ArticleFrontiers in cell and developmental biology2026
Dual molecular and clinical machine-learning prognostic modeling in pancreatic ductal adenocarcinoma: a chaperone-mediated autophagy-based framework integrating multi-cohort molecular signatures and a single-center clinical nomogram.
Article in Frontiers in cell and developmental biology, 2026. 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Pancreatic ductal adenocarcinoma (PDAC) is characterized by marked molecular, cellular, and clinical heterogeneity. Chaperone-mediated autophagy (CMA) supports adaptation to metabolic and environmental stress, but its cell type-specific distribution and prognostic relevance in PDAC remain unclear. Methods: Single-cell RNA sequencing data from GSE212966 were analyzed to characterize CMA-related transcriptional states in PDAC and adjacent non-tumor tissues. Bulk transcriptomic data from TCGA-PAAD were used for differential expression analysis, weighted gene co-expression network analysis, and molecular model development, while ICGC PACA-CA and PACA-AU served as independent validation cohorts. Multiple survival machine-learning approaches were compared to establish a CMA-related prognostic model. Hallmark pathway activity, immune infiltration, and predicted drug sensitivity were evaluated between risk groups. KRT19, the highest-weighted model gene, was selected for Results: CMA-related transcriptional activity varied among cell types, with macrophages showing prominent scores and PDAC-derived macrophages exhibiting higher CMA scores than those from adjacent tissues. Integration of TCGA differential expression analysis and WGCNA identified 105 candidate genes. The StepCox [forward] plus random survival forest model showed favorable overall performance, with C-index values of 0.903, 0.678, and 0.733 in the TCGA, PACA-CA, and PACA-AU cohorts, respectively. High molecular risk was associated with enhanced glycolytic, proliferative, and cell cycle-related signaling, increased M0 macrophages, reduced CD8 Conclusion: This study identified CMA-related cellular heterogeneity, established a molecular prognostic model that retained prognostic discrimination in two independent validation cohorts, demonstrated the functional relevance of KRT19, and developed an independent clinical prediction tool. These molecular and clinical models provide complementary perspectives on PDAC prognosis and warrant further evaluation in matched prospective cohorts.
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.