Evidence map›Paper›PMID 37143651›Full record

ArticleFrontiers in immunology2023

Insights into IGH clonal evolution in BCP-ALL: frequency, mechanisms, associations, and diagnostic implications.

Franziska Darzentas, Monika Szczepanowski, Michaela Kotrová, Alina Hartmann, Thomas Beder, Nicola Gökbuget, Stefan Schwartz, Lorenz Bastian, Claudia Dorothea Baldus, Karol Pál and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 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
2.6field-weighted citation impact, top 11% 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, 9 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

12 authors at 6 institutions in 2 countries.

Franziska DarzentasMedical Department II, Hematology and Oncology, University Hospital Schleswig-Holstein, Kiel, Germany.
Monika SzczepanowskiMedical Department II, Hematology and Oncology, University Hospital Schleswig-Holstein, Kiel, Germany.
Michaela KotrováMedical Department II, Hematology and Oncology, University Hospital Schleswig-Holstein, Kiel, Germany.
Alina HartmannMedical Department II, Hematology and Oncology, University Hospital Schleswig-Holstein, Kiel, Germany.
Thomas BederMedical Department II, Hematology and Oncology, University Hospital Schleswig-Holstein, Kiel, Germany.
Nicola GökbugetDepartment of Medicine II, Hematology/Oncology, Goethe University Hospital, Frankfurt/M, Germany.
Stefan SchwartzDepartment of Hematology, Oncology and Tumor Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Lorenz BastianMedical Department II, Hematology and Oncology, University Hospital Schleswig-Holstein, Kiel, Germany.
Claudia Dorothea BaldusMedical Department II, Hematology and Oncology, University Hospital Schleswig-Holstein, Kiel, Germany.
Karol PálCentral European Institute of Technology, Masaryk University, Brno, Czechia.
Nikos DarzentasMedical Department II, Hematology and Oncology, University Hospital Schleswig-Holstein, Kiel, Germany.
Monika BrüggemannMedical Department II, Hematology and Oncology, University Hospital Schleswig-Holstein, Kiel, Germany.
University Hospital Schleswig-Holstein · DEUniversity of Lübeck · DEDeutsche Forschungsgemeinschaft · DECentral European Institute of Technology – Masaryk University · CZCharité - Universitätsmedizin Berlin · DEUniversity Hospital Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: The malignant transformation leading to a maturation arrest in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) occurs early in B-cell development, in a pro-B or pre-B cell, when somatic recombination of variable (V), diversity (D), and joining (J) segment immunoglobulin (IG) genes and the B-cell rescue mechanism of V Methods: Utilizing high-throughput sequencing assays and bespoke bioinformatics we identified BCP-ALL-derived clonally-related IGH sequences by their shared 'DNJ-stem'. Results: We introduce the concept of 'marker DNJ-stem' to cover the entirety of, even lowly abundant, clonally-related family members. In a cohort of 280 adult patients with BCP-ALL, IGH clonal evolution at diagnosis was identified in one-third of patients. The phenomenon was linked to contemporaneous recombinant and editing activity driven by aberrant ongoing D Discussion: Consequently, we suggest to follow the marker DNJ-stem (capturing all family members) rather than specific clonotypes as the MRD target, as well as to follow both VDJ

Indexed as

Burkitt LymphomaPrecursor B-Cell Lymphoblastic Leukemia-LymphomaAdultBone MarrowGenes, ImmunoglobulinHumansPolymerase Chain Reactionacute lymphoblastic leukemiaclonal evolutionDNJ-stemhigh-throughput sequencingIGH rearrangementsminimal residual diseaseVH replacement

Identifiers

PMID37143651
PMCPMC10151743
OpenAlexW4366290719

What OpenQuestion holds

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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.