Evidence map›Paper›PMID 37840445›Full record

ReviewCancer medicine2023

Immunomodulatory properties of CD38 antibodies and their effect on anticancer efficacy in multiple myeloma.

Kamlesh Bisht, Taro Fukao, Marielle Chiron, Paul Richardson, Djordje Atanackovic, Eduardo Chini, Wee Joo Chng, Helgi Van De Velde, Fabio Malavasi

Open access · goldAbstract readReview
In one paragraph

Review in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
9.8field-weighted citation impact, top 1% 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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 38 citations in OpenAlex.

  1. Pooled it
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  14. Immunological Disorders: Gradations and the Current Approach in Laboratory Diagnostics.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Review
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  16. Review
  17. Targeting CD38 in Antibody-Mediated Rejection.Transplant international : official journal of the European Society for Organ Transplantation · 2025
    Review
  18. Article
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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

9 authors at 8 institutions in 4 countries.

Kamlesh BishtSanofi Oncology, Cambridge, Massachusetts, USA.
Taro FukaoSanofi Oncology, Cambridge, Massachusetts, USA.
Marielle ChironSanofi Research & Development, Vitry-sur-Seine, France.
Paul RichardsonDepartment of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA.
Djordje AtanackovicUniversity of Maryland Marlene and Stewart Greenebaum Comprehensive Cancer Center, Baltimore, Maryland, USA.
Eduardo ChiniDepartment of Anesthesiology and Perioperative Medicine, Mayo Clinic, Jacksonville, Florida, USA.
Wee Joo ChngCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Helgi Van De VeldeSanofi Oncology, Cambridge, Massachusetts, USA.
Fabio MalavasiDepartment of Medical Sciences, University of Turin, Torino, Italy.
AVEO Oncology (United States) · USDana-Farber Cancer Institute · USFondazione Ricerca Molinette · ITJacksonville College · USNational University of Singapore · SGSanofi (France) · FRSanofi (United States) · USUniversity of Maryland Marlene and Stewart Greenebaum Comprehensive Cancer Center

Funding

Sanofi
6 · The paper itself

Abstract

backgroundCD38 has been established as an important therapeutic target for multiple myeloma (MM), for which two CD38 antibodies are currently approved-daratumumab and isatuximab. CD38 is an ectoenzyme that degrades NAD and its precursors and is involved in the production of adenosine and other metabolites.

aimAmong the various mechanisms by which CD38 antibodies can induce MM cell death is immunomodulation, including multiple pathways for CD38-mediated T-cell activation. Patients who respond to anti-CD38 targeting treatment experience more marked changes in T-cell expansion, activity, and clonality than nonresponders. IMPLICATIONS: Resistance mechanisms that undermine the immunomodulatory effects of CD38-targeting therapies can be tumor intrinsic, such as the downregulation of CD38 surface expression and expression of complement inhibitor proteins, and immune microenvironment-related, such as changes to the natural killer (NK) cell numbers and function in the bone marrow niche. There are numerous strategies to overcome this resistance, which include identifying and targeting other therapeutic targets involved in, for example, adenosine production, the activation of NK cells or monocytes through immunomodulatory drugs and their combination with elotuzumab, or with bispecific T-cell engagers.

Indexed as

Multiple MyelomaAdenosineADP-ribosyl Cyclase 1HumansImmunologic FactorsImmunomodulationTumor MicroenvironmentAdenosineADP-ribosyl Cyclase 1Immunologic Factorsadenosinebone marrow nicheCD38 antibodiesdaratumumabimmunomodulationisatuximabmultiple myeloma

Identifiers

PMID37840445
PMCPMC10652336
OpenAlexW4387662079

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.