Evidence that SOX2 overexpression is oncogenic in the lung.

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BACKGROUND: SOX2 (Sry-box 2) is required to maintain a variety of stem cells, is overexpressed in some solid tumors, and is expressed in epithelial cells of the lung. METHODOLOGY/PRINCIPAL FINDINGS: We show that SOX2 is overexpressed in human squamous cell lung tumors and some adenocarcinomas. We have generated mouse models in which Sox2 is upregulated in epithelial cells of the lung during development and in the adult. In both cases, overexpression leads to extensive hyperplasia. In the terminal bronchioles, a trachea-like pseudostratified epithelium develops with p63-positive cells underlying columnar cells. Over 12-34 weeks, about half of the mice expressing the highest levels of Sox2 develop carcinoma. These tumors resemble adenocarcinoma but express the squamous marker, Trp63 (p63). CONCLUSIONS: These findings demonstrate that Sox2 overexpression both induces a proximal phenotype in the distal airways/alveoli and leads to cancer.





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Lu, Y, C Futtner, JR Rock, X Xu, W Whitworth, BL Hogan and MW Onaitis (2010). Evidence that SOX2 overexpression is oncogenic in the lung. PLoS One, 5(6). p. e11022. 10.1371/journal.pone.0011022 Retrieved from https://hdl.handle.net/10161/4546.

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Brigid L. M. Hogan

Research Professor of Cell Biology
  1. Genetic regulation of embryo development using the mouse as a research model.
    2. The role of genes and signaling pathways in directing and co-ordinating the development of the lung.
    3. The identity and regulation of the different stem cells in the adult lung and their role in repair, fibrosis and cancer.

Mark William Onaitis

Adjunct Associate Professor in the Department of Surgery

Mouse Models of Foregut Malignancies
Normal Tissue and Cancer Stem Cells
Risk Prediction in Thoracic Malignancies

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