GP73 is an accurate serum marker for the detection of HCC and its recurrence after surgery, with higher sensitivity and specificity than AFP. Clinical implementation of serum GP73 measurement as a standard test for HCC is recommended.

The interaction between tumor and the immune system is still poorly understood. Significant clinical responses have been achieved in cancer patients treated with antibodies against the CTLA4 and PD-1/PD-L1 checkpoints; however, only a small portion of patients responded to the therapies, indicating a need to explore additional co-inhibitory molecules for cancer treatment. B7-H3, a member of the B7 superfamily, was previously shown by us to inhibit T-cell activation and autoimmunity. In this study, we have analyzed the function of B7-H3 in tumor immunity. Expression of B7-H3 was found in multiple tumor lines, tumor-infiltrating dendritic cells, and macrophages. B7-H3-deficient mice or mice treated with an antagonistic antibody to B7-H3 showed reduced growth of multiple tumors, which depended on NK and CD8 T cells. With a putative receptor expressed by cytotoxic lymphocytes, B7-H3 inhibited their activation, and its deficiency resulted in increased cytotoxic lymphocyte function in tumor-bearing mice. Combining blockades of B7-H3 and PD-1 resulted in further enhanced therapeutic control of late-stage tumors. Taken together, our results indicate that the B7-H3 checkpoint may serve as a novel target for immunotherapy against cancer.

Clinical symptoms are unreliable for these diagnoses and their differential diagnosis. Imaging evaluations and CA19-9 are of value for the recognition of cystadenoma and cystadenocarcinoma, but not for their differential diagnosis. Any recurrence of liver cyst after surgery or other treatments should lead one to suspect one of these diseases. Invasive examination and percutaneous fine-needle aspiration cytology are not recommended. Complete excision or careful enucleation should be the first treatment choice for a better prognosis.

Colorectal carcinoma (CRC) is one of the most common malignancies in the world. PD-1/PD-L1 inhibitors have benefited cancer patients with multiple tumor types. However, their efficacy for CRC is low and this treatment in melanoma patients results in adaptive resistance through upregulation of VISTA, another checkpoint inhibitory pathway. Thus, there is an urgent need to explore additional co-inhibitory molecular pathways such as VISTA for CRC treatment. In this study, C10orf54 (encoding VISTA) expression was analyzed by RNA-seq data from 367 CRC patients in human cancer datasets. Moreover, 28 clinical CRC specimens were used to assess VISTA protein expression. Human cancer datasets showed that CRC tumors expressed higher levels of C10orf54 than CD274 (encoding PD-L1). Moreover, C10orf54 mRNA expression was significantly correlated with genes responsible for tumor immune evasion. VISTA protein expression was high in tumors compared with para-tumors and normal tissues, which is similar to PD-L1 expression. However, in contrast to PD-L1, VISTA was mainly expressed by tumor-infiltrating lymphocytes. This study is the first investigation of VISTA expression in human resected CRC tumors, and the results justify the need for future studies on the role of VISTA in anti-CRC immunity in clinical samples.

Recurrences are more likely to develop within the first 6 months after resection for HCC. Multifocal HCC is an important risk factor associated with early recurrence of advanced HCC after hepatectomy. DSA may serve as an important surveillance for early detection of intrahepatic recurrence after surgery.

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Lung cancer is a leading cause of cancer-related mortalities worldwide. In the present study, a comparison of To determine the roles of ARHGAP10 in the proliferation, migration and invasion of lung cancer cells expression levels between normal lung tissues and lung cancer tissues were compared using immunoblotting, and CCK-8 and Transwell assays. Lung cancer tissues had a decreased ARHGAP10 mRNA expression level compared to the adjacent normal tissues. The ectopic expression of ARHGAP10 significantly suppressed the migration, invasion and proliferation of lung cancer cells. Gene set enrichment analysis revealed that metastasis and Wnt signaling pathways were negatively correlated with ARHGAP10 expression. Immunoblotting analysis revealed that ARHGAP10 overexpression inhibited metastasis [matrix metalloproteinase (MMP)-2, MMP-9 and VEGF] and the expression of Wnt pathway-related proteins (β-catenin and c-Myc). Moreover, the stimulation effects of lithium chloride, a GSK3β inhibitor, on the accumulation of β-catenin were notably suppressed by ARHGAP10 overexpression. Collectively, ARHGAP10 acts to suppress tumor within lung cancer by affecting metastasis and Wnt signaling pathways. The results therefore suggest that ARHGAP10 is a potentially attractive target for the treatment of lung cancer.

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