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Pancreatic cancer relies on opposing signalling pathways to drive its cellular diversity

Communication between epithelial and mesenchymal cells in pancreatic cancer leads to a poor prognosis. The molecular basis for this signalling has now been revealed.
By
  1. Marc P. Stemmler

    1. Marc P. Stemmler is in the Department of Experimental Medicine I, Nikolaus-Fiebiger-Center of Molecular Medicine, Friedrich-Alexander University of Erlangen-Nürnberg, Erlangen 91054, Germany.

Tumour progression and spread are influenced by a variety of factors. These include communication between cells, the presence of differing types of cellular lineage in a cancer (tumour heterogeneity) and variations in cellular states (a phenomenon called plasticity, which describes the adaptability of these cells). Plasticity is often coupled to a process called the epithelial–mesenchymal transition (EMT), which is associated with one type of cell (an epithelial cell) losing its usual characteristics and switching to resemble a different type of cell (a mesenchymal cell). All of the above contribute to a poor prognosis1,2. Writing in Nature, Li et al.3 present evidence as to how communication between epithelial and mesenchymal cancer cells promotes tumour heterogeneity and cellular plasticity to drive malignant pancreatic cancer.

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Nature 648, 46-48 (2025)

doi: https://doi.org/10.1038/d41586-025-03133-1

References

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Competing Interests

The author declares no competing interests.

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