Evidence map›Paper›PMID 38125947›Full record

ArticleFrontiers in oncology2023

Combined inhibition of Wee1 and Chk1 as a therapeutic strategy in multiple myeloma.

Angélique Bruyer, Laure Dutrieux, Hugues de Boussac, Thibaut Martin, Djamila Chemlal, Nicolas Robert, Guilhem Requirand, Guillaume Cartron, Laure Vincent, Charles Herbaux and 5 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

7 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 4 institutions in 1 country.

Angélique Bruyer *Diag2Tec, Montpellier, France.
Laure Dutrieux *Institute of Human Genetics, UMR CNRS-UM 9002, Montpellier, France.
Hugues de BoussacDiag2Tec, Montpellier, France.
Thibaut MartinInstitute of Human Genetics, UMR CNRS-UM 9002, Montpellier, France.
Djamila ChemlalDiag2Tec, Montpellier, France.
Nicolas RobertDepartment of Biological Hematology, CHU Montpellier, Montpellier, France.
Guilhem RequirandDepartment of Biological Hematology, CHU Montpellier, Montpellier, France.
Guillaume CartronDepartment of Clinical Hematology, CHU Montpellier, Montpellier, France.
Laure VincentDepartment of Clinical Hematology, CHU Montpellier, Montpellier, France.
Charles HerbauxInstitute of Human Genetics, UMR CNRS-UM 9002, Montpellier, France.
Malik LutzmannInstitute of Human Genetics, UMR CNRS-UM 9002, Montpellier, France.
Caroline BretInstitute of Human Genetics, UMR CNRS-UM 9002, Montpellier, France.
Philippe PaseroInstitute of Human Genetics, UMR CNRS-UM 9002, Montpellier, France.
Jérôme Moreaux *Institute of Human Genetics, UMR CNRS-UM 9002, Montpellier, France.
Sara Ovejero *Institute of Human Genetics, UMR CNRS-UM 9002, Montpellier, France.
Centre Hospitalier Universitaire de Montpellier · FRCentre National de la Recherche Scientifique · FRInstitut de Génétique Humaine · FRUniversité de Montpellier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) is a hematological malignancy characterized by an abnormal clonal proliferation of malignant plasma cells. Despite the introduction of novel agents that have significantly improved clinical outcome, most patients relapse and develop drug resistance. MM is characterized by genomic instability and a high level of replicative stress. In response to replicative and DNA damage stress, MM cells activate various DNA damage signaling pathways. In this study, we reported that high

Indexed as

Chk1multiple myelomareplicative stresstherapeutic targetsWee1

Identifiers

PMID38125947
PMCPMC10730928
OpenAlexW4389393365

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.