ArticleCell reports. Medicine2026
Proteomics landscape of early T-cell precursor acute lymphoblastic leukemia reveals deficient oxidative phosphorylation signatures.
Article in Cell reports. Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Early T-cell precursor acute lymphoblastic leukemia (ETP-ALL) represents a therapeutically challenging, high-risk leukemia subtype whose comprehensive proteomic characterization remains limited. Our integrated 4D label-free proteomic analysis delineates a distinct molecular signature featuring profound oxidative phosphorylation (OxPhos) deficiency, characterized by compromised mitochondrial ATP synthesis and significant reductions in electron transport chain complexes I and IV. Single-cell RNA sequencing validation establishes that stem-like ETP-ALL populations exhibit substantially diminished ETC activity relative to T-lineage-differentiated counterparts. Pharmacological intervention using dichloroacetate to restore OxPhos functionality effectively suppresses leukemic proliferation and xenograft engraftment through ROS-mediated endoplasmic reticulum stress activation. Furthermore, we identify CD109 as an attractive immunophenotypic marker that not only distinguishes ETP-ALL from other hematologic malignancies but also defines a subset with enhanced ETC suppression and heightened metabolic vulnerability to dichloroacetate. These findings elucidate the mechanistic basis of mitochondrial dysregulation in ETP-ALL pathogenesis and nominate CD109 as a promising biomarker for targeted therapeutic strategies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.