Corn Paul G
Department of Genitourinary Medical Oncology, MD Anderson Cancer Center, Houston, TX, USA.
Cancer Manag Res. 2012;4:183-93. doi: 10.2147/CMAR.S32839. Epub 2012 Jul 25.
Mechanisms leading to the development of virulent prostate cancer are not confined to the cancer epithelial cell, but also involve the tumor microenvironment. Multiple signaling pathways exist between epithelial cells, stromal cells, and the extracellular matrix to support tumor progression from the primary site to regional lymph nodes and distant metastases. Prostate cancers preferentially metastasize to the skeleton, prompting considerable research effort into understanding the unique interaction between prostate cancer epithelial cells and the bone microenvironment. This effort has led to the discovery that signaling pathways involved in normal prostate and bone development become dysregulated in cancer. These pathways stimulate excessive cell growth and neovascularization, impart more invasive properties to epithelial cells, weaken antitumor immune surveillance, and promote the emergence of castrate-resistant disease. An improved understanding of the complex relationship between cancer epithelial cells and the organ-specific microenvironments with which they interact has created a powerful opportunity to develop novel therapies.
导致侵袭性前列腺癌发生发展的机制不仅限于癌上皮细胞，还涉及肿瘤微环境。上皮细胞、基质细胞和细胞外基质之间存在多种信号通路，以支持肿瘤从原发部位进展至区域淋巴结和远处转移。前列腺癌优先转移至骨骼，这促使人们开展大量研究，以了解前列腺癌上皮细胞与骨微环境之间的独特相互作用。这些研究发现，参与正常前列腺和骨发育的信号通路在癌症中发生失调。这些通路刺激细胞过度生长和新血管形成，赋予上皮细胞更强的侵袭性，削弱抗肿瘤免疫监视，并促进去势抵抗性疾病的出现。对癌症上皮细胞与其相互作用的器官特异性微环境之间复杂关系的深入理解，为开发新疗法创造了有力契机。
