Evidence map›Paper›PMID 36503430›Full record

ArticleMolecular cancer2022

Intracellular osteopontin protects from autoimmunity-driven lymphoma development inhibiting TLR9-MYD88-STAT3 signaling.

Celeste Rizzello, Valeria Cancila, Sabina Sangaletti, Laura Botti, Chiara Ratti, Matteo Milani, Matteo Dugo, Francesco Bertoni, Claudio Tripodo, Claudia Chiodoni and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 22 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

11 authors at 4 institutions in 2 countries.

Celeste RizzelloMolecular Immunology Unit, Department of Research, Fondazione IRCCS Istituto Nazionale Tumori, Via Venezian 1, 20133, Milan, Italy.
Valeria CancilaTumor Immunology Unit, Department of Health Science, University of Palermo School of Medicine, Palermo, Italy.
Sabina SangalettiMolecular Immunology Unit, Department of Research, Fondazione IRCCS Istituto Nazionale Tumori, Via Venezian 1, 20133, Milan, Italy.
Laura BottiMolecular Immunology Unit, Department of Research, Fondazione IRCCS Istituto Nazionale Tumori, Via Venezian 1, 20133, Milan, Italy.
Chiara RattiMolecular Immunology Unit, Department of Research, Fondazione IRCCS Istituto Nazionale Tumori, Via Venezian 1, 20133, Milan, Italy.
Matteo MilaniMolecular Immunology Unit, Department of Research, Fondazione IRCCS Istituto Nazionale Tumori, Via Venezian 1, 20133, Milan, Italy.
Matteo DugoPlatform of Integrated Biology, Department of Applied Research and Technology Development, Fondazione IRCCS Istituto Nazionale Tumori, Via Venezian 1, 20133, Milan, Italy.
Francesco BertoniInstitute of Oncology Research, Faculty of Biomedical Sciences, USI, Via F. Chiesa 5, 6500, Bellinzona, Switzerland.
Claudio TripodoTumor Immunology Unit, Department of Health Science, University of Palermo School of Medicine, Palermo, Italy.
Claudia Chiodoni *Molecular Immunology Unit, Department of Research, Fondazione IRCCS Istituto Nazionale Tumori, Via Venezian 1, 20133, Milan, Italy. claudia.chiodoni@istitutotumori.mi.it.
Mario P Colombo *Molecular Immunology Unit, Department of Research, Fondazione IRCCS Istituto Nazionale Tumori, Via Venezian 1, 20133, Milan, Italy. mariopaolo.colombo@istitutotumori.mi.it.
Fondazione IRCCS Istituto Nazionale dei Tumori · ITUniversity of Palermo · ITEnte Ospedaliero Cantonale · CHIRCCS Ospedale San Raffaele · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutoimmune disorders, including Systemic Lupus Erythematosus (SLE), are associated with increased incidence of hematological malignancies. The matricellular protein osteopontin (OPN) has been linked to SLE pathogenesis, as SLE patients show increased serum levels of OPN and often polymorphisms in its gene. Although widely studied for its pro-tumorigenic role in different solid tumours, the role of OPN in autoimmunity-driven lymphomagenesis has not been investigated yet.

methodsTo test the role of OPN in the SLE-associated lymphomagenesis, the SLE-like prone Fas

resultsDespite reduced autoimmunity signs, OPN-/-Fas

conclusionThese data indicate that, in the setting of SLE-like syndrome in which double strand-DNA chronically circulates and activates TLRs, B cell intracellular OPN exerts a protective role in autoimmunity-driven DLBCL development, mainly acting as a brake in the TLR9-MYD88-STAT3 signaling pathway.

Indexed as

Autoimmune DiseasesLupus Erythematosus, SystemicLymphomaAdaptor Proteins, Signal TransducingAnimalsHumansMiceMice, Inbred C57BLMice, Inbred MRL lprMyeloid Differentiation Factor 88Signal TransductionSTAT3 Transcription FactorToll-Like Receptor 9Adaptor Proteins, Signal TransducingMyd88 protein, mouseMyeloid Differentiation Factor 88STAT3 protein, humanSTAT3 Transcription FactorTLR9 protein, humanTlr9 protein, mouseToll-Like Receptor 9AutoimmunityDiffuse large B cell lymphomaOsteopontin

Identifiers

PMID36503430
PMCPMC9743519
OpenAlexW4311125273

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.