ArticleJournal of translational medicine2025
Metabolic, transcriptomic, and proteomic adaptations in pancreatic ductal adenocarcinoma-patient derived xenograft models across serial passages.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The trial behind it
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Who cites it
4 citing papers in PubMed.
- GNL2 plays a critical role in avian reovirus p17-mediated host cellular autophagy and promotes viral proliferation.Poultry science · 2026Article
- Harnessing PDX and PDX 2.0: the next-generation paradigm for precision oncology and translational breakthroughs.Molecular cancer · 2026Review
- Biobanking of gynecologic cancer biospecimens: Development, quality control, and translational applications.PloS one · 2026Article
- ITGB5-mediated biomechanical regulation in pancreatic ductal adenocarcinoma stroma impacts tumor progression and prognosis.Journal of translational medicine · 2025Observational
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
backgroundPatient-derived xenograft (PDX) models are crucial for tumor biology and therapeutic response evaluations. The metabolic, transcriptomic, and proteomic changes in PDX models derived from pancreatic ductal adenocarcinoma (PDAC) during serial passaging remain poorly understood.
methodsWe established 33 PDX models from 43 PDAC patients and collected 40 benign pancreatic tissues as controls for metabolomic analysis using
resultsPDX tumors closely mirrored primary tumors in metabolic characteristics, maintaining key metabolic features of PDAC with minor variations in amino acid metabolism, particularly glutamine and aspartate levels. PDX-2 and PDX-3 showed dysregulation in aminoacyl-tRNA biosynthesis and glycine, serine, and threonine metabolism. DEGs progressively increased across passages, with later-generation PDX models exhibiting transcriptional dysregulation, including enhanced MAPK signaling activity and reduced immune-related pathway expression. Proteomic analysis identified five consistently altered proteins (ZDHHC20, ZNF644, GNL2, PDGFRB, INO80E), indicative of enhanced signal transduction, cell cycle regulation, and DNA repair. Gene-protein interaction analysis identified four core functional modules involved in protein degradation, DNA repair, ribosome biogenesis, and inflammatory response.
conclusionPDX models undergo adaptive changes during serial passaging while retain primary tumor characteristics, making them a valuable tool for understanding tumor evolution and informing therapeutic strategies, provided that passage-related drift is carefully considered.
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