Evidence map›Paper›PMID 30203262›Full record

ReviewCancer immunology, immunotherapy : CII2018

Oncogenic MYD88 mutations in lymphoma: novel insights and therapeutic possibilities.

Alexander N R Weber, Yamel Cardona Gloria, Özcan Çınar, H Christian Reinhardt, Antonio Pezzutto, Olaf-Oliver Wolz

Open access · greenAbstract readReview
In one paragraph

Review in Cancer immunology, immunotherapy : CII, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

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  17. Absence of Non-Canonical, InhibitoryFrontiers in immunology · 2021
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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 3 institutions in 2 countries.

Alexander N R WeberInterfaculty Institute for Cell Biology, Department of Immunology, University of Tübingen, Auf der Morgenstelle 15, 72076, Tübingen, Germany. alexander.weber@uni-tuebingen.de.ORCID http://orcid.org/0000-0002-8627-7056
Yamel Cardona GloriaInterfaculty Institute for Cell Biology, Department of Immunology, University of Tübingen, Auf der Morgenstelle 15, 72076, Tübingen, Germany.
Özcan ÇınarInterfaculty Institute for Cell Biology, Department of Immunology, University of Tübingen, Auf der Morgenstelle 15, 72076, Tübingen, Germany.
H Christian ReinhardtClinic I of Internal Medicine, University Hospital of Cologne, Cologne, Germany.
Antonio PezzuttoBerlin Institute for Health Charité and Max-Delbrück Center, Campus Buch, Building 42-53, Lindenberger Weg 80, 13125, Berlin, Germany.
Olaf-Oliver WolzInterfaculty Institute for Cell Biology, Department of Immunology, University of Tübingen, Auf der Morgenstelle 15, 72076, Tübingen, Germany. oliver.wolz@uni-tuebingen.de.
University of Tübingen · DEMax Delbrück Center · DEUniversity of Cologne · DE

Funding

Deutsche Forschungsgemeinschaft SFB 685 "Immunotherapy"Medizinischen Fakultät, Eberhard Karls Universität Tübingen (DE) Fortüne Junior GrantMinisterium für Wissenschaft, Forschung und Kunst Baden-Württemberg Juniorprofessoren-Programm
6 · The paper itself

Abstract

Oncogenic MYD88 mutations, most notably the Leu 265 Pro (L265P) mutation, were recently identified as potential driver mutations in various B-cell non-Hodgkin Lymphomas (NHLs). The L265P mutation is now thought to be common to virtually all NHLs and occurs in between 4 and 90% of cases, depending on the entity. Since it is tumor-specific, the mutation, and the pathways it regulates, might serve as advantageous therapeutic targets for both conventional chemotherapeutic intervention, as well as immunotherapeutic strategies. Here, we review recent progress on elucidating the molecular and cellular processes affected by the L265P mutation of MYD88, describe a new in vivo model for MyD88 L265P-mediated oncogenesis, and summarize how these findings could be exploited therapeutically by specific targeting of signaling pathways. In addition, we summarize current and explore future possibilities for conceivable immunotherapeutic approaches, such as L265P-derived peptide vaccination, adoptive transfer of L265P-restricted T cells, and use of T-cell receptor-engineered T cells. With clinical trials regarding their efficacy rapidly expanding to NHLs, we also discuss potential combinations of immune checkpoint inhibitors with the described targeted chemotherapies of L265P signaling networks, and/or with the above immunological approaches as potential ways of targeting MYD88-mutated lymphomas in the future.

Indexed as

Molecular Targeted TherapyMutationAntineoplastic AgentsHumansLymphomaMyeloid Differentiation Factor 88Antineoplastic AgentsMYD88 protein, humanMyeloid Differentiation Factor 88Diffuse large B-cell lymphoma (DLBCL)ImmunotherapyMyD88Non-Hodgkin lymphomaToll-like receptorWaldenström’s macroglobulinemia

Identifiers

PMID30203262
PMCPMC11028221
OpenAlexW2891559729

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.