Notch plays the skin field | Nature Medicine
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A recent report (_Cell_ 149, 1207–1220) uncovers a role for the stromal compartment in skin carcinogenesis. Skin cancer often appears in the form of field cancerization, a constellation of
alterations in the epithelial and mesenchymal tissues that surround a tumorigenic lesion, and is likely to emerge from broad exposure to carcinogens such as sunlight. However, it was not
known whether stromal changes could drive this widespread transformation process. Bing Hu _et al_. investigated the contribution of the stroma to tumorigenesis in mice by inactivating the
tumor-suppressive Notch signaling pathway in mesenchymal cells. Interestingly, when they aged, these mice developed spontaneous, multifocal squamous carcinomas of diverse cellular origin,
which were infiltrated by inflammatory cells. The formation of these lesions could be prevented by anti-inflammatory drug treatment. In further studies, the authors confirmed that mouse and
human skin fibroblasts with dysfunctional Notch signaling could foster the neoplastic transformation of epithelial cells by a mechanism that involved increased transcriptional activation by
AP-1 factors. Importantly, the stroma surrounding human preneoplastic skin lesions showed similar alterations in Notch signaling to those in the authors' mouse model, and these changes
could be induced by exposure to ultraviolet A radiation. These new results expand the protumorigenic role of the stroma that has previously been observed in other tissues such as the mammary
gland and draw attention to the role of mesenchymal components as cancer drivers. Authors * Victoria Aranda View author publications You can also search for this author inPubMed Google
Scholar RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Aranda, V. Notch plays the skin field. _Nat Med_ 18, 1026 (2012). https://doi.org/10.1038/nm.2872
Download citation * Published: 06 July 2012 * Issue Date: July 2012 * DOI: https://doi.org/10.1038/nm.2872 SHARE THIS ARTICLE Anyone you share the following link with will be able to read
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