Evidence map›Paper›PMID 41965886›Full record

ArticleCommunications medicine2026

An integrative molecular map of pediatric B-cell precursor acute lymphoblastic leukemia.

Olga Krali, Anna Pia Enblad, Julia Sulyaeva, Dea Gogishvili, Anders Lundmark, Arja Harila, Claes Andersson, Tom Erkers, Merja Heinäniemi, Gudmar Lönnerholm and 1 more

Abstract read
In one paragraph

Article in Communications medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

11 authors.

Olga KraliDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.ORCID http://orcid.org/0000-0002-6436-9531
Anna Pia EnbladDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Julia SulyaevaDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Dea GogishviliDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Anders LundmarkDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Arja HarilaDepartment of Women's and Children's Health, Uppsala University, Uppsala, Sweden.
Claes AnderssonDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Tom ErkersDepartment of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.
Merja HeinäniemiInstitute of Biomedicine, School of Medicine, University of Eastern Finland, Kuopio, Finland.ORCID http://orcid.org/0000-0001-6190-3439
Gudmar LönnerholmDepartment of Women's and Children's Health, Uppsala University, Uppsala, Sweden.
Jessica NordlundDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden. jessica.nordlund@medsci.uu.se.ORCID http://orcid.org/0000-0001-8699-9959

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe molecular landscape of pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL) has been extensively characterized through single-modality studies. However, the interplay between molecular modalities and their collective influence on treatment response and outcomes remains poorly understood.

methodsWe integrated genomic, epigenomic, transcriptomic, and ex vivo drug response data from 1231 patients diagnosed with BCP-ALL. Using Multi-Omics Factor Analysis, we identified signatures explaining key aspects of the integrative molecular landscape, referred to as cross-modal elements (CMEs). The CME-derived signatures were introduced into pathway and intermodal network analyses, while their impact on patient outcomes was assessed through survival modeling.

resultsPathway and network analyses annotate the resulting integrative CMEs, linking them to key biological processes, including disease development, cellular regulatory processes, metabolic pathways, and drug response. By leveraging correlations between DNA methylation and ex vivo response to doxorubicin, we stratify patients with hyperdiploidy into subgroups that differ in relapse-free survival. These signatures are independent of clinical variables. Survival models incorporating CME-selected ex-vivo drug responses combined with clinical data improve risk prediction compared to clinical models alone (FDR < 0.05), demonstrating the potential of integrative multiomics in refining risk stratification.

conclusionsOur study highlights the importance of multimodal data integration in BCP-ALL to provide biological insights with potential relevance for precision medicine.

Identifiers

PMID41965886
PMCPMC13079846

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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.