ArticleHuman mutation2026
Article in Human mutation, 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
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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.
- Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Posttranslational modification (PTM) plays an important role in protein regulation and may influence tumor initiation and progression. However, the role of PTM-related programs in lung adenocarcinoma (LUAD) remains incompletely understood. Materials and Methods: Single-cell RNA sequencing (scRNA-seq) data were analyzed to quantify the activity of PTM-related gene set using the AUCell algorithm and to characterize intercellular communication using CellChat. Molecular subtypes and differentially expressed genes (DEGs) were identified using ConsensusClusterPlus and limma packages, respectively, followed by functional enrichment analysis. Univariate Cox regression, LASSO regression with 10-fold cross-validation, and stepwise multivariable Cox regression based on the Akaike information criterion (AIC) were used to construct a prognostic model. Immune infiltration was evaluated using ESTIMATE, CIBERSORT, MCP-counter, and TIMER algorithms, and drug sensitivity was predicted using oncoPredict package. The IMvigor210 cohort was used for exploratory assessment of immunotherapy response. Quantitative real-time reverse transcription PCR (qRT-PCR) was used to measure the expressions of the model genes. CCK-8, wound-healing, and Transwell assays were performed to evaluate the effects of Results: Comparison between two PTM groups revealed that receptor ligands such as MIF-(CD74+CXCR4) and MIF-(CD74+CD44) had higher communication probabilities in the high-PTM-score group. Two molecular subtypes were identified, and a six-gene risk model for LUAD was established based on Conclusion: The PTM-related six-gene model showed potential for prognostic stratification and characterization of immune-related features in LUAD. However, further prospective and experimental validation is required before direct clinical application.
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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.