Abstract
Considering the increasing importance of immune checkpoints in tumor immunity we investigated the clinical relevance of serum T-cell immunoglobulin and mucin domain-3 (TIM-3) in patients with hepatocellular carcinoma (HCC). Serum TIM-3 levels were measured and their association with HCC stage and the detection of serum programmed death ligand-1 (PD-L1) were assessed. In patients submitted to transarterial chemoembolization (TACE), pre- and 1-week post-treatment TIM-3 levels were also evaluated. We studied 53 HCC patients with BCLC stages: 0 (5.7%), A (34%), B (32.1%), C (22.6%), and D (5.7%). The patients with advanced HCC (BCLC C) had significantly higher TIM-3 levels than patients with BCLC A (p = 0.009) and BCLC B (p = 0.019). TIM-3 levels were not associated with HCC etiology (p = 0.183). PD-L1 detection (9/53 patients) correlated with TIM-3 levels (univariate analysis, p = 0.047). In 33 patients who underwent TACE, post-treatment TIM-3 levels (231 pg/mL, 132–452) were significantly higher than pre-TACE levels (176 pg/mL, 110–379), (p = 0.036). Complete responders had higher post-TACE TIM-3 levels (534 pg/mL, 370–677) than partial responders (222 pg/mL, 131–368), (p = 0.028). Collectively, TIM-3 may have a role in anti-tumor immunity following TACE, setting a basis for combining immunotherapy and chemoembolization.
Highlights
Hepatocellular carcinoma (HCC) is the fifth most common cancer globally and develops mainly in the presence of cirrhosis, as a result of chronic viral hepatitis or other chronic liver disease [1]
According to the findings of this study, serum T-cell immunoglobulin and mucin domain-3 (TIM-3) levels are associated with HCC stage in patients with various types of underlying liver disease
Treatment with transarterial chemoembolization (TACE) causes an escalation of circulating TIM-3 levels, while higher post-treatment serum TIM-3 values were observed in patients with complete response comparing to patients with partial response
Summary
Hepatocellular carcinoma (HCC) is the fifth most common cancer globally and develops mainly in the presence of cirrhosis, as a result of chronic viral hepatitis or other chronic liver disease [1]. It has been proven that the upregulated expression of immune inhibitory molecules such as programmed death-1 (PD-1) by antigen presenting cells (APCs) and by T cells in the tumor microenvironment has a critical role in the establishment of a defective immune response against HCC [3,4]. This effect is further enhanced through the secretion of activating ligands such as PD-1-ligand (PD-L1) by tumor cells and by tumor associated macrophages (TAMs). An anti-PD-1 monoclonal antibody, is the first immunotherapeutic agent that
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