Evidence map›Paper›PMID 36270731›Full record

ReviewJournal for immunotherapy of cancer2022

Combining precision oncology and immunotherapy by targeting the MALT1 protease.

Thorsten R Mempel, Daniel Krappmann

Open access · goldAbstract readReview
In one paragraph

Review in Journal for immunotherapy of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  6. Review
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  15. Review
  16. Article
  17. MALT1 substrate cleavage: what is it good for?Frontiers in immunology · 2024
    Review
  18. Unrestrained cleavage of Roquin-1 by MALT1 induces spontaneous T cell activation and the development of autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  19. Translational Studies Using the MALT1 Inhibitor (Journal of immunotherapy and precision oncology · 2023
    Article
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

2 authors at 2 institutions in 2 countries.

Thorsten R MempelCenter for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, Massachusetts, USA tmempel@mgh.harvard.edu daniel.krappmann@helmholtz-muenchen.de.ORCID 0000-0001-8635-5424
Daniel KrappmannResearch Unit Cellular Signal Integration, Molecular Targets and Therapeutics Center, Helmholtz Center Munich - German Research Center for Environmental Health, Neuherberg, Germany tmempel@mgh.harvard.edu daniel.krappmann@helmholtz-muenchen.de.ORCID 0000-0001-7640-3234
Harvard University · USHelmholtz Zentrum München · DE

Funding

Strategies to Overcome Immune Resistance in Head and Neck CancersP01CA240239 · NCI · YALE UNIVERSITY · PI SARTOR, MAUREEN AGNES · 2019 to 2023
$8.4M
Cellular mechanisms by which exhausted T cell responses are restoredR01AI123349 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI Thorsten Roman Mempel · 2017 to 2026
$4.5M
NCI NIH HHS P01 CA240239NIAID NIH HHS R01 AI123349
6 · The paper itself

Abstract

An innovative strategy for cancer therapy is to combine the inhibition of cancer cell-intrinsic oncogenic signaling with cancer cell-extrinsic immunological activation of the tumor microenvironment (TME). In general, such approaches will focus on two or more distinct molecular targets in the malignant cells and in cells of the surrounding TME. In contrast, the protease Mucosa-associated lymphoid tissue protein 1 (MALT1) represents a candidate to enable such a dual approach by engaging only a single target. Originally identified and now in clinical trials as a lymphoma drug target based on its role in the survival and proliferation of malignant lymphomas addicted to chronic B cell receptor signaling, MALT1 proteolytic activity has recently gained additional attention through reports describing its tumor-promoting roles in several types of non-hematological solid cancer, such as breast cancer and glioblastoma. Besides cancer cells, regulatory T (Treg) cells in the TME are particularly dependent on MALT1 to sustain their immune-suppressive functions, and MALT1 inhibition can selectively reprogram tumor-infiltrating Treg cells into Foxp3-expressing proinflammatory antitumor effector cells. Thereby, MALT1 inhibition induces local inflammation in the TME and synergizes with anti-PD-1 checkpoint blockade to induce antitumor immunity and facilitate tumor control or rejection. This new concept of boosting tumor immunotherapy in solid cancer by MALT1 precision targeting in the TME has now entered clinical evaluation. The dual effects of MALT1 inhibitors on cancer cells and immune cells therefore offer a unique opportunity for combining precision oncology and immunotherapy to simultaneously impair cancer cell growth and neutralize immunosuppression in the TME. Further, MALT1 targeting may provide a proof of concept that modulation of Treg cell function in the TME represents a feasible strategy to augment the efficacy of cancer immunotherapy. Here, we review the role of MALT1 protease in physiological and oncogenic signaling, summarize the landscape of tumor indications for which MALT1 is emerging as a therapeutic target, and consider strategies to increase the chances for safe and successful use of MALT1 inhibitors in cancer therapy.

Indexed as

NeoplasmsForkhead Transcription FactorsHumansImmunotherapyMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinPeptide HydrolasesPrecision MedicineReceptors, Antigen, B-CellTumor MicroenvironmentForkhead Transcription FactorsMALT1 protein, humanMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinPeptide HydrolasesReceptors, Antigen, B-CellLymphocyte ActivationLymphocytes, Tumor-InfiltratingProgrammed Cell Death 1 ReceptorT-LymphocytesTumor Microenvironment

Identifiers

PMID36270731
PMCPMC9594517
OpenAlexW4307046644

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.