Evidence map›Paper›PMID 25992555›Full record

ArticlePloS one2015

Altered HLA Class I Profile Associated with Type A/D Nucleophosmin Mutation Points to Possible Anti-Nucleophosmin Immune Response in Acute Myeloid Leukemia.

Kateřina Kuželová, Barbora Brodská, Ota Fuchs, Marie Dobrovolná, Petr Soukup, Petr Cetkovský

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

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  9. Oncoimmunology · 2022
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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

6 authors at 1 institution in 1 country.

Kateřina KuželováDepartment of Proteomics, Institute of Hematology and Blood Transfusion, Prague, Czech Republic.
Barbora BrodskáDepartment of Proteomics, Institute of Hematology and Blood Transfusion, Prague, Czech Republic.
Ota FuchsDepartment of Genomics, Institute of Hematology and Blood Transfusion, Prague, Czech Republic.
Marie DobrovolnáDepartment of HLA, Institute of Hematology and Blood Transfusion, Prague, Czech Republic.
Petr SoukupClinical Department, Institute of Hematology and Blood Transfusion, Prague, Czech Republic.
Petr CetkovskýClinical Department, Institute of Hematology and Blood Transfusion, Prague, Czech Republic.
Institute of Haematology and Blood Transfusion · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nucleophosmin 1 (NPM1) mutations are frequently found in patients with acute myeloid leukemia (AML) and the newly generated sequences were suggested to induce immune response contributing to the relatively favorable outcome of patients in this AML subset. We hypothesized that if an efficient immune response against mutated nucleophosmin can be induced in vivo, the individuals expressing HLA alleles suitable for presenting NPM-derived peptides should be less prone to developing AML associated with NPM1 mutation. We thus compared HLA class I frequencies in a cohort of patients with mutated NPM1 (63 patients, NPMc+), a cohort of patients with wild-type NPM1 (94 patients, NPMwt) and in normal individuals (large datasets available from Allele Frequency Net Database). Several HLA allelic groups were found to be depleted in NPMc+ patients, but not in NPMwt compared to the normal distribution. The decrease was statistically significant for HLA B(*)07, B(*)18, and B(*)40. Furthermore, statistically significant advantage in the overall survival was found for patients with mutated NPM1 expressing at least one of the depleted allelic groups. The majority of the depleted alleles were predicted to bind potent NPM-derived immunopeptides and, importantly, these peptides were often located in the unmutated part of the protein. Our analysis suggests that individuals expressing specific HLA allelic groups are disposed to develop an efficient anti-AML immune response thanks to aberrant cytoplasmic localization of the mutated NPM protein.

Indexed as

ImmunityAmino Acid SequenceCase-Control StudiesHistocompatibility Antigens Class IHumansLeukemia, Myeloid, AcuteMiddle AgedMolecular Sequence DataMutant ProteinsMutationNuclear ProteinsNucleophosminPeptidesSurvival AnalysisHistocompatibility Antigens Class IMutant ProteinsNPM1 protein, humanNuclear ProteinsNucleophosminPeptides

Identifiers

PMID25992555
PMCPMC4439052
OpenAlexW1519889213

What OpenQuestion holds

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LicenceCC BY
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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.