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TGFβ and cancer metastasis: an inflammation link

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Abstract

Dysregulated transforming growth factor beta (TGFβ) signaling is observed in a variety of human cancers. TGFβ is produced in large quantities by many tumor types and is known to be pro-oncogenic. Therapeutic strategies directed against TGFβ signaling using neutralizing antibodies and small molecular inhibitors have been developed. However, TGFβ is also found to function as a tumor suppressor. This switch from a tumor suppressor in premalignant stages of tumorigenesis to a tumor promoter in later stages of the disease poses great challenges in TGFβ-targeted cancer therapy. It remains unclear what mechanisms underlie the dual role of TGFβ and what factors mediate the switch. In the past, most work on dissecting underlying mechanisms was focused on differential regulation of signaling pathways by tumor cell autonomous TGFβ signaling. Recent progress in elucidating TGFβ effects on host immune/inflammatory reactions in the tumor microenvironment and distant organs brings exciting new perspectives to the field.

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Acknowledgments

We thank Dr B.R. Achyut for graphic assistance and Nan Roche for editorial assistance.

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Yang, L. TGFβ and cancer metastasis: an inflammation link. Cancer Metastasis Rev 29, 263–271 (2010). https://doi.org/10.1007/s10555-010-9226-3

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