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Pancreatic cancer

FAK regulates sensitivity to immunotherapy

Nature Reviews Clinical Oncology volume 13, page 528 (2016)Cite this article

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Newly published research in mouse models of pancreatic ductal adenocarcinoma (PDAC), in which immunotherapy alone is largely ineffective, has revealed that inhibition of focal adhesion kinase (FAK) promotes sensitivity to adoptive T-cell transfer and inhibition of both cytotoxic T-lymphocyte protein-4 (CTLA-4) and programmed cell death-1 (PD-1). Based upon the finding of increased FAK expression in human PDAC biopsy samples, researchers inhibited FAK in a mouse model of PDAC. FAK inhibition delayed tumour progression and markedly reduced the extent of tumour fibrosis. When FAK inhibition was combined with other therapies, such as gemcitabine, it significanty increased overall survival, and the addition of adoptive T-cell transfer resulted in further inhibition of tumour growth. The combination of anti-PD1/anti-CTLA-4 with FAK inhibition resulted in significantly improved overall survival: ∼20% of mice treated with this regimen survived for 180 days from the start of treatment, thus indicating a need for further investigation of FAK inhibition in patients with PDAC.

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References

  1. Jiang, H. et al. Targeting focal adhesion kinase renders pancreatic cancers responsive to checkpoint immunotherapy. Nature http://dx.doi.org/10.1038/nm.4123 (2016)

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  1. Peter Sidaway
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Sidaway, P. FAK regulates sensitivity to immunotherapy. Nat Rev Clin Oncol 13, 528 (2016). https://doi.org/10.1038/nrclinonc.2016.116

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