ArticleDiscover oncology2025
Identification of cell adhesion related signature for molecular subtyping and prognostic prediction in acute myeloid leukemia.
Article in Discover oncology, 2025. 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
3 authors.
Funding
Abstract
backgroundAcute Myeloid Leukemia (AML) is a heterogeneous hematologic malignancy, characterized by complex molecular features that significantly impact prognosis and therapeutic responses. Despite considerable progress, effective risk stratification and predictive biomarkers for personalized therapies remain inadequate. The involvement of cell adhesion-related genes in the progression of AML has yet to be fully explored.
methodsAML patients were grouped into distinct molecular subtypes based on the expression patterns of cell adhesion-related genes. Enrichment analyses were subsequently performed to identify associated biological pathways. Differentially expressed genes were identified, and through Lasso regression and multivariate Cox regression, eight prognostically significant genes were selected. These genes were then used to construct a prognostic model, which was validated using external datasets. Furthermore, analyses of immune cell infiltration and drug sensitivity were conducted to evaluate the practical applicability of the model.
resultsTwo AML molecular subtypes were identified, each linked to distinct biological pathways. A prognostic model comprising 8 genes was developed, showing strong predictive power for overall survival and significant correlations with immune cell infiltration patterns. Drug sensitivity analyses identified potential therapeutic targets and candidate drugs, offering new directions for AML treatment.
conclusionThis study reveals novel AML subtypes driven by cell adhesion-related genes, providing insights into genetic heterogeneity, immune landscape, and therapeutic vulnerabilities. The developed prognostic model and identified therapeutic candidates offer valuable tools for prognosis prediction and personalized treatment strategies in AML.
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.