Department of Molecular Toxicology, Graduate School of Medical Sciences, Nagoya City University, 1-Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Japan.
Breast Cancer. 2013 Jul;20(3):195-203. doi: 10.1007/s12282-013-0439-5. Epub 2013 Jan 19.
Advanced breast cancer commonly spreads to the bones, lungs, liver or brain, and bone is the most common site of breast cancer metastasis. Nearly all patients with advanced breast cancer develop bone metastasis and suffer from serious bone metastasis-associated complications, including chronic pain, fracture, spinal cord compression and hypercalcemia. Metastasis formation in the bone is a complex process that requires cooperative reciprocal interactions between tumor cells and the cellular environment of the bone, which includes osteoclasts and osteoblasts. We have developed a murine bone invasion model of breast cancer, which required a simple surgical technique and mimics the biology of the disease. Osteolytic and/or osteoblastic lesions induced in the tumor-bone interface allowed us to explore cellular and molecular interactions between malignant cells and skeletal tissue in a syngeneic setting. In this review, we will discuss a different animal model that provides a consistent and reproducible platform for investigating the molecular mechanisms underlying tumor-bone interaction and breast cancer-induced osteolytic changes.
晚期乳腺癌通常会扩散到骨骼、肺部、肝脏或大脑，而骨骼是乳腺癌转移最常见的部位。几乎所有晚期乳腺癌患者都会发生骨转移，并患有严重的骨转移相关并发症，包括慢性疼痛、骨折、脊髓压迫和高钙血症。骨骼中的转移形成是一个复杂的过程，需要肿瘤细胞与骨骼的细胞环境之间的协同相互作用，其中包括破骨细胞和成骨细胞。我们已经开发出一种乳腺癌骨侵袭模型，该模型需要一种简单的手术技术，并模拟疾病的生物学特性。在肿瘤-骨骼界面诱导的溶骨性和/或成骨性病变使我们能够在同基因环境中探索恶性细胞与骨骼组织之间的细胞和分子相互作用。在这篇综述中，我们将讨论一种不同的动物模型，该模型为研究肿瘤-骨骼相互作用和乳腺癌诱导的溶骨性变化的分子机制提供了一个一致且可重复的平台。
