Lu-Nan Qi1,2,3, Liang Ma4,5,6, Fei-Xiang Wu4,5,6, Yuan-Yuan Chen7, Wan-Ting Xing4,6, Zhi-Jun Jiang4,6, Jian-Hong Zhong4, Zu-Shun Chen4, Wen-Feng Gong4, Jia-Zhou Ye4, Hong-Hao Li6, Jin-Jie Shang8, Bang-De Xiang9,10,11, Le-Qun Li12,13,14. 1. Department of Hepatobiliary Surgery, Affiliated Tumor Hospital of Guangxi Medical University, No. 71 Hedi Road, Nanning, 530021, Guangxi, China. wangzhennuo@aliyun.com. 2. Guangxi Liver Cancer Diagnosis and Treatment Engineering and Technology Research Center, Nanning, 530021, Guangxi, China. wangzhennuo@aliyun.com. 3. Key Laboratory of Early Prevention and Treatment for Regional High Frequency Tumor, Ministry of Education, Nanning, 530021, Guangxi, China. wangzhennuo@aliyun.com. 4. Department of Hepatobiliary Surgery, Affiliated Tumor Hospital of Guangxi Medical University, No. 71 Hedi Road, Nanning, 530021, Guangxi, China. 5. Guangxi Liver Cancer Diagnosis and Treatment Engineering and Technology Research Center, Nanning, 530021, Guangxi, China. 6. Key Laboratory of Early Prevention and Treatment for Regional High Frequency Tumor, Ministry of Education, Nanning, 530021, Guangxi, China. 7. Department of Ultrasound, First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, Guangxi, China. 8. Jiangsu Key Laboratory for Microbes and Functional Genomics, College of Life Sciences, Nanjing Normal University, Nanjing, 210000, Jiangsu, China. 9. Department of Hepatobiliary Surgery, Affiliated Tumor Hospital of Guangxi Medical University, No. 71 Hedi Road, Nanning, 530021, Guangxi, China. xiangbangde@163.com. 10. Guangxi Liver Cancer Diagnosis and Treatment Engineering and Technology Research Center, Nanning, 530021, Guangxi, China. xiangbangde@163.com. 11. Key Laboratory of Early Prevention and Treatment for Regional High Frequency Tumor, Ministry of Education, Nanning, 530021, Guangxi, China. xiangbangde@163.com. 12. Department of Hepatobiliary Surgery, Affiliated Tumor Hospital of Guangxi Medical University, No. 71 Hedi Road, Nanning, 530021, Guangxi, China. li_lequn@263.net. 13. Guangxi Liver Cancer Diagnosis and Treatment Engineering and Technology Research Center, Nanning, 530021, Guangxi, China. li_lequn@263.net. 14. Key Laboratory of Early Prevention and Treatment for Regional High Frequency Tumor, Ministry of Education, Nanning, 530021, Guangxi, China. li_lequn@263.net.
Abstract
BACKGROUND: Portal vein tumor thrombus (PVTT) and microvascular invasion (MVI) are types of intrahepatic vascular metastasis of hepatocellular carcinoma (HCC) and are highly correlated with poor prognosis. However, the underlying biomarkers of PVTT and MVI are unclear. METHODS: We identified a PVTT/MVI-associated gene S100P by cDNA microarray analysis, and assess the potential value of serum S100P measurement in the differential diagnosis of HCC and prediction of MVI status with large retrospective and perspective cohort studies. RESULTS: The mRNA and protein of S100P was increased in HCCs with PVTT or MVI. High S100P immunostaining in tumors was correlated with inferior tumor-free survival. Serum S100P values discriminated patients with HCCs from those with benign liver tumors, and it showed predictive potential of MVI status in both retrospective and perspective cohorts. S100P may regulate HCC tumorigenicity and invasive ability; S100P also was associated with up-regulation of CD44, which may mediate HCC cell adhesion to form PVTT/MVI. CONCLUSIONS: Serum S100P may be a novel differential diagnostic marker for HCC and a potential predictor of MVI status pre-surgery for HCC patients. S100P overexpression in HCC is highly correlated with the formation of PVTT and MVI, which may make S100P as a potential therapeutic target for HCC metastasis.
BACKGROUND: Portal vein tumor thrombus (PVTT) and microvascular invasion (MVI) are types of intrahepatic vascular metastasis of hepatocellular carcinoma (HCC) and are highly correlated with poor prognosis. However, the underlying biomarkers of PVTT and MVI are unclear. METHODS: We identified a PVTT/MVI-associated gene S100P by cDNA microarray analysis, and assess the potential value of serum S100P measurement in the differential diagnosis of HCC and prediction of MVI status with large retrospective and perspective cohort studies. RESULTS: The mRNA and protein of S100P was increased in HCCs with PVTT or MVI. High S100P immunostaining in tumors was correlated with inferior tumor-free survival. Serum S100P values discriminated patients with HCCs from those with benign liver tumors, and it showed predictive potential of MVI status in both retrospective and perspective cohorts. S100P may regulate HCC tumorigenicity and invasive ability; S100P also was associated with up-regulation of CD44, which may mediate HCC cell adhesion to form PVTT/MVI. CONCLUSIONS: Serum S100P may be a novel differential diagnostic marker for HCC and a potential predictor of MVI status pre-surgery for HCC patients. S100P overexpression in HCC is highly correlated with the formation of PVTT and MVI, which may make S100P as a potential therapeutic target for HCC metastasis.
Authors: Thiruvengadam Arumugam; Vijaya Ramachandran; Sobeyda B Gomez; Ann M Schmidt; Craig D Logsdon Journal: Clin Cancer Res Date: 2012-06-20 Impact factor: 12.531
Authors: A Vogel; A Cervantes; I Chau; B Daniele; J M Llovet; T Meyer; J-C Nault; U Neumann; J Ricke; B Sangro; P Schirmacher; C Verslype; C J Zech; D Arnold; E Martinelli Journal: Ann Oncol Date: 2018-10-01 Impact factor: 32.976