Evidence map›Paper›PMID 41701537›Full record

ArticleJCI insight2026

Deletion of 9p drives B-ALL through heterozygous inactivation of Pax5 and Cd72 in preleukemic cells.

Belén Ruiz-Corzo, Ana Casado-García, Ninad Oak, Paula Somoza-Cotillas, Andrea López-Álvarez de Neyra, Jorge Martínez-Cano, Alba Pérez-Pons, Elena G Sánchez, Oscar Blanco, Diego Alonso-López and 11 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JCI insight, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

21 authors.

Belén Ruiz-CorzoExperimental Therapeutics and Translational Oncology Program, Instituto de Biología Molecular y Celular del Cáncer, CSIC-USAL, Campus M. de Unamuno s/n, Salamanca, Spain.
Ana Casado-GarcíaExperimental Therapeutics and Translational Oncology Program, Instituto de Biología Molecular y Celular del Cáncer, CSIC-USAL, Campus M. de Unamuno s/n, Salamanca, Spain.
Ninad OakDepartment of Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Paula Somoza-CotillasExperimental Therapeutics and Translational Oncology Program, Instituto de Biología Molecular y Celular del Cáncer, CSIC-USAL, Campus M. de Unamuno s/n, Salamanca, Spain.
Andrea López-Álvarez de NeyraExperimental Therapeutics and Translational Oncology Program, Instituto de Biología Molecular y Celular del Cáncer, CSIC-USAL, Campus M. de Unamuno s/n, Salamanca, Spain.
Jorge Martínez-CanoImmune system development and function Unit, Centro de Biología Molecular Severo Ochoa (Consejo Superior de Investigaciones Científicas -Universidad Autónoma de Madrid), Madrid, Spain.
Alba Pérez-PonsCancer Research Center (IBMCC, USAL-CSIC), Department of Medicine and Cytometry Service (NUCLEUS), University of Salamanca, Salamanca, Spain, and Biomedical Research Institute of Salamanca (IBSAL), Salamanca, Spain.
Elena G SánchezOncohematology Laboratory, Advance Terapy Unit, Fundación para la Investigación Biomédica del Hospital Universitario Niño Jesús (FIB HUNJ), Madrid, Spain.
Oscar BlancoInstitute of Biomedical Research of Salamanca (IBSAL), Universidad de Salamanca, Campus Miguel de Unamuno s/n, Salamanca, Spain.
Diego Alonso-LópezBioinformatics Unit, and.
Javier De Las RivasInstitute of Biomedical Research of Salamanca (IBSAL), Universidad de Salamanca, Campus Miguel de Unamuno s/n, Salamanca, Spain.
Susana RiescoInstitute of Biomedical Research of Salamanca (IBSAL), Universidad de Salamanca, Campus Miguel de Unamuno s/n, Salamanca, Spain.
Pablo Prieto-MatosInstitute of Biomedical Research of Salamanca (IBSAL), Universidad de Salamanca, Campus Miguel de Unamuno s/n, Salamanca, Spain.
Francisco Javier García CriadoInstitute of Biomedical Research of Salamanca (IBSAL), Universidad de Salamanca, Campus Miguel de Unamuno s/n, Salamanca, Spain.
María Begoña García CenadorInstitute of Biomedical Research of Salamanca (IBSAL), Universidad de Salamanca, Campus Miguel de Unamuno s/n, Salamanca, Spain.
Alberto OrfaoCancer Research Center (IBMCC, USAL-CSIC), Department of Medicine and Cytometry Service (NUCLEUS), University of Salamanca, Salamanca, Spain, and Biomedical Research Institute of Salamanca (IBSAL), Salamanca, Spain.
Manuel Ramírez-OrellanaDepartment of Pediatric Hematology and Oncology, Hospital Infantil Universitario Niño Jesús and Institute of Biomedical Research Hospital Universitario La Princesa, Madrid, Spain.
César CobaledaImmune system development and function Unit, Centro de Biología Molecular Severo Ochoa (Consejo Superior de Investigaciones Científicas -Universidad Autónoma de Madrid), Madrid, Spain.
Carolina Vicente-DueñasInstitute of Biomedical Research of Salamanca (IBSAL), Universidad de Salamanca, Campus Miguel de Unamuno s/n, Salamanca, Spain.
Kim E NicholsDepartment of Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Isidro Sánchez-GarcíaExperimental Therapeutics and Translational Oncology Program, Instituto de Biología Molecular y Celular del Cáncer, CSIC-USAL, Campus M. de Unamuno s/n, Salamanca, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The contribution of 9p deletion to B cell acute lymphoblastic leukemia (B-ALL) has remained elusive since its discovery more than 40 years ago. Here we show that loss of CD72 is recurrent in B-ALL cases containing PAX5 deletions, and that Cd72 haploinsufficiency drives B-ALL development in Pax5+/- mice. Mechanistically, Cd72+/-;Pax5+/- precursor B cells exhibited an inflammatory transcriptional profile characterized by a decrease in Myd88 expression, a finding that aligns with our previous studies of B-ALL development in Pax5+/- mice following exposure to immune stressors. These combined genomic analyses and functional models provide compelling evidence that co-deletion of 2 contiguous genes, Pax5 and Cd72, drives B cell leukemogenesis.

Indexed as

Chromosome DeletionChromosomes, Human, Pair 9PAX5 Transcription FactorPrecursor B-Cell Lymphoblastic Leukemia-LymphomaAnimalsHeterozygoteHumansMiceMice, KnockoutPAX5 protein, humanPax5 protein, mousePAX5 Transcription FactorGenetic risk factorsHematologyLeukemiasMouse modelsOncology

Identifiers

PMID41701537
PMCPMC13134721

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Registered trials

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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.