Evidence map›Paper›PMID 30079070›Full record

ArticleFrontiers in immunology2018

CD38 as Immunotherapeutic Target in Light Chain Amyloidosis and Multiple Myeloma-Association With Molecular Entities, Risk, Survival, and Mechanisms of Upfront Resistance.

Anja Seckinger, Jens Hillengass, Martina Emde, Susanne Beck, Christoph Kimmich, Tobias Dittrich, Michael Hundemer, Anna Jauch, Ute Hegenbart, Marc-Steffen Raab and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 44 citations in OpenAlex.

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  15. Molecular Mechanisms of Cardiac Amyloidosis.International journal of molecular sciences · 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

13 authors at 2 institutions in 1 country.

Anja SeckingerMedizinische Klinik V, Universitätsklinikum Heidelberg, Heidelberg, Germany.
Jens HillengassMedizinische Klinik V, Universitätsklinikum Heidelberg, Heidelberg, Germany.
Martina EmdeMedizinische Klinik V, Universitätsklinikum Heidelberg, Heidelberg, Germany.
Susanne BeckMedizinische Klinik V, Universitätsklinikum Heidelberg, Heidelberg, Germany.
Christoph KimmichMedizinische Klinik V, Universitätsklinikum Heidelberg, Heidelberg, Germany.
Tobias DittrichMedizinische Klinik V, Universitätsklinikum Heidelberg, Heidelberg, Germany.
Michael HundemerMedizinische Klinik V, Universitätsklinikum Heidelberg, Heidelberg, Germany.
Anna JauchInstitut für Humangenetik, Universität Heidelberg, Heidelberg, Germany.
Ute HegenbartMedizinische Klinik V, Universitätsklinikum Heidelberg, Heidelberg, Germany.
Marc-Steffen RaabMedizinische Klinik V, Universitätsklinikum Heidelberg, Heidelberg, Germany.
Anthony D HoMedizinische Klinik V, Universitätsklinikum Heidelberg, Heidelberg, Germany.
Stefan SchönlandMedizinische Klinik V, Universitätsklinikum Heidelberg, Heidelberg, Germany.
Dirk HoseMedizinische Klinik V, Universitätsklinikum Heidelberg, Heidelberg, Germany.
Heidelberg University · DEUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Monoclonal antibodies against the cell surface antigen CD38, e.g., isatuximab, daratumumab, or Mor202, have entered the therapeutic armamentarium in multiple myeloma due to single agent overall response rates of 29 vs. 36 vs. 31%, effectivity in combination regimen, e.g., with lenalidomide or bortezomib plus dexamethasone, and tolerable side effects. Despite clinical use, many questions remain. In this manuscript, we address three of these: first, upfront CD38 target-expression in AL-amyloidosis, monoclonal gammopathy of unknown significance (MGUS), asymptomatic, symptomatic, and relapsed multiple myeloma. Second, relation of CD38-expression to survival, disease stages, molecular entities, and high-risk definitions. Third, alternative splicing or lack of CD38-expression as potential mechanisms of upfront resistance. We assessed CD138-purified plasma cell samples from 196 AL-amyloidosis, 62 MGUS, 259 asymptomatic, 764 symptomatic, and 90 relapsed myeloma patients, including longitudinal pairs of asymptomatic/symptomatic (

Indexed as

alternative splicingamyloidosisCD38immunotherapymultiple myelomasurvival

Identifiers

PMID30079070
PMCPMC6062598
OpenAlexW2883541595

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.