Evidence map›Paper›PMID 22086231›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2012

An artificial PAP gene breaks self-tolerance and promotes tumor regression in the TRAMP model for prostate carcinoma.

Elmar Spies, Wilfried Reichardt, Gerardo Alvarez, Marcus Groettrup, Peter Ohlschläger

Open access · bronzeAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

7 citing papers in PubMed, 15 citations in OpenAlex.

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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

5 authors at 4 institutions in 2 countries.

Elmar SpiesDivision of Immunology, Department of Biology, University of Constance, Constance, Germany. elmar.spies@uni-konstanz.de
Wilfried Reichardt
Gerardo Alvarez
Marcus Groettrup
Peter Ohlschläger
Biotechnology Institute Thurgau · CHFH Aachen · DEUniversity Medical Center Freiburg · DEUniversity of Konstanz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PCa) is the most commonly diagnosed type of cancer in men in western industrialized countries. As a public health burden, the need for the invention of new cost-saving PCa immunotherapies is apparent. In this study, we present a DNA vaccine encoding for the prostate-specific antigen prostatic acid phosphatase (PAP) linked to the J-domain and the SV40 enhancer sequence. The PAP DNA vaccine induced a strong PAP-specific cellular immune response after electroporation (EP)-based delivery in C57BL/6 mice. Splenocytes from mice immunized with PAP recognized the naturally processed PAP epitopes, indicating that vaccination with the PAP-J gene broke its self-tolerance against PAP. Remarkably, DNA vaccination with PAP-J inhibited tumor growth in the Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) mouse model that closely resembled human PCa. Therefore, this study highlights a novel cancer immunotherapy approach with the potential to control PCa in clinical settings.

Indexed as

Acid PhosphataseAmino Acid MotifsAmino Acid SequenceAnimalsAntibodiesAntigens, NeoplasmCancer VaccinesCell LineDisease Models, AnimalDisease ProgressionEpitopesGenetic VectorsH-2 AntigensMaleMiceMice, Inbred C57BLAcid PhosphataseAntibodiesAntigens, NeoplasmCancer VaccinesEpitopesH-2 AntigensPeptidesprostatic acid phosphataseProtein Tyrosine PhosphatasesVaccines, DNA

Identifiers

PMID22086231
PMCPMC3293618
OpenAlexW1984421040

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.