Evidence map›Paper›PMID 33924378›Full record

ArticleCancers2021

Murlentamab, a Low Fucosylated Anti-Müllerian Hormone Type II Receptor (AMHRII) Antibody, Exhibits Anti-Tumor Activity through Tumor-Associated Macrophage Reprogrammation and T Cell Activation.

Mélissa Prat, Marie Salon, Thibault Allain, Olivier Dubreuil, Grégory Noël, Laurence Preisser, Bérangère Jean, Lydie Cassard, Fanny Lemée, Isabelle Tabah-Fish and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 43% 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

10 citing papers in PubMed, 8 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

15 authors at 5 institutions in 2 countries.

Mélissa PratUMR 152 Pharma Dev, Université de Toulouse, IRD, UPS, 31062 Toulouse, France.
Marie SalonUMR 152 Pharma Dev, Université de Toulouse, IRD, UPS, 31062 Toulouse, France.
Thibault AllainUMR 152 Pharma Dev, Université de Toulouse, IRD, UPS, 31062 Toulouse, France.
Olivier DubreuilGamaMabs Pharma, 31106 Toulouse, France.
Grégory NoëlInstitut Jules Bordet, Université Libre de Bruxelles, 1000 Brussels, Belgium.
Laurence PreisserUniv Angers, Université de Nantes, CHU Angers, Inserm, CRCINA, SFR ICAT, 49000 Angers, France.
Bérangère JeanGamaMabs Pharma, 31106 Toulouse, France.
Lydie CassardLaboratory of Immunomonitoring in Oncology, Gustave Roussy, 94905 Villejuif, France.ORCID 0000-0001-8373-041X
Fanny LeméeGamaMabs Pharma, 31106 Toulouse, France.
Isabelle Tabah-FishGamaMabs Pharma, 31106 Toulouse, France.
Bernard PipyUMR 152 Pharma Dev, Université de Toulouse, IRD, UPS, 31062 Toulouse, France.
Pascale JeanninUniv Angers, Université de Nantes, CHU Angers, Inserm, CRCINA, SFR ICAT, 49000 Angers, France.
Jean-François ProstGamaMabs Pharma, 31106 Toulouse, France.
Jean-Marc BarretGamaMabs Pharma, 31106 Toulouse, France.ORCID 0000-0001-8085-3422
Agnès CosteUMR 152 Pharma Dev, Université de Toulouse, IRD, UPS, 31062 Toulouse, France.ORCID 0000-0001-7781-3323
Centre National de la Recherche Scientifique · FRInserm · FRUniversité Toulouse III - Paul Sabatier · FRInstitut Gustave Roussy · FRUniversité Libre de Bruxelles · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AMHRII, the anti-Müllerian hormone receptor, is selectively expressed in normal sexual organs but is also re-expressed in gynecologic cancers. Hence, we developed murlentamab, a humanized glyco-engineered anti-AMHRII monoclonal antibody currently in clinical trial. Low-fucosylated antibodies are known to increase the antibody-dependent cell-mediated cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP) potency of effector cells, but some preliminary results suggest a more global murlentamab-dependent activation of the immune system. In this context, we demonstrate here that the murlentamab opsonization of AMHRII-expressing ovarian tumor cells, in the presence of unstimulated- or tumor-associated macrophage (TAM)-like macrophages, significantly promotes macrophage-mediated ADCC and shifts the whole microenvironment towards a pro-inflammatory and anti-tumoral status, thus triggering anti-tumor activity. We also report that murlentamab orients both unstimulated- and TAM-like macrophages to an M1-like phenotype characterized by a strong expression of co-stimulation markers, pro-inflammatory cytokines and chemokines, favoring T cell recruitment and activation. Moreover, we show that murlentamab treatment shifts CD4

Indexed as

adaptive immunityglyco-engineered antibodyimmunotherapymurlentamabovarian cancertumor-associated macrophages

Identifiers

PMID33924378
PMCPMC8070390
OpenAlexW3156822015

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.