing C57BL/6 mice with human c-MYC protein or non-homologous peptides, we show that the human c-MYC protein, despite its high homology between mouse and man, contains several immunogenic epitopes presented in the context of murine H2(b) haplotype. We identified an MHC class II-restricted CD4⁺ T-cell epitope and therein an MHC class I-restricted CD8⁺ T-cell epitope (SSPQGSPEPL) that, after prime/boost immunization, protected up to 25% of mice against a lethal lymphoma challenge. Lymphoma-rejecting animals contained MHC multimer-binding CD8⁺ cell within the peripheral blood and displayed in vivo cytolytic activity with specificity for SSPQGSPEPL. Taken together these data suggest that oncogenic c-MYC can be targeted with specific T-cells.

Indexed as

Amino Acid SequenceAnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesEpitopes, T-LymphocyteHumansInterferon-gammaLymphomaMiceMice, Inbred C57BLProto-Oncogene MasProto-Oncogene Proteins c-mycVaccinationEpitopes, T-LymphocyteInterferon-gammaMAS1 protein, humanMYC protein, humanProto-Oncogene MasProto-Oncogene Proteins c-myc

Identifiers

PMID24130880
PMCPMC3795085
OpenAlexW2150782606

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.