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Microenvironment

An exercise in restraint

Nature Reviews Cancer volume 14, page 449 (2014)Cite this article

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The prevailing opinion is that cancer-associated fibroblasts promote tumour progression, but two groups have found surprising results about the role of myofibroblasts and desmoplasia in pancreatic ductal adenocarcinoma (PDAC).

Özdemir et al. used PKT mice — a genetically-engineered mouse model (GEMM) of PDAC — in which cells expressing α-smooth muscle actin (αSMA; a myofibroblast marker) are ablated owing to induction of thymidine kinase (TK) by ganciclovir administration. These PKT–αSMA–TK mice were treated with ganciclovir at early stages of pancreatic cancer development and at late stages when PDACs were established. In both cases, invasive and highly undifferentiated tumours developed that significantly reduced survival compared with controls, despite ∼80% depletion of proliferating myofibroblasts in the tumours. In addition, patients with therapy-naive PDAC with low αSMA levels (which were usually poorly differentiated) had a poor prognosis.

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References

  1. Özdemir, B. C. et al. Depletion of carcinoma-associated fibroblasts and fibrosis induces immunosuppression and accelerates pancreas cancer with reduced survival. Cancer Cell http://dx.doi.org/10.1016/j.ccr.2014.04.005 (2014)

  2. Rhim, A. D. et al. Stromal elements act to restrain, rather than support, pancreatic ductal adenocarcinoma. Cancer Cell http://dx.doi.org/10.1016/j.ccr.2014.04.021 (2014)

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  1. Gemma K. Alderton
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Stoker, M. G., Shearer, M. & O'Neill, C. Growth inhibition of polyoma-transformed cells by contact with static normal fibroblasts. J. Cell Sci. 1, 297–310 (1966)

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Alderton, G. An exercise in restraint. Nat Rev Cancer 14, 449 (2014). https://doi.org/10.1038/nrc3769

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