Abstract
Hepatocellular carcinoma (HCC) is one of the most common tumors in the world, and its mortality is still on the rise. Limited treatments and low chemotherapy sensitivity of HCC make new therapeutic strategies urgently needed. With the rise of immune checkpoint blockade, anti-CTLA-4 antibodies and anti-PD-1 antibodies have shown therapeutic effects in various tumors. T cell immunoglobulin mucin-3 (Tim-3), a newly discovered immune checkpoint molecule, plays a major role in the development of HCC. Tim-3 can be used to evaluate the prognosis and therapeutic effects in HCC, and Tim-3 intervention has shown anti-tumor effects in preclinical experiments. This review summarizes findings regarding Tim-3 and HCC in recent years and discusses the rationale of Tim-3 as a therapeutic target for HCC.
Highlights
Hepatocellular carcinoma (HCC) is the most common primary liver cancer
Liu et al Journal of Hematology & Oncology (2018) 11:126 immunoglobulin mucin-3 (Tim-3) antibodies have curative effects in laboratory-scale studies in several tumors, and some of them have entered phase I/II clinical trials (Table 1); T cell immunoglobulin mucin-3 (Tim-3) has the potential to become a new target for cancer immunotherapy
The results indicate that Tim-3+CD8+ T cells in sustained responders (SRs) obtain potential anti-tumor effects when appropriately stimulated by tumor antigens released under radiotherapy
Summary
Hepatocellular carcinoma (HCC) is the most common primary liver cancer. It is the sixth most common tumor and the third leading cause of cancer death [1]. Liu et al Journal of Hematology & Oncology (2018) 11:126 immunoglobulin mucin-3 (Tim-3) antibodies have curative effects in laboratory-scale studies in several tumors, and some of them have entered phase I/II clinical trials (Table 1); Tim-3 has the potential to become a new target for cancer immunotherapy. Ligands and functions of Tim-3 Tim-3 plays a key role in inhibiting both adaptive and innate immune responses. The most studied Tim-3 ligands are galectin-9 (Gal-9), phosphatidylserine (PtdSer), highmobility group box-1 protein (HMGB1), and carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM-1) (Table 2). Interaction of PtdSer with Tim-3 on DCs mediates elimination of apoptosis cells and cross-presentation [17], while interaction of HMGB1 and Tim-3 on DCs suppresses nucleic acidmediated innate immune responses in tumor site [18]. GT+TT genotypes of rs10053538 in chronic hepatitis B (CHB) patients
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