ArticleiScience2025
Interplay between acute Type A aortic dissection and pan-cancer: Clinical evidence, bioinformatics, and experimental validation.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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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.
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute Type A Aortic Dissection (ATAAD) and cancer represent major global health burdens, yet shared mechanisms remain elusive. Epidemiological analyses linked ATAAD to increased risks of lung adenocarcinoma (LUAD) and head and neck squamous cell carcinoma (HNSCC). Integrated multi-omics identified mitochondrial peptidylprolyl isomerase F (PPIF) as a key ATAAD biomarker, specifically overexpressed in monocytes, with experimentally validated. Pan-cancer analyses revealed PPIF overexpression correlated with poor prognosis across malignancies, and functional assays also confirmed PPIF drives proliferation, migration, and invasion in LUAD and HNSCC. These findings nominate PPIF as a shared mechanistic node connecting ATAAD pathogenesis to cancer progression, highlighting its potential as a therapeutic target worth further investigation.
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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 OpenQuestion graph.