ArticleCells2025
Extracellular Vesicles Profiling in Acute Myeloid Leukemia Cell Lines: A Proteomic Characterization.
Article in Cells, 2025. 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.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular vesicles (EVs) express features of parental cells and are fundamental in modulating the crosstalk between cancer cells and their environment. Increasing evidence suggests that EVs have a pivotal role in tumorigenesis, cancer development, and drug resistance. EVs are also involved in controlling the communication between hematopoietic stem cells and the surrounding microenvironment in the bone marrow (BM), during several processes such as self-renewal, mobilization, and lineage differentiation. Proteins expressed in cancer cell-derived EVs can be useful to further understand the regulation of hematopoietic stem cell fate, a fundamental mechanism in acute myeloid leukemia (AML). Furthermore, EVs are implicated in transmitting drug-resistance mechanisms in solid and not-solid cancer types. Here, using a proteomic approach, we analyze and validate the protein profile of EVs from three AML cell lines with different genotypes, namely OCI-AML-2, OCI-AML-3, and HL-60. The majority of the identified proteins were significantly enriched in the Gene Ontology category 'Extracellular Exosome'. Network model analysis of EV proteins revealed several significantly modulated pathways, including inflammation activation and metastatic processes in AML cell-derived EVs. The EVs proteomic profiling allows us to identify the EVs-associated molecules and pathways that could impact cancer progression and drug resistance.
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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 Socratic graph.