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Targeting tumor–stroma crosstalk: the example of the NT157 inhibitor

Oncogene volume 35, pages 2562–2564 (2016)Cite this article

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Abstract

Recent clinical research has provided evidence that cancer progression and therapy resistance is driven not only by tumor’s genetic profile but also by complex paracrine interactions within the tumor microenvironment (TME). The role of TME in modulating tumor drug sensitivity is increasingly recognized and targeting TME has been the focus of novel therapeutic approaches. Two recent reports show that a new anti-cancer drug, the inhibitor NT157 has the potential to inhibit IGF-1R and STAT3 signaling pathways in cancer cells and stroma cells of TME leading to a decrease in cancer cell survival.

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Acknowledgements

We are grateful to Action Against Cancer for their continued support.

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Authors and Affiliations

  1. Department of Biochemistry and Biomedicine, School of Life Sciences, University of Sussex, Brighton, UK

    T Rampias & G Giamas

  2. Department of Surgery and Cancer, Imperial College, Hammersmith Hospital Campus, London, UK

    R Favicchio, J Stebbing & G Giamas

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  1. T Rampias
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  2. R Favicchio
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Correspondence to T Rampias or G Giamas.

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Rampias, T., Favicchio, R., Stebbing, J. et al. Targeting tumor–stroma crosstalk: the example of the NT157 inhibitor. Oncogene 35, 2562–2564 (2016). https://doi.org/10.1038/onc.2015.392

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