ArticlePloS one2026
DC-STAMP activates the PI3K/AKT/mTOR signaling pathway to regulate PANoptosis in acute myeloid leukemia.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Mechanisms ofFood science & nutrition · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPANoptosis is a newly defined form of programmed cell death that integrates features of apoptosis, pyroptosis and necroptosis, playing a critical role in immune regulation and tumor biology. Clinically, Acute Myeloid Leukemia (AML) patients with high DC‑STAMP expression exhibited notably poorer cytogenetic risk profiles and shorter overall survival. Gene set enrichment analysis of primary AML samples from public databases revealed significant enrichment of the mTORC1 signaling pathway, a core signaling axis regulating the apoptotic process, in AML samples with high DC-STAMP expression.
methodsDC-STAMP knockdown and overexpression models were established in the AML cell line THP-1 using small interfering RNA (siRNA) and lentiviral plasmids, respectively. Western blotting and RT-PCR were used to assess changes in PI3K/AKT/mTOR pathway activity in response to altered DC-STAMP expression. Flow cytometry and other cellular phenotypic assays were employed to evaluate the impact of DC-STAMP on PANoptosis in AML cells. Finally, PI3K inhibitors were introduced to assess the functional reversal of DC-STAMP-driven malignant phenotypes through downstream PI3K pathway inhibition.
resultsHigh DC-STAMP expression in AML activated the PI3K/AKT/mTOR signaling pathway and suppressed the PANoptosis process, thereby enhancing leukemic cell survival and chemoresistance. In contrast, genetic silencing of DC-STAMP or pharmacological inhibition of downstream PI3K restored normal apoptotic processes and significantly attenuated the malignant phenotypes driven by mTOR hyperactivation.
conclusionsActivation of DC-STAMP is an essential mechanism that suppresses PANoptosis and promotes chemoresistance in AML cells. Targeting the downstream PI3K/mTOR signaling pathway may offer a promising therapeutic strategy for this high-risk AML subtype.
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.