Background: Thanks to the rapid development of computer-based systems and deep-learning-based algorithms, artificial intelligence (AI) has long been integrated into the healthcare field. AI is also particularly helpful in image recognition, surgical assistance and basic research. Due to the unique nature of dermatology, AI-aided dermatological diagnosis based on image recognition has become a modern focus and future trend. Key scientific concepts of review: The use of 3D imaging systems allows clinicians to screen and label skin pigmented lesions and distributed disorders, which can provide an objective assessment and image documentation of lesion sites. Dermatoscopes combined with intelligent software help the dermatologist to easily correlate each close-up image with the corresponding marked lesion in the 3D body map. In addition, AI in the field of prosthetics can assist in the rehabilitation of patients and help to restore limb function after amputation in patients with skin tumors. The aim of the study: For the benefit of patients, dermatologists have an obligation to explore the opportunities, risks and limitations of AI applications. This study focuses on the application of emerging AI in dermatology to aid clinical diagnosis and treatment, analyzes the current state of the field and summarizes its future trends and prospects so as to help dermatologists realize the impact of new technological innovations on traditional practices so that they can embrace and use AI-based medical approaches more quickly.

Background. The DNA repair enzyme poly(ADP-ribose) polymerase (PARP) is involved in DNA damage repair and cell death. However, the association between PARPs biological activities and the immune microenvironment in hepatocellular carcinoma (HCC) is unclear. The present study will explore whether combining a PARP inhibitor with anti-PD1 might improve the anti-HCC impact and explain how it works. Method. The PARP inhibitor olaparib was screened out of 867 drugs through Cell Counting Kit 8 (CCK-8) assay. The expression of PARP was verified through the TCGA and TISIDB databases. The impacts exerted by PARP inhibitor olaparib to HCC cells were assessed via wound healing, Transwell, and proliferation assay. In vivo, experiments were performed in a C57BL/6 mouse model to evaluate the function of PARP inhibitor olaparib combination with anti-PD1 in HCC and mice tumors were further detected by immunohistochemically staining. Result. Olaparib was selected as the research object on the basis of drug screening. The results of the TCGA and Human Protein Atlas databases revealed that PARP was significantly upregulated in carcinoma cell cluster of HCC tissues compared to normal tissues. Higher expression of PARP showed a poorer prognosis based on Kaplan-Meier Plotter. qRT-PCR experiments confirmed that olaparib could increase PD-L1 expression through inhibiting miR-513 in HCC cells. In vivo, experiment confirmed that the combination of olaparib and anti-PD1 could enhance the immunotherapy effect of HCC. Conclusion. The present study reveals that inhibition of PARP potentiates immune checkpoint therapy through the miR-513/PD-L1 pathway in HCC and the combination of PARP inhibitor olaparib and anti-PD1 is beneficial to HCC therapy.

Background. Breast cancer (BC) is the most common cause of cancer death worldwide, and its incidence is increasing every year. This study aims to investigate the expression characteristics of ADAR gene in breast cancer and to explore its role in the occurrence and development of BC and its possible mechanism. Methods. TCGA portal was used to detect the expression of ADAR in cancer including BC, and its correlation with clinicopathological data as well as other genes was analyzed via UALCAN database. The TISCH database evaluated the expression of ADAR in different types of cell populations in BC at the single-cell level. The KaplanMeier plotter database was used to predict the correlation between ADAR expression and BC patient prognosis. The Human Protein Atlas was used to detect the expression of ADAR in tissues and location of ADAR mRNA in cells. Moreover, the relationships between immune response and ADAR expression in BC were assessed with the use of the TISIDB. Metascape and STRING were applied to predict ADAR with other protein interactions. Finally, the effect generated by ADAR expression on cell proliferating, invading, and migrating processes was assessed in vitro with knockdown and overexpression strategies. Results. ADAR was significantly upregulated in BC tissues compared to paracancerous tissues. Single-cell RNA analysis showed that ADAR was specifically upregulated in cancer cell clusters and was also expressed in stromal and immune cell clusters. The upregulation of ADAR was positively correlated with clinicopathological stage and negatively correlated with BC prognosis. Experimental processes in vitro revealed ADAR knockdown hindered, proliferated, invaded, and migrated levels of BC cells, whereas over expression of ADAR played the opposite effect. ADAR protein, which may interact with OASL, STAT2, and IFIT3, was mainly located in the nucleoli in cells and primarily involved DNA modification and apoptotic signaling pathway. Immune factors may interact with ADAR in BC, and ADAR was found noticeably linked with immunosuppressor such as IL10, CD274, and IDO1. Conclusion. ADAR is significantly upregulated in breast cancer tissues, which may promote the progression of BC through the interaction of cancer cells, stromal cells, and immune cells. Targeting ADAR may offer new hope in treating breast cancer.

Ablation is one of the main methods for local treatment of hepatocellular carcinoma (HCC). Different from radiofrequency ablation (RFA), microwave ablation (MWA) is not limited by tissue conductivity, and can use multiple electrodes at the same time to improve ablation efficiency. In addition, MWA can form a larger ablation area, which makes it possible to completely ablate large HCC. However, MWA may be incomplete due to factors such as larger tumors or tumors in high-risk areas. The mechanism by which the cellular and tumor immune microenvironment (TIME) is involved in the in vitro effects of incomplete microwave ablation (iMWA) needs to be further elucidated. H22 tumor-bearing C57BL/6 mice were treated with iMWA with several combinations of ablation power and time duration. The effects of iMWA on the genes of HCC cancer cells and the TIME were investigated by RNA sequencing, mass cytometry, immunohistochemistry, and immunofluorescence. The effect of iMWA in combination with anti-Gr-1 on HCC tumor growth was also evaluated. Thermal stress generated by iMWA induced coagulative necrosis and apoptosis in the region of the ablation center of HCC. RNA sequencing analysis showed that iMWA can boost chemokine CXCL5, which was further confirmed by quantitative real time polymerase chain reaction (qRT-PCR). Mass cytometry results showed that relative to Ctrl group, iMWA-treated led to decreased CD4+ T, CD8+ T, Natural killer (NK), macrophages including both M1 and M2 types but increased monocytes and bone marrow-derived suppressor cells (MDSC). Therefore, inhibiting MDSC is the main target in the later stage of iMWA. In vivo results showed that the tumor volume and weight of iMWA+ anti-Gr-1 group were significantly reduced compared with iMWA+ anti-IgG group. In addition, the merged expressions of CD11b and Gr-1 proteins were found reduced in the iMWA+ anti-Gr-1 group compared with the iMWA+ anti-IgG group by immunofluorescence staining. Immunohistochemistry suggested that CD8 was enriched in the iMWA+ anti-Gr-1 group but not in the iMWA+ anti-IgG group. Our data suggests that iMWA and Gr-1 blocking combined therapy can further inhibit HCC growth and significantly improve the CD8+ T cells in the mouse subcutaneous tumor model, which brings good news to HCC patients.