Evidence map›Paper›PMID 36964168›Full record

ArticleCell death & disease2023

Type I interferon signaling in malignant blasts contributes to treatment efficacy in AML patients.

Peter Holicek, Iva Truxova, Jana Rakova, Cyril Salek, Michal Hensler, Marek Kovar, Milan Reinis, Romana Mikyskova, Josef Pasulka, Sarka Vosahlikova and 10 more

Open access · goldFull text read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Refining favorable-risk classification in pediatricBlood science (Baltimore, Md.) · 2026
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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

20 authors at 7 institutions in 3 countries.

Peter HolicekSotio Biotech, Prague, Czech Republic.ORCID 0000-0002-0268-4915
Iva TruxovaSotio Biotech, Prague, Czech Republic.
Jana RakovaSotio Biotech, Prague, Czech Republic.
Cyril SalekInstitute of Hematology and Blood Transfusion, Prague, Czech Republic.
Michal HenslerSotio Biotech, Prague, Czech Republic.
Marek KovarLaboratory of Tumor Immunology, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czech Republic.
Milan ReinisLaboratory of Immunological and Tumour Models, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Romana MikyskovaLaboratory of Immunological and Tumour Models, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Josef PasulkaSotio Biotech, Prague, Czech Republic.
Sarka VosahlikovaSotio Biotech, Prague, Czech Republic.
Hana RemesovaInstitute of Hematology and Blood Transfusion, Prague, Czech Republic.
Iva ValentovaSotio Biotech, Prague, Czech Republic.
Daniel LysakDepartment of Hematology and Oncology, Faculty Hospital in Pilsen, Pilsen, Czech Republic.
Monika HolubovaBiomedical Center, Medical Faculty in Pilsen, Charles University, Pilsen, Czech Republic.
Petr KasparCzech Centre for Phenogenomics, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Jan ProchazkaCzech Centre for Phenogenomics, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Lenka KasikovaSotio Biotech, Prague, Czech Republic.
Radek SpisekSotio Biotech, Prague, Czech Republic.
Lorenzo GalluzziDepartment of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA. deadoc80@gmail.com.ORCID 0000-0003-2257-8500
Jitka FucikovaSotio Biotech, Prague, Czech Republic. fucikova@sotio.com.ORCID 0000-0002-8423-479X
Charles University · CZSotio (Czechia) · CZCzech Academy of Sciences, Institute of Molecular Genetics · CZCornell University · USCzech Academy of Sciences · CZInstitute of Haematology and Blood Transfusion · CZPilsen Tools (Czechia) · CZ

Funding

Radiation Effect on Immune Cells and the MicrobiomeU54CA274291 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI Joseph O Deasy · 2022 to 2026
$9.1M
NCI NIH HHS U54 CA274291
6 · The paper itself

Abstract

While type I interferon (IFN) is best known for its key role against viral infection, accumulating preclinical and clinical data indicate that robust type I IFN production in the tumor microenvironment promotes cancer immunosurveillance and contributes to the efficacy of various antineoplastic agents, notably immunogenic cell death inducers. Here, we report that malignant blasts from patients with acute myeloid leukemia (AML) release type I IFN via a Toll-like receptor 3 (TLR3)-dependent mechanism that is not driven by treatment. While in these patients the ability of type I IFN to stimulate anticancer immune responses was abolished by immunosuppressive mechanisms elicited by malignant blasts, type I IFN turned out to exert direct cytostatic, cytotoxic and chemosensitizing activity in primary AML blasts, leukemic stem cells from AML patients and AML xenograft models. Finally, a genetic signature of type I IFN signaling was found to have independent prognostic value on relapse-free survival and overall survival in a cohort of 132 AML patients. These findings delineate a clinically relevant, therapeutically actionable and prognostically informative mechanism through which type I IFN mediates beneficial effects in patients with AML.

Indexed as

Antineoplastic AgentsInterferon Type ILeukemia, Myeloid, AcuteHumansSignal TransductionTreatment OutcomeTumor MicroenvironmentAntineoplastic AgentsInterferon Type I

Identifiers

PMID36964168
PMCPMC10039058
OpenAlexW4360861214

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read59
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.