Evidence map›Paper›PMID 34568318›Full record

ArticleFrontiers in cell and developmental biology2021

MCL-1 Inhibition Overcomes Anti-apoptotic Adaptation to Targeted Therapies in B-Cell Precursor Acute Lymphoblastic Leukemia.

Albert Manzano-Muñoz, Clara Alcon, Pablo Menéndez, Manuel Ramírez, Felix Seyfried, Klaus-Michael Debatin, Lüder H Meyer, Josep Samitier, Joan Montero

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

8 citing papers in PubMed, 10 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

9 authors at 5 institutions in 2 countries.

Albert Manzano-MuñozInstitute for Bioengineering of Catalonia (IBEC), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
Clara AlconInstitute for Bioengineering of Catalonia (IBEC), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
Pablo MenéndezStem Cell Biology, Developmental Leukemia and Immunotherapy, Josep Carreras Leukemia Research Institute-Campus Clinic, Department of Biomedicine, School of Medicine, University of Barcelona, Barcelona, Spain.
Manuel RamírezDepartment of Pediatric Hematology and Oncology, Niño Jesús University Children's Hospital, Madrid, Spain.
Felix SeyfriedDepartment of Pediatrics and Adolescent Medicine, Ulm University Medical Center, Ulm, Germany.
Klaus-Michael DebatinDepartment of Pediatrics and Adolescent Medicine, Ulm University Medical Center, Ulm, Germany.
Lüder H MeyerDepartment of Pediatrics and Adolescent Medicine, Ulm University Medical Center, Ulm, Germany.
Josep SamitierInstitute for Bioengineering of Catalonia (IBEC), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
Joan MonteroInstitute for Bioengineering of Catalonia (IBEC), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
Institute for Bioengineering of Catalonia · ESUniversität Ulm · DEBiomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine · ESHospital Infantil Universitario Niño Jesús · ESUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple targeted therapies are currently explored for pediatric and young adult B-cell precursor acute lymphoblastic leukemia (BCP-ALL) treatment. However, this new armamentarium of therapies faces an old problem: choosing the right treatment for each patient. The lack of predictive biomarkers is particularly worrying for pediatric patients since it impairs the implementation of new treatments in the clinic. In this study, we used the functional assay dynamic BH3 profiling (DBP) to evaluate two new treatments for BCP-ALL that could improve clinical outcome, especially for relapsed patients. We found that the MEK inhibitor trametinib and the multi-target tyrosine kinase inhibitor sunitinib exquisitely increased apoptotic priming in an NRAS-mutant and in a

Indexed as

apoptosisBH3 mimeticspediatric leukemiaresistancetargeted therapies

Identifiers

PMID34568318
PMCPMC8458912
OpenAlexW3200924307

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.