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08 June 2021, Volume 48 Issue 6 Previous Issue    Next Issue

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Effects of NFAT5 inhibition on proliferation, invasion, migration and apoptosis of lung adenocarcinoma cells Jiang Mengting, Wang Jiachun, Zong Jing 2021, 48 (6):  321-327.  doi: 10.3760/cma.j.cn371439-20201026-00062 Abstract ( 359 )   HTML ( 34 )   PDF (2052KB) ( 220 )   Save Objective To investigate the expressions of nuclear factor of activated T cell 5 (NFAT5) in lung adenocarcinoma tissues and cells, and the effects of NFAT5 on the proliferation, invasion, migration and apoptosis of lung adenocarcinoma cells. Methods The clinical pathological specimens and paracancerous tissues of 61 patients with lung adenocarcinoma diagnosed and treated in 904th Hospital of Joint Logistic Support Force of People's Liberation Army from June 2017 to June 2019 were collected. The expression levels of NFAT5 in lung adenocarcinoma tissues and paracancerous tissues were detected by quantitative real-time PCR (qRT-PCR), and the relationships between the expression of NFAT5 and clinicopathological features of patients were analyzed. H1975 cells were divided into control group (no treatment), NC group (transfecting siRNA-NC) and si-NFAT5 group (transfecting siRNA-NFAT5) . qRT-PCR was used to detect the expression level of NFAT5 in cell line. MTT and clone formation assay were used to detect cell proliferation. Transwell and scratch test were used to detect cell invasion and migration ability. Flow cytometry was used to detect cell apoptosis. The expressions of mitogen-activated protein kinase (MAPK) signaling pathway related proteins were detected by Western blotting. Results The expression level of NFAT5 mRNA in lung adenocarcinoma (3.22±0.20) was significantly higher than that in paracancerous tissues (1.00±0.12), and there was a statistically significant difference (t=75.662, P<0.001). The expression level of NFAT5 in lung adenocarcinoma tissue was associated with TNM stage (χ2=10.357, P=0.001) and lymph node metastasis (χ2=18.268, P<0.001). The expression levels of NFAT5 in the control group, NC group and si-NFAT5 group were 1.00±0.06, 1.01±0.05 and 0.31±0.06, and there was a statistically significant difference (F=140.498, P<0.001). The absorbance (A) values in the control group, NC group and si-NFAT5 group were 0.70±0.01, 0.55±0.01 and 0.35±0.01 at 24 h after transfection, 0.92±0.03, 0.87±0.06 and 0.57±0.06 at 48 h after transfection, 1.05±0.01, 0.90±0.01 and 0.66±0.01 at 72 h after transfection, and there were statistically significant differences (F=9.815, P=0.013; F=45.977, P<0.001; F=129.494, P<0.001). Further pairwise comparison showed that the proliferation abilities of the si-NFAT5 group at 24, 48 and 72 h were significantly lower than those of the control group and NC group (all P<0.001). The cell clone numbers in the three groups were 452.33±31.50, 421.00±17.35 and 129.00±17.35 respectively, with a statistically significant difference (F=128.200, P<0.001). The cell clone number in the si-NFAT5 group was significantly lower than that in the control group and NC group (both P<0.001). The invasion numbers of cells in the three groups were 262.67±28.02, 278.00±27.50 and 46.00±12.00 respectively, and there was a statistically significant difference (F=89.896, P<0.001). The cell invasive ability in the si-NFAT5 group was significantly lower than that in the control group and NC group (both P<0.001). The relative scratch widths in the three groups were 0.28±0.04, 0.32±0.04 and 0.54±0.04 respectively, and there was a statistically significant difference (F=42.889, P<0.001). The relative scratch width in the si-NFAT5 group was significantly increased than that in the control group and NC group (both P<0.001). The apoptosis rates in the three groups were (3.38±0.56)%, (3.14±0.62)% and (13.82±0.75)% respectively, and there was a statistically significant difference (F=264.705, P<0.001). The apoptosis rate in the si-NFAT5 group was significantly higher than that in the control group and NC group (both P<0.001). The differences of protein expressions of NFAT5, p-P38/P38, p-ERK1/2/ERK1/2, p-JNK/JNK among the three groups were statistically significant (F=91.245, P<0.001; F=132.896, P<0.001; F=243.332, P<0.001; F=118.358, P<0.001). The protein expressions of NFAT5, p-P38/P38, p-ERK1/2/ERK1/2, p-JNK/JNK in the si-NFAT5 group were all significantly lower than those in the control group and NC group, and there were statistically significant differences (all P<0.001). Conclusion The expression of NFAT5 is increased in lung adenocarcinoma tissues and cells. Inhibition of NFAT5 can inhibit proliferation, invasion and migration of lung adenocarcinoma H1975 cells, and promote apoptosis of H1975 cells. The mechanism may be related to the inhibition of MAPK signal pathway by NFAT5. Figures and Tables | References | Related Articles | Metrics

BMXΔN mediates gefitinib resistance of lung cancer cells through ERK/MAPK signaling pathway Yan Xingyu, Lian Zhenying, Diao Yutao, Liu Hongyan 2021, 48 (6):  328-334.  doi: 10.3760/cma.j.cn371439-20201230-00063 Abstract ( 320 )   HTML ( 24 )   PDF (1369KB) ( 210 )   Save Objective To explore the mechanism of a novel BMX splicing variant induced epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) gefitinib resistance in lung cancer. Methods Stable transgenic cell line PC9-BMXΔN and HCC827-BMXΔN were constructed by lentivirus infection of PC9 and HCC827 cells carrying EGFR mutation. The cells were divided into PC9-Vec group (PC9 cells transfected with empty vector), PC9-BMX group (PC9 cells stably expressing BMX), PC9-BMXΔN group (PC9 cells stably expressing BMXΔN) and HCC827-Vec group (HCC827 cells transfected with empty vector), HCC827-BMXΔN group (HCC827 cells stably expressing BMXΔN). Quantitative real-time PCR was used to detect the expression levels of mRNA. The protein expression levels in each group were detected by Western blotting. The cells in the PC9-Vec group and PC9-BMXΔN group were treated with 0, 0.01, 2.00, 50.00, 100.00, 200.00 nmol/L and 2.00, 4.00 μmol/L gefitinib. The cells in the HCC827-Vec group and HCC827-BMXΔN group were treated with 0, 0.01, 1.00, 10.00, 100.00 nmol/L and 1.00 μmol/L gefitinib. MTT method was used to detect cell viabilities. Results The PC9-BMXΔN cells were scattered and showed a fibroblast-like morphology. Compared with the PC9-Vec cells, the relative expression levels of fibronectin, N-cadherin, vimentin, Snail, Slug and TWIST 2 mRNA in PC9-BMXΔN cells were up-regulated. Compared with the PC9-Vec cells and PC9-BMX cells, the expression levels of fibronectin and vimentin protein in PC9-BMXΔN cells were up-regulated; while the expression level of E-cadherin protein in PC9-BMXΔN cells was significantly down-regulated. Compared with the PC9-Vec cells, the cell viabilities of PC9-BMXΔN cells treated with 0.01 nmol/L [(99.11±2.16)% vs. (91.29±1.91)%, t=-4.701, P=0.011], 2.00 nmol/L [(80.41±1.48)% vs. (63.36±2.14)%, t=-11.324, P<0.001], 50.00 nmol/L [(80.83±5.38)% vs. (60.22±3.61)%, t=-5.507, P=0.005], 100.00 nmol/L [(75.54±3.46)% vs. (59.93±1.91)%, t=-6.836, P=0.002], 200.00 nmol/L [(77.57±6.53)% vs. (56.70±2.88)%, t=-5.064, P=0.007], 2.00 μmol/L [(70.22±3.45)% vs. (53.14±0.89)%, t=-8.309, P=0.001], 4.00 μmol/L [(68.66±4.67)% vs. (52.30±2.59)%, t=-4.882, P=0.008] gefitinib were significantly increased, with statistically significant differences. Similarly, compared with the HCC827-Vec cells, the cell viabilities of HCC827-BMXΔN cells treated with 1.00 nmol/L [(64.36±2.49 )% vs. (47.13±4.21)%, t=-7.067, P=0.019], 10.00 nmol/L [(63.25±5.87)% vs. (43.28±2.95)%, t=-5.267, P=0.006], 100.00 nmol/L [(49.47±5.74)% vs. (37.12±4.92)%, t=-2.830, P=0.047], 1.00 μmol/L [(49.05±3.34)% vs. (32.06±4.73)%, t=-5.073, P=0.007] gefitinib were significantly increased, with statistically significant differences. Gefitinib treatment could significantly inhibit the expression levels of p-EGFR and p-ERK1/2 both in PC9-Vec cells, PC9-BMX cells and PC9-BMXΔN cells. Compared with the PC9-Vec cells and PC9-BMX cells, the expression level of p-EGFR in PC9-BMXΔN cells was significantly increased after gefitinib treatment for 8 h (0.91±0.04 vs. 0.81±0.04 vs. 0.80±0.05, all P<0.05); the expression levels of p-ERK1/2 in PC9-BMXΔN cells were significantly increased after gefitinib treatment for 2 h (0.64±0.06 vs. 0.38±0.12 vs. 0.37±0.14), 4 h (1.28±0.06 vs. 1.08±0.06 vs. 1.11±0.07), and 8 h (0.75±0.04 vs. 0.55±0.05 vs. 0.60±0.07), with statistically significant differences (all P<0.05). Conclusion BMXΔN is involved in EGFR-TKI gefitinib resistance in lung cancer, which may be achieved by inducing cells to undergo epithelial-mesenchymal transition and activating the ERK/MAPK signaling pathway. Figures and Tables | References | Related Articles | Metrics

Effects of decorin on proliferation, migration and invasion of bladder cancer cells Wang Ziyi, Chen Hongjie, Yang Ninggang, Zhang Jun, Zhang Xiangjun, Yu Xinning, Ma Zhongyi, Dai Enlai 2021, 48 (6):  335-340.  doi: 10.3760/cma.j.cn371439-20201007-00064 Abstract ( 246 )   HTML ( 11 )   PDF (2202KB) ( 139 )   Save Objective To investigate the effects of decorin (DCN) on the proliferation, migration and invasion of bladder cancer cells. Methods Bladder cancer T24 cell line was used as the research object. MTT assay was used to detect the inhibitory effect of DCN at different concentrations (0, 5, 10, 20, 30, 40, 50 mg/L) on T24 cell proliferation at 24, 48, 72 and 96 h. The effects of DCN on T24 cell cycle and apoptosis were analyzed by flow cytometry. MTT assay, Transwell migration and invasion experiments were used to detect the effects of DCN on the adhesion, migration and invasion ability of T24 cells. The effects of DCN on TGF-β1 and P21 protein expression were detected by ELISA and Western blotting. Results T24 cells were treated with 0, 5, 10, 20, 30, 40 and 50 mg/L DCN at 24, 48, 72 and 96 h, and there were statistically significant diffe-rences in cell proliferation activity (F=168.64, P<0.001; F=165.81, P<0.001; F=291.02, P<0.001; F=148.93, P<0.001). T24 cells were treated with 0, 5, 10, 20, 30, 40 and 50 mg/L DCN for 72 h, and the cell proliferation activities were (60.71±3.03)%, (40.82±2.09)%, (37.24±1.63)%, (25.65±2.55)%, (23.00±2.67)%, (10.78±1.17)%, (11.04±0.96)%, respectively, and there was a statistically significant difference. At the concentration of 40 mg/L, the proliferation activity reached the lowest level, and the inhibitory effect on cell proliferation was the strongest. At concentrations of 40 and 50 mg/L, the cells in G1 phase reached the peak value, while the cells in S phase reached the lowest value, and the cells in G2 phase remained unchanged throughout the treatment process. T24 cells were treated with 0, 5, 10, 20, 30, 40 and 50 mg/L DCN for 72 h, and the apoptosis rates of cells were (12.18±1.17)%, (21.24±1.05)%, (19.80±1.20)%, (26.52±1.40)%, (30.86±1.40)%, (52.99±1.22)%, (43.04±2.16)%, respectively, and there was a statistically significant difference (F=178.54, P<0.001). The differences between 5, 10, 20, 30, 40, 50 mg/L DCN and 0 mg/L DCN were all statistically significant (all P<0.001). When T24 cells were treated with 0, 40 mg/L DCN for 72 h, the cell adhesion rates were (37.14±1.35)% and (59.86±1.95)%, the numbers of migrated cells were 53.86±3.18 and 12.86±1.35, and there were statistically significant differences (t=25.25, P<0.001; t=31.36, P<0.001). When DCN was applied to T24 cells for 48 h, the numbers of invasion at 0, 40 mg/L were 235.14±3.44 and 160.86±3.13, and there was a statistically significant difference (t=2.27, P<0.001). When T24 cells were treated with 0, 5, 10, 20, 30, 40 and 50 mg/L DCN for 72 h, the relative expression levels of TGF-β1 were 85.67±3.35, 45.51±1.19, 49.93±4.15, 47.64±3.53, 46.05±3.18, 25.54±2.25, 33.44±4.05, and there was a statistically significant difference (F=324.58, P<0.001). Compared with 0 mg/L DCN, 5, 10, 20, 30, 40 and 50 mg/L DCN could significantly inhibited the expression of TGF-β1 (all P<0.001). Compared with 0 mg/L DCN, P21 protein was upregulated 72 h after treatment with 40 mg/L DCN. Conclusion DCN can inhibit proliferation and induce apoptosis of T24 cells in vitro, and has the effect of anti-metastasis of T24 cells. Figures and Tables | References | Related Articles | Metrics

Analysis of clinical characteristics and dosimetric factors on long-term survival in locally advanced thoracic esophageal squamous cell carcinoma Li Xiaoqin, Zhang Kaixian, Li Guang, Zheng Anping, Li Baosheng 2021, 48 (6):  341-349.  doi: 10.3760/cma.j.cn371439-20210205-00065 Abstract ( 306 )   HTML ( 18 )   PDF (959KB) ( 207 )   Save Objective To explore the effects of clinical characteristics and dosimetric factors on the survival and prognosis of patients with locally advanced thoracic esophageal squamous cell carcinoma after concurrent chemoradiotherapy (CCRT). Methods A total of 158 patients with locally advanced thoracic esophageal squamous cell carcinoma undergoing CCRT in Shandong Cancer Hospital, Anyang Cancer Hospital of Henan Province, Tengzhou Central People's Hospital of Shandong Province and the First Affiliated Hospital of China Medical University from August 2015 to October 2018 were selected as the research subjects. These patients were divided into standard-dose group (50.0-50.4 Gy, n=59) and high-dose group (>50.4 Gy, n=99) according to the radiotherapy dose. The overall survival (OS) and progression-free survival (PFS) of the two groups after treatment were compared. Kaplan-Meier method was used to calculate survival rate and survival comparison was performed by log-rank test. Cox proportional hazard regression model was used to analyze the adverse prognostic factors. The receiver operating characteristic (ROC) curve was used to analyze the predictive value of lung V30 for patient prognosis. Results In 158 patients with locally advanced esophageal squamous cell carcinoma, 19 cases (12.03%) had complete remission after CCRT, 103 cases (65.19%) had partial remission, 27 cases (17.09%) had stable disease, 9 cases (5.70%) had progression disease, and the total effective rate was 77.22%. The median OS of 158 patients was 41 months (95%CI: 25-57 months), and the 1- and 3-year OS rates were 76% and 51%, respectively. The median PFS was 24 months (95%CI: 13-35 months), and the 1- and 3-year PFS rates were 60% and 39%, respectively. The 1- and 3-year OS rates in the standard-dose group were 74% and 56%, and those in the high-dose group were 77% and 49%, with no statistically significant difference (χ2=0.300, P=0.584). The 1- and 3-year PFS rates in the standard-dose group were 62% and 37%, and those in the high-dose group were 59% and 40%, with no statistically significant difference (χ2<0.001, P=0.990). Univariate analysis showed that the length of the lesion, N stage, clinical stage, short-term efficacy of CCRT, planning target volume (PTV) Dmax, gross tumor volume (GTV) Dmean, V5, V10, V20, V30, Dmean of the left, right and bilateral lung were all the prognostic factors for OS and PFS (all P<0.05). Multivariate analysis showed that the length of the lesion (HR=2.226, 95%CI: 1.244-3.985, P=0.007), N stage (HR=2.819, 95%CI: 1.137-6.991, P=0.025), clinical stage (HR=1.897, 95%CI: 1.079-3.334, P=0.026), short-term efficacy of CCRT (HR=1.805, 95%CI: 1.250-2.606, P=0.002), left lung V10 (HR=0.811, 95%CI: 0.668-0.986, P=0.035), left lung V30 (HR=0.617, 95%CI: 0.408-0.933, P=0.022), right lung V20 (HR=2.067, 95%CI: 1.010-4.231, P=0.047), bilateral lung V10 (HR=1.299, 95%CI: 1.016-1.662, P=0.037) and bilateral lung V30 (HR=2.368, 95%CI: 1.142-4.910, P=0.021) were independent prognostic factors affecting OS. N stage (HR=2.433, 95%CI: 1.201-4.931, P=0.014), short-term efficacy of CCRT (HR=2.067, 95%CI: 1.391-3.071, P<0.001) and bilateral lung V30 (HR=0.113, 95%CI: 0.018-0.719, P=0.021) were independent prognostic factors affecting PFS. The ROC curve for predicting OS and PFS showed that the optimal cut-off value of bilateral lung V30 was 9.5%. Conclusion Compared with the standard-dose group, increasing the dose of radiotherapy fails to improve the long-term survival of patients with locally advanced thoracic squamous cell carcinoma. Lesion length, N stage, clinical stage, short-term efficacy of CCRT, left lung V10 and V30, right lung V20 , bilateral lung V10 and V30 are independent prognostic factors for OS in patients with locally advanced thoracic squamous cell carcinoma. N stage, short-term efficacy of CCRT and bilateral lung V30 are independent prognostic factors for PFS. When bilateral lung V30≤9.5%, the patients' OS and PFS will benefit from the treatment. Figures and Tables | References | Related Articles | Metrics

Reviews

Correlation between PD-L1 and Tregs in tumor immunity and immunotherapy Ou Huiyi, Wang Yue, Peng Chenghong 2021, 48 (6):  350-353.  doi: 10.3760/cma.j.cn371439-20200907-00066 Abstract ( 517 )   HTML ( 28 )   PDF (607KB) ( 206 )   Save Programmed death-1 (PD-1) and programmed death ligand-1 (PD-L1) are important co-inhibitory molecules, while regulatory T cells (Tregs) are important suppressor cells. The increase of them in tumor microenvironment is closely related to tumor immune escape and tumor development. PD-L1 plays an important role in the development and function of Tregs. The application of PD-1/PD-L1 blockade also affects the proliferation and function of Tregs, which further participates in the occurrence of drug resistance and hyperprogressive disease. Further understanding of the role and correlation of PD-L1 and Tregs in tumor immunity and immunotherapy can provide new ideas for improving the efficacy of PD-1/PD-L1 blockade. References | Related Articles | Metrics

Role of new immune checkpoints in tumor treatment Wu Yuanling, Shou Weizhen 2021, 48 (6):  354-357.  doi: 10.3760/cma.j.cn371439-20201119-00067 Abstract ( 263 )   HTML ( 15 )   PDF (609KB) ( 155 )   Save New immune checkpoint targets such as lymphocyte activation gene-3, T-cell immunoglobulin mucin-3, T cell immunoglobulin and ITIM domain, V-domain immunoglobulin suppressor of T cell activation, B7 Homolog 3, B and T lymphocyte attenuator play an important role in tumor treatment. Blocking them can delay tumor growth, enhance the anti-tumor effect of immune cells, and improve the survival rate of the host. Although these new immune checkpoints are in the early stages of research, with the continuous development of science and technology, they will play an increasingly important role in tumor immunotherapy. References | Related Articles | Metrics

Research and application of liquid biopsy based on epigenetic markers in the diagnosis and treatment of solid tumors Zhuang Weitao, Qiao Guibin 2021, 48 (6):  358-361.  doi: 10.3760/cma.j.cn371439-20200918-00068 Abstract ( 263 )   HTML ( 11 )   PDF (609KB) ( 155 )   Save Epigenetic changes are closely related to carcinogenesis, tumor progression and prognosis, which have a considerable potential in assisting the precision and minimally invasive management of cancers. The progress of detection techniques for DNA methylation, hydroxymethylation and histone modification has promoted the research works of liquid biopsy targeting epigenetic markers, and recently, important progress has been made in tumor location, early diagnosis, clinical staging, evaluation of treatment response, monitoring of recurrence and prognostic prediction of solid tumors. References | Related Articles | Metrics

Molecular mechanism of vasculogenic mimicry in brain glioma Guo Shihao, Ren Yeqing, Guo Geng 2021, 48 (6):  362-365.  doi: 10.3760/cma.j.cn371439-20200617-00069 Abstract ( 286 )   HTML ( 10 )   PDF (607KB) ( 165 )   Save Vasculogenic mimicry (VM) is a new tumor angiogenesis mode independent of endothelial cells and an important component of tumor microcirculation. The formation mechanism of VM in glioma is complex and variable. Various molecules and signal pathways (such as hypoxia induction factor and matrix metalloproteasefamily) interact in the formation process, to jointly regulate the formation of VM. The in-depth study of molecular mechanism can provide a theoretical basis for drug research and development against VM formation. References | Related Articles | Metrics

MET14 exon skipping mutation and non-small cell lung cancer Zhou Ye, Yu Yan 2021, 48 (6):  366-369.  doi: 10.3760/cma.j.cn371439-20201207-00070 Abstract ( 951 )   HTML ( 26 )   PDF (609KB) ( 280 )   Save The molecular mechanism of the skipping mutation of MET14 exon (METex14) is mainly that the skipping of METex14 leads to the loss of the c-Cbl tyrosine binding site, which causes the proteasome-mediated degradation of MET protein to decrease, which continuously activates the MET signal, and finally leads to tumorigenesis. The incidence of METex14 skipping mutations in non-small cell lung cancer is 3%-4%. Drugs that act on skipping mutations of METex14 include crizotinib, capmatinib, tepotinib, savolitinib, and have a high objective remission rate and good safety. However, due to gene amplification, second site mutations, bypass activation and pathological type conversion, drug resistance after targeted drug therapy requires attention. References | Related Articles | Metrics

Research on the correlation between driver genes of lung adenocarcinoma and venous thromboembolism Li Tiantian, Shi Licheng, Kong Hui, Qi Xu 2021, 48 (6):  370-373.  doi: 10.3760/cma.j.cn371439-20201119-00071 Abstract ( 250 )   HTML ( 8 )   PDF (607KB) ( 117 )   Save Venous thromboembolism (VTE) is one of the common complications of lung adenocarci-noma. The state of the driver genes of lung adenocarcinoma is related to the risk of VTE. The common driver genes include epidermal growth factor receptor, anaplastic lymphoma kinase, c-ros oncogene 1 receptor kinase and Kirsten rat sarcoma viral oncogene, etc.. Based on the study of the correlation between lung adenocarci-noma driver genes and VTE, it is of great significance for the early clinical prevention of VTE in patients with lung adenocarcinoma to screen out patients with high risk of VTE according to the state of the driver genes and finally evaluate the risk of VTE in patients with lung adenocarcinoma by combining conventional risk factors with the driver genes. References | Related Articles | Metrics

CDX2 and gastrointestinal neoplasms Ju Xinyue, Hu Chunmei, Zhao Yue, Tang Yan 2021, 48 (6):  374-376.  doi: 10.3760/cma.j.cn371439-20201118-00072 Abstract ( 415 )   HTML ( 16 )   PDF (599KB) ( 198 )   Save Caudal type homeobox transcription factor 2 (CDX2) is an enteric-specific nuclear transcription factor, which is mainly expressed in the small intestine and colorectum and not expressed in normal gastric mucosa. CDX2 is involved in the occurrence, development, invasion and metastasis of gastrointestinal tumors, and its expression state is related to the clinicopathological characteristics and prognosis of patients with gastrointestinal tumors. It is expected to provide a new idea for the diagnosis and treatment of gastrointestinal tumors by further studying the mechanism of CDX2 involvement in tumor genesis and development and its relationship with clinicopathological features and prognosis. References | Related Articles | Metrics

Mechanism and immunotherapy of Kaposi sarcoma-associated herpesvirus and host immunity in the pathogenesis of Kaposi sarcoma Wang Fang, Wang Peng, Kang Xiaojing 2021, 48 (6):  377-380.  doi: 10.3760/cma.j.cn371439-20200923-00073 Abstract ( 240 )   HTML ( 9 )   PDF (606KB) ( 150 )   Save Kaposi sarcoma is a multiple pigmented hemangioma of soft tissue. The etiology of Kaposi sarcoma is still unclear. Its occurrence is related to Kaposi sarcoma-related herpesvirus. Kaposi sarcoma-associated herpes virus plays an important role in the occurrence and development of Kaposi sarcoma by interfering with the pattern recognition receptors, complement system, or effecting on the immune cells directly to evasive host immune system. The immune modulators, immunotherapy of targeted drugs and vaccines are expected to be the new methods for the prevention and treatment of Kaposi sarcoma. References | Related Articles | Metrics

Immune, targeted therapy and related issues of relapsed/refractory multiple myeloma Sun Ruijie, Shan Ningning 2021, 48 (6):  381-384.  doi: 10.3760/cma.j.cn371439-20200622-00074 Abstract ( 289 )   HTML ( 8 )   PDF (606KB) ( 174 )   Save The new immune and targeted therapy medicines of multiple myeloma and recurrence of refractory multiple myeloma mainly include immunomodulatory drugs, proteasome inhibitors, monoclonal antibody, immune monitoring point inhibitors, histone deacetylase and chimeric antigen receptor. Although the emergence of new drugs and the application of autologous hematopoietic stem cell transplantation have significantly improved the prognosis of patients, more effective treatment methods and treatment strategies are still required to deal with the adverse reactions and the condition of recurrence during treatment. References | Related Articles | Metrics