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2018 ; 37
(1
): 110
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Immune checkpoint therapy in liver cancer
#MMPMID29843754
Xu F
; Jin T
; Zhu Y
; Dai C
J Exp Clin Cancer Res
2018[May]; 37
(1
): 110
PMID29843754
show ga
Immune checkpoints include stimulatory and inhibitory checkpoint molecules. In
recent years, inhibitory checkpoints, including cytotoxic T lymphocyte-associated
antigen 4 (CTLA-4), programmed cell death protein-1 (PD-1), and programmed cell
death ligand 1 (PD-L1), have been identified to suppress anti-tumor immune
responses in solid tumors. Novel drugs targeting immune checkpoints have
succeeded in cancer treatment. Specific PD-1 blockades were approved for
treatment of melanoma in 2014 and for treatment of non-small-cell lung cancer in
2015 in the United States, European Union, and Japan. Preclinical and clinical
studies show immune checkpoint therapy provides survival benefit for greater
numbers of patients with liver cancer, including hepatocellular carcinoma and
cholangiocarcinoma, two main primary liver cancers. The combination of
anti-PD-1/PD-L1 with anti-CTLA-4 antibodies is being evaluated in phase 1, 2 or 3
trials, and the results suggest that an anti-PD-1 antibody combined with
locoregional therapy or other molecular targeted agents is an effective treatment
strategy for HCC. In addition, studies on activating co-stimulatory receptors to
enhance anti-tumor immune responses have increased our understanding regarding
this immunotherapy in liver cancer. Epigenetic modulations of checkpoints for
improving the tumor microenvironment also expand our knowledge of potential
therapeutic targets in improving the tumor microenvironment and restoring immune
recognition and immunogenicity. In this review, we summarize current knowledge
and recent developments in immune checkpoint-based therapies for the treatment of
hepatocellular carcinoma and cholangiocarcinoma and attempt to clarify the
mechanisms underlying its effects.
|*Molecular Targeted Therapy
[MESH]
|Animals
[MESH]
|Antineoplastic Agents, Immunological/*pharmacology/*therapeutic use
[MESH]