ArticleTranslational cancer research2025
CD69 predicts prognosis through immune cell infiltration and decitabine treatment response in acute myeloid leukemia.
Article in Translational cancer research, 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.
- Flow cytometric detection of leukemic stem cells in Acute Myeloid Leukemia: current status and future directions.Frontiers in pharmacology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Acute myeloid leukemia (AML) is a heterogeneous myeloid neoplasm. Recent studies have focused on unraveling the complexities of the tumor microenvironment (TME) and its impact on AML, with a specific emphasis on CD69, a potential TME regulator. However, the precise relationship between CD69 and AML is yet to be fully elucidated. This study aimed to analyze the heterogeneous gene expression landscape of AML patients using public databases, and to elucidate the relationship between CD69 expression and the pathophysiology of AML. Methods: Three gene datasets from Gene Expression Omnibus (GEO), ribonucleic acid (RNA) sequence data from The Cancer Genome Atlas (TCGA) and Therapeutically Applicable Research to Generate Effective Treatments (TARGET), and tumor cell lines data from Cancer Cell Line Encyclopedia (CCLE) were used. The Cox proportional hazards regression model was employed to assess the impact of differentially expressed genes on the overall survival (OS) rate of AML. Spearman's rank correlation coefficient analysis was conducted to determine the relationship between CD69 and immune cell infiltration in AML patients. Western blot analysis was utilized to verify CD69 expression in AML cell lines. Results: (I) Gene expression: 13 differentially expressed genes were identified in AML. (II) Impact on survival: CD69 expression was inversely related to OS of AML patients, with lower CD69 levels correlating with improved survival outcomes. (III) Independent risk factors: CD69, ITGB7, SCD and age were identified as independent risk factors in AML. (IV) Immune cell infiltration: a higher expression of CD69 was associated with reduced infiltration of CD8+ T cells and macrophages in AML. (V) Effect of decitabine (DA) treatment: AML patients treated with DA exhibited decreased CD69 expression. Conclusions: The study established a correlation between the expression of ITGB7, SCD, CD69 and the OS in AML patients. SCD, ITGB7 and age were identified as key prognostic factors. The multifaceted role of CD69 in AML, encompassing its association with prognosis, immune cell infiltration, and response to chemotherapy, underscores its potential as a key player in the complex landscape of AML pathogenesis and treatment response.
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.