Abstract

// Chang Liu 1, * , Guo-Jun Zeng 2, * , Bang-Sheng Jia 3 , Jia-Yin Yang 1 , Li Jiang 1 , Hua Du 1 , Wu-Ran Wei 4 , Bing-Wen Zou 5 and Wu-Sheng Lu 1 1 Department of Liver Surgery and Liver Transplantation Center, West China Hospital, Sichuan University, Chengdu, 610041, China 2 Department of Vascular Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China 3 Department of Radiology, West China Hospital, Sichuan University, Chengdu, 610041, China 4 Department of Urology, West China Hospital, Sichuan University, Chengdu, 610041, China 5 Division of Thoracic Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan, 610041, China * These authors contributed equally to this work Correspondence to: Wu-Sheng Lu, email: luwu8@126.com Keywords: neutrophil-to-lymphocyte ratio; platelet-to-lymphocyte ratio; hepatocellular carcinoma (HCC); transarterial chemoembolization (TACE); 131 I-labeled-metuxima (Licartin) Received: May 27, 2017      Accepted: November 08, 2017      Published: January 02, 2018 ABSTRACT Background: The prognostic value of NLR and PLR in unresectable HCC patients undergoing 131 I-labeled-metuximab plus transarterial chemoembolization has not been studied. Materials and Methods: 184 patients with unresectable HCC were enrolled from 2009 to 2011. Data were acquired through patients' medical records and follow-up. Receiver operating curves (ROC) were used to determine the optimal cut-off levels of NLR and PLR. Kaplan-Meier univariate analysis and multivariate Cox regression analysis were used to evaluate the correlation of the NLR, PLR, and other potential prognostic factors with overall survival. Results: The optimal cutoff levels were 2.5 for NLR and 105 for PLR by ROC curve analysis. Patients with NLR ≥ 2.5 and PLR ≥ 105 groups had significantly worse OS. The median survival time for patients with low NLR and high NLR were 19 months (2–35 months) and 10 months (2–34 months) respectively. And median survival time were 13 months (2–35 months) and 21 months (2–35 months) in the high and low PLR group respectively. Multivariate analysis showed that NLR ≥ 2.5 (HR, 2.41; 95% CI, 1.26–4.13; P = 0.034, PLR ≥ 105 (HR, 1.79; 95% CI, 1.17–3.41; P = 0.028), tumor ≥ 10 cm (HR, 1.81; 95% CI, 1.04–2.62; P = 0.016), BCLC C stage (HR,3.12; 95% CI, 1.72–4.98; P = 0.021) and albumin 35 < g/L (HR, 0.56; 95% CI, 0.34–0.95; P = 0.03) were independent risk factors for OS. Conclusions: Elevated NLR and PLR were independent factors of a poor prognosis in unresectable patients undergoing 131 I-labeled-metuximab plus TACE.

Highlights

  • Hepatocellular carcinoma (HCC) is among the most prevalent cancers worldwide, and is the third leading cause of cancer-related mortality [1]

  • Multivariate analysis showed that neutrophilto-lymphocyte ratio (NLR) ≥ 2.5 (HR, 2.41; 95% confidence interval (CI), 1.26–4.13; P = 0.034, platelet-to-lymphocyte ratio (PLR) ≥ 105 (HR, 1.79; 95% CI, 1.17–3.41; P = 0.028), tumor ≥ 10 cm (HR, 1.81; 95% CI, 1.04–2.62; P = 0.016), Barcelona Clinic Liver Cancer system (BCLC) C stage (HR, 3.12; 95% CI, 1.72–4.98; P = 0.021) and albumin 35 < g/L (HR, 0.56; 95% CI, 0.34–0.95; P = 0.03) were independent risk factors for OS

  • Licartin is an F(ab)2 fragment of a mouse-derived HAb18/CD147 antibody, studies have demonstrated that HAb18G/ CD147 expression is high in HCC tissues (75%) but is not present in normal liver tissue, and its expression is closely related with HCC metastasis [8, 9]

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Summary

Introduction

Hepatocellular carcinoma (HCC) is among the most prevalent cancers worldwide, and is the third leading cause of cancer-related mortality [1]. Radioimmunotherapy (RIT) has provided a new therapeutic approach for patients with HCC resulting in improved clinical outcome without severe side effects [5,6,7] as radiolabeled antibodies injected via the tumor feeding artery can bind and accumulated in cancer tissues, thereby destroying as much as tumor cells without normal tissue and the surrounding organs. The therapeutic effects of Licartin are primarily performed via the following mechanisms [5]: first, metuximab blocks HAb18G/CD147 antigen-induced signal transduction pathways by binding to the HAb18G/ CD147 antigen on the surface of HCC cells, as a result, reducing liver cancer metastasis and recurrence [5]. A previous multicenter phase IV clinical study [10] and other research [11, 12] have demonstrated satisfactory tumor targeting, suggesting high efficacy and a favorable toxicity profile of this combination therapy in treatment of intermediate to advanced HCC. The prognostic value of NLR and PLR in unresectable HCC patients undergoing 131I-labeled-metuximab plus transarterial chemoembolization has not been studied

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