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RANK和Akt1激活在人骨肉瘤进展中的作用：一项临床病理研究。

Role of RANK and Akt1 activation in human osteosarcoma progression: A clinicopathological study.

作者信息

Zhu Jianxi, Liu Yuwei, Zhu Yong, Zeng Min, Xie Jie, Lei Pengfei, Li Kanghua, Hu Yihe

机构信息

Department of Orthopedics, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.

出版信息

Exp Ther Med. 2017 Jun;13(6):2862-2866. doi: 10.3892/etm.2017.4360. Epub 2017 Apr 19.

DOI:10.3892/etm.2017.4360
PMID:28587351
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5450667/
Abstract

The receptor activator of nuclear factor κB (RANK) axis is the fundamental signaling pathway in bone formation as well as bone tumor pathophysiology. The aim of the present study was to evaluate the impact of the expression of RANK and its downstream signaling molecule Akt1 on tumor progression in patients with osteosarcoma. Expression of RANK and Akt1 was examined in 78 human osteosarcoma samples by immunohistochemistry using formalin-fixed samples. Following this, each graded immunohistochemistry result was correlated with clinicopathological parameters and patient survival. In total, 60 osteosarcomas (76.9%) expressed RANK and 58 cases (74.4%) showed expression of Akt1. In addition, expression of RANK was negatively correlated with disease-free survival by Kaplan-Meier analysis. A resistance was observed to chemotherapy in RANK-expressing cases, which was statistically significant (P<0.05). In addition, chemotherapy and staging of the tumor were found to independent factors that have an effect on patient survival (P<0.05). Thus, RANK was identified as a negative prognostic factor of osteosarcoma survival.

摘要

核因子κB受体激活剂（RANK）轴是骨形成以及骨肿瘤病理生理学中的基本信号通路。本研究的目的是评估RANK及其下游信号分子Akt1的表达对骨肉瘤患者肿瘤进展的影响。使用福尔马林固定样本，通过免疫组织化学检测了78例人类骨肉瘤样本中RANK和Akt1的表达。在此之后，将每个分级的免疫组织化学结果与临床病理参数和患者生存率相关联。总共，60例骨肉瘤（76.9%）表达RANK，58例（74.4%）显示Akt1表达。此外，通过Kaplan-Meier分析，RANK的表达与无病生存率呈负相关。在表达RANK的病例中观察到对化疗的耐药性，具有统计学意义（P<0.05）。此外，发现化疗和肿瘤分期是影响患者生存的独立因素（P<0.05）。因此，RANK被确定为骨肉瘤生存的负性预后因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a140/5450667/e3dd10f3e75c/etm-13-06-2862-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a140/5450667/850685a24d67/etm-13-06-2862-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a140/5450667/0d8c8ab82cc6/etm-13-06-2862-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a140/5450667/fb10e78907f9/etm-13-06-2862-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a140/5450667/e3dd10f3e75c/etm-13-06-2862-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a140/5450667/850685a24d67/etm-13-06-2862-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a140/5450667/0d8c8ab82cc6/etm-13-06-2862-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a140/5450667/fb10e78907f9/etm-13-06-2862-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a140/5450667/e3dd10f3e75c/etm-13-06-2862-g03.jpg

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