Evidence map›Paper›PMID 41514266›Full record

ArticleBMC biology2026

Proteomics analysis of human mesenchymal stromal/stem cell sarcomagenesis model identifies ALDH1A3 and CD99 as potential targets in the transformation process.

Jonathan M Gobin, Jun Gao, Veronica Rey, Juan Tornín, Gauri Muradia, Hala Halabi, Clara Bueno, Mercedes Guerrero-Murillo, Belen Lopez-Millan, Pablo Menendez and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC biology, 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. Article
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

13 authors.

Jonathan M GobinDepartment of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, 451 Smyth Road, Ottawa, ON, K1H 8M5, Canada.
Jun GaoCentre for Oncology, Radiopharmaceuticals and Research, Biologic and Radiopharmaceutical Drugs Directorate, Health Products and Food Branch, Health Canada, Ottawa, ON, K1A 0K9, Canada.
Veronica ReyInstituto de Investigacion Sanitaria del Principado de Asturias (ISPA) - Hospital Universitario Central de Asturias, Oviedo, 33011, Spain.
Juan TornínInstituto de Investigacion Sanitaria del Principado de Asturias (ISPA) - Hospital Universitario Central de Asturias, Oviedo, 33011, Spain.
Gauri MuradiaCentre for Oncology, Radiopharmaceuticals and Research, Biologic and Radiopharmaceutical Drugs Directorate, Health Products and Food Branch, Health Canada, Ottawa, ON, K1A 0K9, Canada.
Hala HalabiCentre for Oncology, Radiopharmaceuticals and Research, Biologic and Radiopharmaceutical Drugs Directorate, Health Products and Food Branch, Health Canada, Ottawa, ON, K1A 0K9, Canada.
Clara BuenoJosep Carreras Leukaemia Research Institute, Department of Biomedicine, School of Medicine, University of Barcelona, Barcelona, Spain.
Mercedes Guerrero-MurilloJosep Carreras Leukaemia Research Institute, Department of Biomedicine, School of Medicine, University of Barcelona, Barcelona, Spain.
Belen Lopez-MillanJosep Carreras Leukaemia Research Institute, Department of Biomedicine, School of Medicine, University of Barcelona, Barcelona, Spain.
Pablo MenendezCentro de Investigación Biomédica en Red-Oncología (CIBERONC), Instituto de Salud Carlos III, Madrid, 28029, Spain.
Michael Rosu-MylesDepartment of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, 451 Smyth Road, Ottawa, ON, K1H 8M5, Canada.
Rene RodriguezInstituto de Investigacion Sanitaria del Principado de Asturias (ISPA) - Hospital Universitario Central de Asturias, Oviedo, 33011, Spain. rene.rodriguez@ispasturias.es.
Jessie R LavoieDepartment of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, 451 Smyth Road, Ottawa, ON, K1H 8M5, Canada. jessie.lavoie@hc-sc.gc.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMesenchymal stromal/stem cells (MSC) may represent the cell-of-origin for sarcoma development. A collection of human MSCs sequentially mutated with an increasing number of oncogenic hits served to recreate a step-wise process of sarcomagenesis. To identify potential protein targets of interest in the MSC-sarcoma transformation process, quantitative mass spectrometry-based (LC-MS/MS) proteomics was performed.

resultsAmong the protein hits identified as significantly regulated in the transformation process, ALDH1A3 and CD99 were selected and further studied. Both ALDH1A3 abundance levels and activity were significantly upregulated in early-phase (immortalized) and fully transformed (sarcoma forming) cells as compared to normal MSCs. Inversely, CD99 total protein and cell-surface abundance levels were downregulated in immortalized and transformed MSCs. Downregulated CD99 was also identified in several human bone and soft tissue sarcoma subtypes.

conclusionsProteomics investigation of a MSC-transformation model of sarcoma has yielded ALDH1A3 and CD99 as potential targets for sarcomagenesis that may contribute to a greater understanding of the disease and the development of novel therapeutic approaches.

Indexed as

12E7 AntigenAldehyde OxidoreductasesCell Transformation, NeoplasticMesenchymal Stem CellsProteomicsSarcomaHumans12E7 Antigenaldehyde dehydrogenase (NAD(P)+)Aldehyde OxidoreductasesCD99 protein, humanALDH1A3CD99MSC-sarcoma modelProteomicsSarcomagenesis

Identifiers

PMID41514266
PMCPMC12882515

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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.