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Expression of hypoxia‐inducible factor 1α, glucose transporter 1, and hexokinase 2 in primary central nervous system lymphoma and the correlation with the biological behaviors

Authors :
Yuedan Chen
Hong Zhu
Na Shen
Yuchen Wu
Jinglan He
Shengjun Sun
Yaming Wang
Qing Liu
Xuefei Sun
Qu Cui
Nan Ji
Xueyan Bai
Wenyuan Lai
Ruixian Xing
Jun Qian
Yuanbo Liu
Junhong Li
Source :
Brain and Behavior, Brain and Behavior, Vol 10, Iss 8, Pp n/a-n/a (2020)
Publication Year :
2020
Publisher :
Wiley, 2020.

Abstract

Background It has been indicated that abnormal glucose metabolism mediated by hypoxia‐inducible factor 1α (HIF‐1α) played an essential role in the development of solid tumor. However, there were rare studies about the role of them in primary central nervous system lymphoma (PCNSL). Objective To investigate the protein levels of HIF‐1α, glucose transporter 1 (GLUT1), and hexokinase 2 (HK2) in PCNSL and whether their levels are associated with prognostic factors. Methods Expression of HIF‐1α, GLUT1, and HK2 in 39 tumor tissues was evaluated by immunohistochemical stainning. The correlation of the expression of HIF‐1α with the protein level of GLUT1 and HK2 was investigated. In addition, the association between these protein expression levels and clinical parameters and prognosis was analyzed. Results In the tumor specimens of PCNSL, positive stainings of HIF‐1α, GLUT1, and HK2 were in 23 patients (58.97%), 25 patients (64.1%), and 26 patients (66.67%), respectively, which were associated with the expression level of lactic dehydrogenase (LDH), but not with age, gender, number of lesion, ECOG score, or deep structure. The expression of HIF‐1α was positively correlated with the expression of GLUT1 (p<br />There was a hypoxic microenvironment, and HIF‐1α was involved in the regulation of glycolysis pathway in PCNSL. GLUT1 might be a potential marker for shorter PFS in PCNSL.

Details

ISSN :
21623279
Volume :
10
Database :
OpenAIRE
Journal :
Brain and Behavior
Accession number :
edsair.doi.dedup.....16c12224b384d69d5051eb0cdba19ee3
Full Text :
https://doi.org/10.1002/brb3.1718