RESPONSE OF BONE TO INVADING BREAST ADENOCARCINOMA CELLS

骨对侵袭乳腺癌细胞的反应

• 批准号: 6104573
• 负责人: JAY SISON
• 金额: $ 5.57万
• 依托单位: HARVARD MEDICAL SCHOOL
• 依托单位国家: 美国
• 财政年份: 1999
• 资助国家: 美国
• 起止时间: 1999-07-01 至 2000-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6104573
• 关键词: RESPONSE; BONE; INVADING; BREAST; ADENOCARCINOMA

Our general goal is to understand the pathophysiology osteolytic response of bone to invading breast adenocarcinoma cells. Osteolysis primarily requires cancer-mediated dysregulation of cells from the osteoclasi lineage, but other cells types are also critically involved e.g. stromal cells, osteoblasts, and endothelial cells. We plan to identify some of the regulatory factors relevant to osteolysis which are produced by metastatic adenocarcinoma cells. The specific aim of this study is to analyze the expression of the ligand RANKL and its decoy receptor OPG by bone cells in response to breast carcinoma cells grown under different co-culture conditions, and to determine whether breast carcinoma cells also express RANKL or OPG or whether proteinases induced in bone or secreted by breast carcinoma cells inactivate RANKL or OPG.

我们的总体目标是了解骨溶解的病理生理学。 骨骼对乳腺癌细胞侵袭的反应。骨溶解 主要需要癌症介导的细胞调节失调 破骨细胞系，但其他类型的细胞也是关键因素 例如基质细胞、成骨细胞和内皮细胞。我们计划 找出一些与骨溶解有关的调节因素，包括 由转移性腺癌细胞产生。 本研究的具体目的是分析该基因的表达 骨细胞对配体RANKL及其诱骗受体OPG的影响 不同共培养条件下生长的乳腺癌细胞，以及 为了确定乳腺癌细胞是否也表达RANKL或OPG或 无论是骨诱导的还是乳腺癌分泌的蛋白酶 细胞失活RANKL或OPG。