ReviewBiology2026
Decoding Drug Resistance in Pancreatic Cancer: A Subcellular Structure Perspective.
Review in 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
12 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies, with drug resistance representing the primary barrier to effective treatment. Current research has largely focused on individual signaling pathways or isolated organelle functions, yet a comprehensive understanding of how these subcellular structures coordinate to drive resistance remains lacking. This review synthesizes current knowledge through the perspective of subcellular structural homeostasis, the dynamic balance maintained by intracellular organelles. We examine how key subcellular structures, the cell membrane, mitochondria, endoplasmic reticulum, ribosomes, lysosomes, exosomes, and stress granules, undergo functional remodeling to promote drug resistance. It is crucial that these organelles do not work independently but form an integrated and dynamic communication network. Mitochondria serve as the intracellular signaling hub, integrating calcium signals, metabolic progress, and stress responses, while exosomes function as intercellular messengers that spread the anti-drug-resistant phenotype between cells. This framework reveals why targeting individual structures often fails and highlights the therapeutic potential of disrupting inter-organelle communication. We discuss emerging clinical strategies targeting subcellular structures and identify critical knowledge gaps, including the need for non-invasive biomarkers and combination approaches that target multiple network nodes. By shifting the focus from isolated organelles to their coordinated interplay, this review offers a new paradigm for overcoming drug resistance in PDAC.
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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.