ReviewCancer metastasis reviews2026
Early cellular plasticity promotes progression and dissemination in pancreatic adenocarcinoma.
Review in Cancer metastasis reviews, 2026. 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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5 authors.
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Abstract
Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies, with limited therapeutic success and a persistently low 5-year survival rate. Despite significant advances in genomics and tumor biology, a fundamental challenge persists: to identify the elusive transformation from common benign pancreatic lesions to occasional malignant cellular identity. This review addresses a critical missing link in PDAC pathogenesis, focusing on when and where the switch to malignancy occurs, and why surgical intervention is often insufficient. We explore the biological and spatial-temporal evolution of precancerous lesions, such as PanINs and IPMNs, and examine how phenotypic plasticity and overlapping cellular programs-including squamous transdifferentiation, epithelial-to-mesenchymal transition (EMT), and acquisition of mesenchymal features-contribute to early dissemination, treatment resistance, and surgical failure. Recognizing and characterizing these early molecular events is essential for rethinking therapeutic strategies, identifying actionable biomarkers, and redefining the temporal window when curative intervention is feasible.
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