Turner Christina J, Edwards Claire M
Nuffield Department of Surgical Sciences, University of Oxford, Oxford, UK.
Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Old Road, Oxford, OX3 7LD, UK.
Curr Osteoporos Rep. 2016 Oct;14(5):170-7. doi: 10.1007/s11914-016-0323-2.
The bone is a common site for metastasis in patients with advanced prostate carcinoma, and provides a 'fertile' milieu which stimulates tumour growth and associated bone disease. For years, the concept of treatment strategies has remained targeting the tumour itself; however, the occurrence of chemoresistance remains a challenge now more than ever. The attraction of targeting the bone microenvironment in order to disrupt tumour localisation and proliferation stems from the idea that stromal cells are superiorly stable at a genetic level, thus decreasing the risk of resistance manifestation. In this review, we will discuss recent findings with regards to the pathogenesis of prostate cancer-induced bone disease and recent therapeutic strategies in an aim to evaluate the ever increasing role of the microenvironment in disease progression.
骨是晚期前列腺癌患者常见的转移部位，并提供了一个促进肿瘤生长及相关骨病的“肥沃”环境。多年来，治疗策略的理念一直是针对肿瘤本身；然而，化疗耐药的出现如今比以往任何时候都更是一项挑战。靶向骨微环境以破坏肿瘤定位和增殖的吸引力源于这样一种观点，即基质细胞在基因水平上具有更高的稳定性，从而降低了耐药表现的风险。在本综述中，我们将讨论前列腺癌诱导骨病发病机制的最新研究结果以及近期的治疗策略，旨在评估微环境在疾病进展中日益增加的作用。
