Selective Evolution of Stromal Mesenchyme with p53 Loss in Response to Epithelial Tumorigenesis

• Published in: Cell Vol. 123; no. 6; pp. 1001 - 1011
• Main Authors: Hill, Reginald, Song, Yurong, Cardiff, Robert D., Van Dyke, Terry
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 16.12.2005
• Subjects: Actins - analysis; Adenocarcinoma - genetics; Adenocarcinoma - metabolism; Adenocarcinoma - pathology; Animals; Antigens, Polyomavirus Transforming - genetics; Cell Proliferation; Connective Tissue - pathology; Disease Models, Animal; Epithelial Cells - metabolism; Epithelial Cells - pathology; Fibroblasts - metabolism; Fibroblasts - pathology; Gene Deletion; Genotype; Keratin-8; Keratins - analysis; Loss of Heterozygosity - genetics; Male; Mice; Mice, Knockout; Mice, Transgenic; Models, Biological; Mutation - genetics; Paracrine Communication; Prostate - metabolism; Prostate - pathology; Prostatic Neoplasms - genetics; Prostatic Neoplasms - metabolism; Prostatic Neoplasms - pathology; Retinoblastoma Protein - metabolism; S100 Calcium-Binding Protein A4; S100 Proteins - analysis; Stromal Cells - metabolism; Stromal Cells - pathology; Tumor Suppressor Protein p53 - genetics; Tumor Suppressor Protein p53 - metabolism

Our understanding of cancer has largely come from the analysis of aberrations within the tumor cell population. Yet it is increasingly clear that the tumor microenvironment can significantly influence tumorigenesis. For example, the mesenchyme can support the growth of tumorigenic epithelium. Howeve...