11 months ago

2013 Scientific Report

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  • Report
  • Institute
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  • Tumor
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  • Signaling

Figure 1 Figure 2 Figure

Figure 1 Figure 2 Figure 3 Differentiated prostate epithelial cells. Figure 1 shows basal cells (the lowest layer of cells) stained for integrin a6; the red stain is largely on the periphery of the cells. Figure 2 shows secretory cells (the upper layer), which have differentiated from the basal cells. The green stain in the secretory cells, which have lost integrin expression, is for the ING4 molecule in the nucleus. Figure 3 shows a composite image of both stains, plus DAPI stain (blue) for DNA. Images by Penny Berger and Elly Park of the Miranti lab. 33

Xiaohong Li, Ph.D. Laboratory for Tumor Microenvironment and Metastasis Dr. Li received her Ph.D. from the Chinese Academy of Sciences in Beijing in 2000, and she moved to Vanderbilt University in the same year. Dr. Li was a postdoctoral fellow in the laboratory of David Ong until 2005 and in the laboratory of Neil Bhowmick from 2005 to 2009. She was promoted to research assistant professor in the Department of Urologic Surgery in 2009. Dr. Li joined VARI as an Assistant Professor in September 2012. Research Interests The laboratory is committed to understanding cancer and metastasis. We study not only the cancer cells, but also the contributions of the tumor microenvironment, aiming to develop early diagnostic and treatment strategies for breast and prostate cancer metastasis to bone. Our research focuses on the role of stromal transforming growth factor (TGF-b) in the microenvironment of primary and metastatic tumor sites, as well as its effects in bone metastases, and on the development of animal models of cancer-induced osteolytic and osteoblastic bone disease. We have recently been funded by the Department of Defense Prostate Cancer Research Program to study the influence of the primary microenvironment on the development of prostate cancer osteoblastic bone lesions. The objectives are to determine the contribution of prostate mesenchymal TGF-b to lesion development and to determine whether chemokines induced by the loss of TGF-b signaling mediate prostate cancer bone metastasis. Other developing projects include the creation of animal models for studying prostate osteoblastic bone metastases and mechanisms; study of the role of TGF-b on the development of breast cancer-induced osteolytic bone lesions; and the evaluation of anti-TGF-b combination therapies on cancer-induced bone disease. Staff Priscilla Lee, B.S. Diana Lewis, A.S. Jared Murdoch, B.S. 34

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