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Volume 26,Issue 2,2019 Table of Contents
2019, 26(2):137-145.
DOI: 10.3872/j.issn.1007-385X.2019.02.001
Abstract:
[Abstract] In recent years, immune checkpoint inhibitors have been continuously researched and developed, and gradually expanded in clinical practice, rapidly changing the treatment mode of lung cancer. At present, a number of immunotherapeutic drugs are also actively developed in China and gradually applied to clinical research, indicating that China has entered a new era of immunotherapy.However, with the continuous expansion of clinical research and the continuous accumulation of experimental data, it also brings us many new challenges and new thinking. This article mainly analyzes the development status and challenges of immunotherapy for lung cancer in the aspects of breakthroughs in treatment modes, special populations excluded from clinical immunotherapy trials, response evaluation, treatment-related adverse events and predictive biomarkers.
[Abstract] In recent years, immune checkpoint inhibitors have been continuously researched and developed, and gradually expanded in clinical practice, rapidly changing the treatment mode of lung cancer. At present, a number of immunotherapeutic drugs are also actively developed in China and gradually applied to clinical research, indicating that China has entered a new era of immunotherapy.However, with the continuous expansion of clinical research and the continuous accumulation of experimental data, it also brings us many new challenges and new thinking. This article mainly analyzes the development status and challenges of immunotherapy for lung cancer in the aspects of breakthroughs in treatment modes, special populations excluded from clinical immunotherapy trials, response evaluation, treatment-related adverse events and predictive biomarkers.
2019, 26(2):146-151.
DOI: 10.3872/j.issn.1007-385X.2019.02.002
Abstract:
[Abstract] Objective: To investigate whether GSDME affects the sensitivity of breast cancer MCF-7 cells to paclitaxel (PTX) by regulating cell pyroptosis. Methods: GSDME was knocked-down in MCF-7 cells by RNA interference technique. CCK-8 assay, flow cytometry,lactate dehydrogenase (LDH) release method and Wb were respectively used to detect cell proliferation, pyroptotic rate, LDH release, GSDME-N-terminal protein and cleaved-caspase-3 protein levels in PTX-treated MCF-7 cells before and after GSDME knockdown.Results: Compared with the control group, the pyroptotic rate, LDH release, GSDME-N-terminal protein and cleaved-caspase-3 protein levels in the PTX-treatment group significantly increased (all P<0.01). Compared with the si-NC group, the PTX-sensitivity of si-GSDME group decreased, and the pyroptotic rate, LDH release and GSDME-N-terminal protein all significantly decreased (all P<0.01). Conclusion: Knock-down of GSDME in MCF-7 cells significantly inhibited cell pyroptosis and reduced drug sensitivity of MCF-7 cells to PTX.
[Abstract] Objective: To investigate whether GSDME affects the sensitivity of breast cancer MCF-7 cells to paclitaxel (PTX) by regulating cell pyroptosis. Methods: GSDME was knocked-down in MCF-7 cells by RNA interference technique. CCK-8 assay, flow cytometry,lactate dehydrogenase (LDH) release method and Wb were respectively used to detect cell proliferation, pyroptotic rate, LDH release, GSDME-N-terminal protein and cleaved-caspase-3 protein levels in PTX-treated MCF-7 cells before and after GSDME knockdown.Results: Compared with the control group, the pyroptotic rate, LDH release, GSDME-N-terminal protein and cleaved-caspase-3 protein levels in the PTX-treatment group significantly increased (all P<0.01). Compared with the si-NC group, the PTX-sensitivity of si-GSDME group decreased, and the pyroptotic rate, LDH release and GSDME-N-terminal protein all significantly decreased (all P<0.01). Conclusion: Knock-down of GSDME in MCF-7 cells significantly inhibited cell pyroptosis and reduced drug sensitivity of MCF-7 cells to PTX.
HAO Ruidong
,
TIAN Fang
,
YANG Zhenli
,
WANG Minliang
,
Zhang Dating
,
LI Yantao
,
FAN Pengcheng
,
WU Guoxiang
,
ZHU Xuejun
,
LIU Gentao
2019, 26(2):152-158.
DOI: 10.3872/j.issn.1007-385X.2019.02.003
Abstract:
[Abstract] Objective：To explore a novel chimeric antigen receptor (CAR)-T cell treatment to treat Multiple Myeloma (MM) via target B cell maturation antigen (BCMA). Methods：A CAR-BCMA molecular was constructed based on mouse originated BCMA scFv, and was packaged into lentiviral vector and transfected into T cells from healthy donors to construct CAR-BCMA-T cells. The BCMA positive cell lines A549-BCMA, A549-BCMAOFP and K562-BCMA were constructed as target cells. Then, the CAR-BCMA-T cells were co-incubated with the constructed target cells and human myeloma U266 cells, and the cytotoxic effects of CAR-BCMA-T cells were evaluated via CCK-8 and FACS. Finally, the CAR-BCMA-T cells originated from MM patients were constructed, and its cytotoxicity against A549-BCMA were examined; in addition, the IFN-γ release level in CAR-BCMA-T cells was evaluated by ELISA and FACS.Results: After 11 days’incubation, the CAR-BCMA-T cells originated from healthy donors amplified 300 times with a positive rate of 43%. The BCMA positive target cell lines were constructed successfully. Under an effector : target ratio of 5:1, the killing rates of CARBCMA-T cells against A549-BCMA, K562-BCMA and U266 were about 80%, 60%, and 80%, respectively, which were significantly higher than those against BCMA negative cells; and the cytotoxicity was related to the BCMA expression level in target cells. What’s more, at the effector : target ratio of 20:1, the CAR-BCMA-T cells originated from MM patients were demonstrated to exhibit a killing rate of more than 95% against A549-BCMA positive cells, and produced large amount of IFN-γ. Conclusion: CAR-BCMA-T cells originated from both healthy and MM donors were successfully constructed, and they can effectively and specifically kill BCMA positive tumor cells.
[Abstract] Objective：To explore a novel chimeric antigen receptor (CAR)-T cell treatment to treat Multiple Myeloma (MM) via target B cell maturation antigen (BCMA). Methods：A CAR-BCMA molecular was constructed based on mouse originated BCMA scFv, and was packaged into lentiviral vector and transfected into T cells from healthy donors to construct CAR-BCMA-T cells. The BCMA positive cell lines A549-BCMA, A549-BCMAOFP and K562-BCMA were constructed as target cells. Then, the CAR-BCMA-T cells were co-incubated with the constructed target cells and human myeloma U266 cells, and the cytotoxic effects of CAR-BCMA-T cells were evaluated via CCK-8 and FACS. Finally, the CAR-BCMA-T cells originated from MM patients were constructed, and its cytotoxicity against A549-BCMA were examined; in addition, the IFN-γ release level in CAR-BCMA-T cells was evaluated by ELISA and FACS.Results: After 11 days’incubation, the CAR-BCMA-T cells originated from healthy donors amplified 300 times with a positive rate of 43%. The BCMA positive target cell lines were constructed successfully. Under an effector : target ratio of 5:1, the killing rates of CARBCMA-T cells against A549-BCMA, K562-BCMA and U266 were about 80%, 60%, and 80%, respectively, which were significantly higher than those against BCMA negative cells; and the cytotoxicity was related to the BCMA expression level in target cells. What’s more, at the effector : target ratio of 20:1, the CAR-BCMA-T cells originated from MM patients were demonstrated to exhibit a killing rate of more than 95% against A549-BCMA positive cells, and produced large amount of IFN-γ. Conclusion: CAR-BCMA-T cells originated from both healthy and MM donors were successfully constructed, and they can effectively and specifically kill BCMA positive tumor cells.
2019, 26(2):159-165.
DOI: 10.3872/j.issn.1007-385X.2019.02.004
Abstract:
[Abstract] Objective: To investigate whether miR-140 could increase the sensitivity of cervical cancer (CC) to oxaliplatin by downregulating the expression of programmed death-1 (PD-L1). Methods: qPCR was used to analyze miR-140 expression in normal human cervical cells, CC cells and oxaliplatin-resistant CC cells. Cells were transfected with miR-140 mimic, and then, the proliferation of CC cells and oxaliplatin-resistant CC cells was detected by using CCK-8 assay, and the colony formation rate of CC cells was obtained by using colony formation assay. Starbase and TargetScan were used to predict the targeted binding site of miR-140 and PD-L1, and the influence of miR-140 on the expression of PD-L1 was validated by dual luciferase reporter gene assay. Annexin V FITC/PI double staining and Wb assays were used to detect the effect of over-expression of miR-140 or both over-expression of PD-L1 and miR140 on the apoptosis, migration and expression of apoptosis-related proteins in CC cells after treatment with oxaliplatin. Moreover, transplantation tumor of CC cell lines was established in nude mice to assess the effects of miR-140 on enhancing the sensitivity of tumors to oxaliplatin.Results: The expression of miR-140 was significantly decreased in oxaliplatin-resistant CC cells (P<0.01). Over-expression of miR-140 could significantly increase the sensitivity of oxaliplatin-resistant CC cells to oxaliplatin (P<0.05), and inhibit the CC cells proliferation and colony formation (P<0.01). miR-140 showed targeted binding to PD-L1 3'-UTR and inhibited its expression. Over-expression of miR-140 significantly promoted CC cell migration and apoptosis (P<0.01). However, co-transfection of PD-L1 counteracts the ef-fects of miR-140 on cell metastasis and apoptosis (all P<0.05). In addition, xenograft tumor model in mice also verified that miR-140 could promote the sensitivity of tumors to oxaliplatin. Conclusion: miR-140 increases the sensitivity of CC to oxaliplatin through inhibition of PD-L1 expression. Therefore, up-regulation of miR-140 or down-regulation of PD-L1 in combination with oxaliplatin may be a novel strategy for the treatment of Oxaliplatin-resistant CC.
[Abstract] Objective: To investigate whether miR-140 could increase the sensitivity of cervical cancer (CC) to oxaliplatin by downregulating the expression of programmed death-1 (PD-L1). Methods: qPCR was used to analyze miR-140 expression in normal human cervical cells, CC cells and oxaliplatin-resistant CC cells. Cells were transfected with miR-140 mimic, and then, the proliferation of CC cells and oxaliplatin-resistant CC cells was detected by using CCK-8 assay, and the colony formation rate of CC cells was obtained by using colony formation assay. Starbase and TargetScan were used to predict the targeted binding site of miR-140 and PD-L1, and the influence of miR-140 on the expression of PD-L1 was validated by dual luciferase reporter gene assay. Annexin V FITC/PI double staining and Wb assays were used to detect the effect of over-expression of miR-140 or both over-expression of PD-L1 and miR140 on the apoptosis, migration and expression of apoptosis-related proteins in CC cells after treatment with oxaliplatin. Moreover, transplantation tumor of CC cell lines was established in nude mice to assess the effects of miR-140 on enhancing the sensitivity of tumors to oxaliplatin.Results: The expression of miR-140 was significantly decreased in oxaliplatin-resistant CC cells (P<0.01). Over-expression of miR-140 could significantly increase the sensitivity of oxaliplatin-resistant CC cells to oxaliplatin (P<0.05), and inhibit the CC cells proliferation and colony formation (P<0.01). miR-140 showed targeted binding to PD-L1 3'-UTR and inhibited its expression. Over-expression of miR-140 significantly promoted CC cell migration and apoptosis (P<0.01). However, co-transfection of PD-L1 counteracts the ef-fects of miR-140 on cell metastasis and apoptosis (all P<0.05). In addition, xenograft tumor model in mice also verified that miR-140 could promote the sensitivity of tumors to oxaliplatin. Conclusion: miR-140 increases the sensitivity of CC to oxaliplatin through inhibition of PD-L1 expression. Therefore, up-regulation of miR-140 or down-regulation of PD-L1 in combination with oxaliplatin may be a novel strategy for the treatment of Oxaliplatin-resistant CC.
GUO Yanli
,
LIANG Xiaoliang
,
KUANG Gang
,
WU Xuan
,
KANG Xiaoliang
,
DONG Zhiming
,
SHEN Supeng
,
LIANG Jia
,
GUO Wei
2019, 26(2):166-172.
DOI: 10.3872/j.issn.1007-385X.2019.02.005
Abstract:
[Abstract] Objective: To screen the Hub genes associated with the occurrence and development of esophageal squamous cell carcinoma (ESCC) and to analyze their biological functions by using various bioinformatics analysis tools. Methods: ESCC chip profile GSE100942 from GEO database was used as study subject; GEO2R tool was used to analyze the data and to screen the differentially expressed genes (DEGs), and the bioinformatics tools (DAVID, String, Cytoscape) were further used to construct protein-protein interaction (PPI) network and identify the key Hub genes. GO and KEGG were used for the biological function enrichment analysis. In the meanwhile, MiRDB was applied to identify the miRNAs that might regulate Hub genes and to construct Hub gene–miRNA network.Importantly, the expression of DEGs and the patient survival were verified by the GEPIA analysis tool. Results: By analyzing GSE100942 database, a total of 1229 DEGs with difference of 2 times and 223 DEGs with difference of 4 times were screened out. In addition, 20 Hub genes, which were all up-regulated in ESCC tissues, were also identified. The functional enrichment analysis showed that these DEGs were mainly enriched in cancer related pathways and involved in cell division and mitotic nuclear division. Among those 20 Hub genes, DLGAP5, BUB1B, TPX2, TTK, CDC20, CCNB2, AURKA and DEPDC1 were identified as 8 key Hub genes that related with ESCC, and involved in many important biological processes, such as cell proliferation, cell cycle and signal pathway. Five Hub genes, CEP55, ECT2, NEK2, DEPDC1 and NUSAP1, were identified to be highly regulated by the miRNA regulatory network.Conclusion: Microarray combined with bioinformatics can effectively analyze the DEGs associated with the occurrence and develop-ment of ESCC. The identification of the 20 Hub genes and the 8 key Hub genes can provide theoretical guidance for further research on the molecular mechanism and molecular marker screening of ESCC.
[Abstract] Objective: To screen the Hub genes associated with the occurrence and development of esophageal squamous cell carcinoma (ESCC) and to analyze their biological functions by using various bioinformatics analysis tools. Methods: ESCC chip profile GSE100942 from GEO database was used as study subject; GEO2R tool was used to analyze the data and to screen the differentially expressed genes (DEGs), and the bioinformatics tools (DAVID, String, Cytoscape) were further used to construct protein-protein interaction (PPI) network and identify the key Hub genes. GO and KEGG were used for the biological function enrichment analysis. In the meanwhile, MiRDB was applied to identify the miRNAs that might regulate Hub genes and to construct Hub gene–miRNA network.Importantly, the expression of DEGs and the patient survival were verified by the GEPIA analysis tool. Results: By analyzing GSE100942 database, a total of 1229 DEGs with difference of 2 times and 223 DEGs with difference of 4 times were screened out. In addition, 20 Hub genes, which were all up-regulated in ESCC tissues, were also identified. The functional enrichment analysis showed that these DEGs were mainly enriched in cancer related pathways and involved in cell division and mitotic nuclear division. Among those 20 Hub genes, DLGAP5, BUB1B, TPX2, TTK, CDC20, CCNB2, AURKA and DEPDC1 were identified as 8 key Hub genes that related with ESCC, and involved in many important biological processes, such as cell proliferation, cell cycle and signal pathway. Five Hub genes, CEP55, ECT2, NEK2, DEPDC1 and NUSAP1, were identified to be highly regulated by the miRNA regulatory network.Conclusion: Microarray combined with bioinformatics can effectively analyze the DEGs associated with the occurrence and develop-ment of ESCC. The identification of the 20 Hub genes and the 8 key Hub genes can provide theoretical guidance for further research on the molecular mechanism and molecular marker screening of ESCC.
2019, 26(2):173-181.
DOI: 10.3872/j.issn.1007-385X.2019.02.006
Abstract:
[Abstract] Objective: To investigate the molecular mechanism of lncRNA-HCG11 promoting progression and metastasis of colorectal cancer (CRC) via up-regulating zinc finger E box binding homeobox 1 (ZEB1) by regulating miR-144-3p expression in CRC. Methods:A total of 78 pairs of CRC tissues and corresponding adjacent tissues were obtained from patients in Department of Colorectal Surgery,Cancer Hospital of Yunnan Province during January 2013 and January 2018. HCG11 expression level in CRC cell lines and tissues was determined by qPCR; HCG11-knockdown vector, miR-144-3p mimic and miR-144-3p inhibitor were constructed and transfected into CRC cells lines (SW480 and SW620); and then, cell viability was detected by using CCK-8 assay and colony formation assay,while cell migration and invasion was assessed by using transwell assay; the expression levels of ZEB1 and epithelial mesenchymal markers (E-cadherin, Vimentin, ɑ-catenin, Sox2, Nestin, Oct4 and Nanog) were detected by Wb and immunofluorescence assay; and the relationship between HCG11, miR-144-3p and ZEB1 was validated by dual-luciferase reporter gene assay. Nude mice xenograft model was constructed and the effect of HCG11 knock-down on the growth of xenograft was evaluated. Results: The expression of HCG11 was significantly higher in CRC cell lines (all P<0.05) and tissues (P<0.01) compared with that in normal colon epithelial cells and para-cancerous tissues; HCG11 expression was closely related with cancer metastasis, clinical staging and prognosis of CRC patients (all P<0.05). Knockdown of HCG11 significantly inhibited cells proliferation, migration, invasion, epithelial-mesenchymal transition and CRC stem cell formation (all P<0.05). Moreover, knockdown of HCG11 significantly up-regulated miR-144-3p expression (P<0.05),while over-expression of miR-144-3p significantly inhibited ZEB1 expression (P<0.05) and reduced dual-luciferase activity (P＜0.05).Conclusion: HCG11 regulates miR-144-3p to up-regulate ZEB1 expression, and further promotes CRC progression and metastasis;therefore, HCG11 could be used as a target for clinical diagnosis and treatment for CRC.
[Abstract] Objective: To investigate the molecular mechanism of lncRNA-HCG11 promoting progression and metastasis of colorectal cancer (CRC) via up-regulating zinc finger E box binding homeobox 1 (ZEB1) by regulating miR-144-3p expression in CRC. Methods:A total of 78 pairs of CRC tissues and corresponding adjacent tissues were obtained from patients in Department of Colorectal Surgery,Cancer Hospital of Yunnan Province during January 2013 and January 2018. HCG11 expression level in CRC cell lines and tissues was determined by qPCR; HCG11-knockdown vector, miR-144-3p mimic and miR-144-3p inhibitor were constructed and transfected into CRC cells lines (SW480 and SW620); and then, cell viability was detected by using CCK-8 assay and colony formation assay,while cell migration and invasion was assessed by using transwell assay; the expression levels of ZEB1 and epithelial mesenchymal markers (E-cadherin, Vimentin, ɑ-catenin, Sox2, Nestin, Oct4 and Nanog) were detected by Wb and immunofluorescence assay; and the relationship between HCG11, miR-144-3p and ZEB1 was validated by dual-luciferase reporter gene assay. Nude mice xenograft model was constructed and the effect of HCG11 knock-down on the growth of xenograft was evaluated. Results: The expression of HCG11 was significantly higher in CRC cell lines (all P<0.05) and tissues (P<0.01) compared with that in normal colon epithelial cells and para-cancerous tissues; HCG11 expression was closely related with cancer metastasis, clinical staging and prognosis of CRC patients (all P<0.05). Knockdown of HCG11 significantly inhibited cells proliferation, migration, invasion, epithelial-mesenchymal transition and CRC stem cell formation (all P<0.05). Moreover, knockdown of HCG11 significantly up-regulated miR-144-3p expression (P<0.05),while over-expression of miR-144-3p significantly inhibited ZEB1 expression (P<0.05) and reduced dual-luciferase activity (P＜0.05).Conclusion: HCG11 regulates miR-144-3p to up-regulate ZEB1 expression, and further promotes CRC progression and metastasis;therefore, HCG11 could be used as a target for clinical diagnosis and treatment for CRC.
2019, 26(2):182-189.
DOI: 10.3872/j.issn.1007-385X.2019.02.007
Abstract:
[Abstract] Objective: To investigate the mechanism of lncRNA MALAT1 modulating proliferation and metastasis of cervical cancer cells via regulating miR-124-3p/IGF2BP1 axis. Methods: A total of 45 cases of cervical cancer tissues and corresponding paracancerous tissues resected from patients, who were admitted to the Department of Obstetrics and Gynecology of Guiyang Maternal and Child Health Hospital during April 2014 and December 2017, were included in this study; in addition, cervical cancer cell lines SiHa, Caski,HeLa and C33awere also collected for this study. qPCR was applied to detect the expression of MALAT1 in cervical cancer tissues and cell lines. MALAT1-knockdown vectors, miR-124-3p inhibitors and IGF2BP1-overexpression vectors were constructed and used to transfect cervical cancer cells, respectively; the influence of MALAT1 or MALAT1 knockdown on cell proliferation, invasion and epithelial mesenchymal transition (EMT) via miR-124-3p/IGF2BP1 axis were determined by CCK-8 assay, Transwell assay, Wb and immunofluorescence,respectively. The interaction between MALAT1, miR-124-3p, and IGF2BP1 were verified by dual luciferase reporter gene assay. Results: MALAT1 was up-regulated in cervical cancer tissues and cell lines (P<0.05 or P<0.01). Meanwhile, MALAT1 knockdown remarkably inhibited proliferation, invasion and EMT of cervical cancer cells (P<0.05 or P<0.01). Moreover, dual-luciferase reporter gene assay showed that MALAT1 directly interacted with miR-124-3p and down-regulated its expression, while miR-124-3p negatively regulated IGF2BP1 expression. Our experiment further validated that MALAT1 knockdown suppressed proliferative, invasion and EMT of cervical cancer cells via inducing the inhibitory effect of miR-124-3p on IGF2BP1 (P<0.05 or P<0.01). Conclusion:MALAT1 promotes the proliferation, invasion and EMT of cervical cancer cells by down-regulating miR-124-3p/IGF2BP1 axis,which provides potential molecular targets for early diagnosis or treatment of cervical cancer.
[Abstract] Objective: To investigate the mechanism of lncRNA MALAT1 modulating proliferation and metastasis of cervical cancer cells via regulating miR-124-3p/IGF2BP1 axis. Methods: A total of 45 cases of cervical cancer tissues and corresponding paracancerous tissues resected from patients, who were admitted to the Department of Obstetrics and Gynecology of Guiyang Maternal and Child Health Hospital during April 2014 and December 2017, were included in this study; in addition, cervical cancer cell lines SiHa, Caski,HeLa and C33awere also collected for this study. qPCR was applied to detect the expression of MALAT1 in cervical cancer tissues and cell lines. MALAT1-knockdown vectors, miR-124-3p inhibitors and IGF2BP1-overexpression vectors were constructed and used to transfect cervical cancer cells, respectively; the influence of MALAT1 or MALAT1 knockdown on cell proliferation, invasion and epithelial mesenchymal transition (EMT) via miR-124-3p/IGF2BP1 axis were determined by CCK-8 assay, Transwell assay, Wb and immunofluorescence,respectively. The interaction between MALAT1, miR-124-3p, and IGF2BP1 were verified by dual luciferase reporter gene assay. Results: MALAT1 was up-regulated in cervical cancer tissues and cell lines (P<0.05 or P<0.01). Meanwhile, MALAT1 knockdown remarkably inhibited proliferation, invasion and EMT of cervical cancer cells (P<0.05 or P<0.01). Moreover, dual-luciferase reporter gene assay showed that MALAT1 directly interacted with miR-124-3p and down-regulated its expression, while miR-124-3p negatively regulated IGF2BP1 expression. Our experiment further validated that MALAT1 knockdown suppressed proliferative, invasion and EMT of cervical cancer cells via inducing the inhibitory effect of miR-124-3p on IGF2BP1 (P<0.05 or P<0.01). Conclusion:MALAT1 promotes the proliferation, invasion and EMT of cervical cancer cells by down-regulating miR-124-3p/IGF2BP1 axis,which provides potential molecular targets for early diagnosis or treatment of cervical cancer.
2019, 26(2):190-195.
DOI: 10.3872/j.issn.1007-385X.2019.02.008
Abstract:
[Abstract] Objective: To indentify the candidate genes and signaling pathways in lung adenocarcinoma by analyzing gene profiles with bioinformatics. Methods: The expression profiles of GSE40791, GSE68571, GSE43458, and GSE18842 were down-loaded from the Gene Expression Omnibus (GEO) database. The four microarray datasets were integrated to obtain the differentially expressed genes related to lung adenocarcinoma. STRING database was used to construct the protein-protein interaction (PPI) network of differentially expressed genes, and to further explore the gene modules and the key genes. DAVID was used to perform the gene enrichment analysis of each gene module, and to explore the regulatory function of each gene module in adenocarcinoma cells, as well as the relationship between the key genes in the module and the prognosis of the patients. Results: Thirty-seven up-regulated genes and 120 down-regulated genes were obtained from the primary screen, and the protein-protein interaction(PPI) network was successfully constructed. According to MCODE algorithm, we constructed gene modules and calculated the core genes (KIF14, SEPP1, SPP1,RBP4) in the PPI network. Finally, four modules were proved to be involved in regulation of cell cycle, blood coagulation, cell adhesion and cell metabolism, and four key genes were proved to be differentially expressed between lung adenocarcinoma tissues and normal tissues (all P<0.05). Survival analysis showed that expressions of KIF14, SEPP1 and SPP1 had significant effect on the prognosis of lung adenocarcinoma (P<0.01 or P<0.05), while RBP4 exerted insignificant difference in the survival rate of lung adenocarcinoma patients (P>0.05). Conclusion: With bioinformatics, three differentially expressed genes between lung adenocarcinoma tissues and normal adjacent tissues were finally screened out and proved to be closely related to the prognosis of patients, which provided new thoughts in the diagnosis and prognosis prediction of lung adenocarcinoma and improved the study efficiency on the mechanism of lung adenocarcinoma.
[Abstract] Objective: To indentify the candidate genes and signaling pathways in lung adenocarcinoma by analyzing gene profiles with bioinformatics. Methods: The expression profiles of GSE40791, GSE68571, GSE43458, and GSE18842 were down-loaded from the Gene Expression Omnibus (GEO) database. The four microarray datasets were integrated to obtain the differentially expressed genes related to lung adenocarcinoma. STRING database was used to construct the protein-protein interaction (PPI) network of differentially expressed genes, and to further explore the gene modules and the key genes. DAVID was used to perform the gene enrichment analysis of each gene module, and to explore the regulatory function of each gene module in adenocarcinoma cells, as well as the relationship between the key genes in the module and the prognosis of the patients. Results: Thirty-seven up-regulated genes and 120 down-regulated genes were obtained from the primary screen, and the protein-protein interaction(PPI) network was successfully constructed. According to MCODE algorithm, we constructed gene modules and calculated the core genes (KIF14, SEPP1, SPP1,RBP4) in the PPI network. Finally, four modules were proved to be involved in regulation of cell cycle, blood coagulation, cell adhesion and cell metabolism, and four key genes were proved to be differentially expressed between lung adenocarcinoma tissues and normal tissues (all P<0.05). Survival analysis showed that expressions of KIF14, SEPP1 and SPP1 had significant effect on the prognosis of lung adenocarcinoma (P<0.01 or P<0.05), while RBP4 exerted insignificant difference in the survival rate of lung adenocarcinoma patients (P>0.05). Conclusion: With bioinformatics, three differentially expressed genes between lung adenocarcinoma tissues and normal adjacent tissues were finally screened out and proved to be closely related to the prognosis of patients, which provided new thoughts in the diagnosis and prognosis prediction of lung adenocarcinoma and improved the study efficiency on the mechanism of lung adenocarcinoma.
2019, 26(2):196-199.
DOI: 10.3872/j.issn.1007-385X.2019.02.009
Abstract:
[Abstract] Objective: To investigate the inhibitory effect of Triptolide on vasculogenesis of human cervical microvascular endothelial cells, and to explore the mechanism. Methods: Human cervical microvascular endothelial cells (HCerMECs) were used as research subject,and treated with different concentrations of Triptolide (0, 5, 10, 20 and 40 ng/ml) in vitro. The effect of Triptolide on cell proliferation was determined by CCK-8, the cell migration ability was detected by Transwell assay while the expression of vascular endothelial growth factor (VEGF) was examined by western blotting. Results: Triptolide inhibited the proliferation and migration of HCerMECs in a dose-dependent manner (P<0.05). In addition, Triptolide could inhibit the expression of VEGF in HCerMECs in a concentration-dependent manner. Conclusions: Triptolide could inhibit the proliferation and migration activity of HCerMECs which is related with the suppression of VEGF expression.
[Abstract] Objective: To investigate the inhibitory effect of Triptolide on vasculogenesis of human cervical microvascular endothelial cells, and to explore the mechanism. Methods: Human cervical microvascular endothelial cells (HCerMECs) were used as research subject,and treated with different concentrations of Triptolide (0, 5, 10, 20 and 40 ng/ml) in vitro. The effect of Triptolide on cell proliferation was determined by CCK-8, the cell migration ability was detected by Transwell assay while the expression of vascular endothelial growth factor (VEGF) was examined by western blotting. Results: Triptolide inhibited the proliferation and migration of HCerMECs in a dose-dependent manner (P<0.05). In addition, Triptolide could inhibit the expression of VEGF in HCerMECs in a concentration-dependent manner. Conclusions: Triptolide could inhibit the proliferation and migration activity of HCerMECs which is related with the suppression of VEGF expression.
2019, 26(2):200-205.
DOI: 10.3872/j.issn.1007-385X.2019.02.010
Abstract:
[Abstract] Objective: To explore the related factors for efficacy and prognosis of personalized comprehensive treatment for T790Mpositive lung adenocarcinoma patients with bone metastasis. Methods: The clinical data of 68 patients undergoing personalized comprehensive treatment for T790M-positive lung adenocarcinoma with bone metastasis were retrospectively reviewed; chemotherapy, radiotherapy,molecule-targeted agents, Bevacizumab, bisphosphonate and other therapies were chosen for the patients, and the efficacy and prognosis were observed to explore the related factors. Results: Effective rate of personalized comprehensive treatment was 60.3% (41/68), with a median survival time of 23 months. Multiple factors showed significant effects on long-term efficacy, such as no radiotherapy,T790M mutation but no KRAS mutation, adjuvant scheme+rescue scheme in prior chemotherapy treatment, N1 stage, isolated bone metastasis, alternative treatment of osimertinib with chemotherapy, less metastasized organs and ECOG scores<2 (P<0.05). Multivariate analysis revealed that T790M mutation but no KRAS mutation (P=0.012), number of metastasized organs =0 or 1 (P=0.000), alternative treatment of osimertinib with chemotherapy (P=0.020), and isolated bone metastasis (P=0.006) were independent protective factors for long-term results of personalized comprehensive treatment for T790M-positive lung adenocarcinoma patients with bone metastasis.Conclusion: Chemotherapy combined with osimertinib, agents of bisphosphonate and other personalized comprehensive treatment prolongs survival time in T790M-positive lung adenocarcinoma patients without KRAS mutation, providing a potential therapeutic model for those patients.
[Abstract] Objective: To explore the related factors for efficacy and prognosis of personalized comprehensive treatment for T790Mpositive lung adenocarcinoma patients with bone metastasis. Methods: The clinical data of 68 patients undergoing personalized comprehensive treatment for T790M-positive lung adenocarcinoma with bone metastasis were retrospectively reviewed; chemotherapy, radiotherapy,molecule-targeted agents, Bevacizumab, bisphosphonate and other therapies were chosen for the patients, and the efficacy and prognosis were observed to explore the related factors. Results: Effective rate of personalized comprehensive treatment was 60.3% (41/68), with a median survival time of 23 months. Multiple factors showed significant effects on long-term efficacy, such as no radiotherapy,T790M mutation but no KRAS mutation, adjuvant scheme+rescue scheme in prior chemotherapy treatment, N1 stage, isolated bone metastasis, alternative treatment of osimertinib with chemotherapy, less metastasized organs and ECOG scores<2 (P<0.05). Multivariate analysis revealed that T790M mutation but no KRAS mutation (P=0.012), number of metastasized organs =0 or 1 (P=0.000), alternative treatment of osimertinib with chemotherapy (P=0.020), and isolated bone metastasis (P=0.006) were independent protective factors for long-term results of personalized comprehensive treatment for T790M-positive lung adenocarcinoma patients with bone metastasis.Conclusion: Chemotherapy combined with osimertinib, agents of bisphosphonate and other personalized comprehensive treatment prolongs survival time in T790M-positive lung adenocarcinoma patients without KRAS mutation, providing a potential therapeutic model for those patients.
2019, 26(2):206-212.
DOI: 10.3872/j.issn.1007-385X.2019.02.011
Abstract:
[Abstract] Objective:To explore the prognostic significance of thrombospondin 2 (THBS2) expression and its effects on the proliferation and migration of pancreatic cancer ASPC-1 cells for patients with pancreatic cancer, and to investigate its possible molecular mechanism. Methods: The expression of THBS2 in pancreatic cancer tissues and its effects on overall survival rate in patients were analyzed by online database. THBS2 expression in pancreatic cancer ASPC-1 cells was detected by Western Blotting; RNA interference was used to knockdown the expression of THBS2 in ASPC-1 cells, and then the effects of THBS2 knockdown on cell proliferation and migration were detected by MTT and Transwell assays, while its effects on protein expression levels (MMP, E-cadherin, AKT and PI3K) were detected by Wb. Results: Expression of THBS2 in pancreatic cancer tissues was significantly higher than that in normal pancreatic tissues (P<0.01), and the high expression of THBS2 could lead to the decrease of overall survival rate in pancreatic cancer patients. The expression of THBS2 in pancreatic cancer cell lines was significantly up-regulated; however, after interference on the expression of THBS2,the proliferation (P<0.01) and migration ability (P<0.01) of ASPC-1 cells were significantly decreased, and the expression of AKT and PI3K in cells was significantly down-regulated (P<0.01). Conclusion: THBS2 is highly expressed in pancreatic cancer tissues and cells,and is negatively correlated with the prognosis of patients. The mechanism is possibly related with the proliferation and migration of ASPC-1 cells that regulated by AKT/PI3K signaling pathway.
[Abstract] Objective:To explore the prognostic significance of thrombospondin 2 (THBS2) expression and its effects on the proliferation and migration of pancreatic cancer ASPC-1 cells for patients with pancreatic cancer, and to investigate its possible molecular mechanism. Methods: The expression of THBS2 in pancreatic cancer tissues and its effects on overall survival rate in patients were analyzed by online database. THBS2 expression in pancreatic cancer ASPC-1 cells was detected by Western Blotting; RNA interference was used to knockdown the expression of THBS2 in ASPC-1 cells, and then the effects of THBS2 knockdown on cell proliferation and migration were detected by MTT and Transwell assays, while its effects on protein expression levels (MMP, E-cadherin, AKT and PI3K) were detected by Wb. Results: Expression of THBS2 in pancreatic cancer tissues was significantly higher than that in normal pancreatic tissues (P<0.01), and the high expression of THBS2 could lead to the decrease of overall survival rate in pancreatic cancer patients. The expression of THBS2 in pancreatic cancer cell lines was significantly up-regulated; however, after interference on the expression of THBS2,the proliferation (P<0.01) and migration ability (P<0.01) of ASPC-1 cells were significantly decreased, and the expression of AKT and PI3K in cells was significantly down-regulated (P<0.01). Conclusion: THBS2 is highly expressed in pancreatic cancer tissues and cells,and is negatively correlated with the prognosis of patients. The mechanism is possibly related with the proliferation and migration of ASPC-1 cells that regulated by AKT/PI3K signaling pathway.
FENG Zhiping
,
CHEN Fukun
,
YANG Chuanzhou
,
CHEN Ting
,
ZHU Jialun
,
LIU Chao
,
LV Juan
,
LU Jianmei
,
DENG Zhiyong
2019, 26(2):213-219.
DOI: 10.3872/j.issn.1007-385X.2019.02.012
Abstract:
[Abstract] Objective: To investigate the correlation between KRAS gene mutation and differentiated thyroid carcinoma (DTC) treatment effect and prognosis, and to explore the mechanism. Methods: Clinical tissue samples from DTC patients undergoing 131I Radiotherapy were collected. Then single strand conformation polymorphism analysis of polymerase chain reaction products (PCRC-SSCP)was used to detect KRAS mutation rate in thyroid cancer patients of different TNM stages; p21 protein expression level was detected by real-time quantitative polymerase chain reaction (qPCR) and western blotting. DTC cells were treated by sub-lethal dose of 131I Radiotherapy,and then CCK-8 assay, transwell assay and flow cytometry (FCM) were used to evaluate the changes of cells viability. Animal models were then constructed for verification. Results: The results showed that KRAS gene mutants were increased in 131I-resistant DTC patients; KRAS gene mutation suppressed p21 protein expression and was associated with clinical stage and poor prognosis. In vivo and in vitro experiments proved that sub-lethal dose of 131I increased KRAS gene mutation rate, suppressed p21 expression level, and caused 131I radiotherapy resistance. Reversely, over-expression of KRAS gene could significantly increase p21 expression, and inhibit tumor proliferation and metastasis. Conclusion: KRAS gene mutations were associated with DTC TNM stages and 131I resistance in DTC patients. Sub-lethal dose of 131I treatment could improve 131I resistance in DTC cells line, inversely, over-expressed KRAS gene could increase the sensitivity to 131I radiotherapy in DTC patients.
[Abstract] Objective: To investigate the correlation between KRAS gene mutation and differentiated thyroid carcinoma (DTC) treatment effect and prognosis, and to explore the mechanism. Methods: Clinical tissue samples from DTC patients undergoing 131I Radiotherapy were collected. Then single strand conformation polymorphism analysis of polymerase chain reaction products (PCRC-SSCP)was used to detect KRAS mutation rate in thyroid cancer patients of different TNM stages; p21 protein expression level was detected by real-time quantitative polymerase chain reaction (qPCR) and western blotting. DTC cells were treated by sub-lethal dose of 131I Radiotherapy,and then CCK-8 assay, transwell assay and flow cytometry (FCM) were used to evaluate the changes of cells viability. Animal models were then constructed for verification. Results: The results showed that KRAS gene mutants were increased in 131I-resistant DTC patients; KRAS gene mutation suppressed p21 protein expression and was associated with clinical stage and poor prognosis. In vivo and in vitro experiments proved that sub-lethal dose of 131I increased KRAS gene mutation rate, suppressed p21 expression level, and caused 131I radiotherapy resistance. Reversely, over-expression of KRAS gene could significantly increase p21 expression, and inhibit tumor proliferation and metastasis. Conclusion: KRAS gene mutations were associated with DTC TNM stages and 131I resistance in DTC patients. Sub-lethal dose of 131I treatment could improve 131I resistance in DTC cells line, inversely, over-expressed KRAS gene could increase the sensitivity to 131I radiotherapy in DTC patients.
2019, 26(2):220-224.
DOI: 10.3872/j.issn.1007-385X.2019.02.013
Abstract:
[Abstract] Objective：To detect the gene mutation in cholangiocarcinoma patients using the next generation sequencing (NGS) technology,and to analyze its correlation to the prognosis of the patients. Methods: From June 2016 to June 2018, 40 patients diagnosed with cholangiocarcinoma received NGS examination to screen the possible mutations (single base mutation, structural variation, copy number variation and gene fusion, etc.). The disease control rates (DCR), progression-free survival (PFS) and overall survival (OS) of the patients, who received the first line therapy, were retrospectively reviewed to analyze the relationship between signaling pathway as well as its genetic variation and the prognosis of cholangiocarcinoma patients. Results: The median PFS of patients with and without TP53 mutation was 11.0 and 8.3 months, respectively (P=0.332), while OS was 14.3 and 32.9 months, respectively (P=0.041). The median PFS of patients with and without PI3K mutations was 8.3 and 11.0 months, respectively (P=0.285), while OS was 14.3 and 37.0 months, respectively (P=0.020). The median PFS of patients with and without mTOR pathway mutations was 6.3 and 10.3 months, respectively (P=0.020), while OS was 15.6 and 19.6 months, respectively (P=0.892). There was no significant effect of pathway-related gene mutations on patients’survival. Conclusion: The prognosis of cholangiocarcinoma patients with TP53 and PI3K pathway activation had obviously poor prognosis than those without. No significant difference was observed between the patients with and without mTOR pathway activation and IDH mutation.
[Abstract] Objective：To detect the gene mutation in cholangiocarcinoma patients using the next generation sequencing (NGS) technology,and to analyze its correlation to the prognosis of the patients. Methods: From June 2016 to June 2018, 40 patients diagnosed with cholangiocarcinoma received NGS examination to screen the possible mutations (single base mutation, structural variation, copy number variation and gene fusion, etc.). The disease control rates (DCR), progression-free survival (PFS) and overall survival (OS) of the patients, who received the first line therapy, were retrospectively reviewed to analyze the relationship between signaling pathway as well as its genetic variation and the prognosis of cholangiocarcinoma patients. Results: The median PFS of patients with and without TP53 mutation was 11.0 and 8.3 months, respectively (P=0.332), while OS was 14.3 and 32.9 months, respectively (P=0.041). The median PFS of patients with and without PI3K mutations was 8.3 and 11.0 months, respectively (P=0.285), while OS was 14.3 and 37.0 months, respectively (P=0.020). The median PFS of patients with and without mTOR pathway mutations was 6.3 and 10.3 months, respectively (P=0.020), while OS was 15.6 and 19.6 months, respectively (P=0.892). There was no significant effect of pathway-related gene mutations on patients’survival. Conclusion: The prognosis of cholangiocarcinoma patients with TP53 and PI3K pathway activation had obviously poor prognosis than those without. No significant difference was observed between the patients with and without mTOR pathway activation and IDH mutation.
2019, 26(2):225-229.
DOI: 10.3872/j.issn.1007-385X.2019.02.014
Abstract:
[Abstract] Objective: To analyze the correlation between WT1 gene polymorphism and multiple myeloma (MM) susceptibility in 168 patients. Methods: One hundred and sixty eight MM patients, who were hospitalized in our hospital and Hebei Provincial People's Hospital from January 2013 to December 2017, were researched in this study. There were 121 males (72%) and 47 females(28%) with a median age of 62.4 years old (36~83 years old). Polymorphism of WT1 gene of the samples was detected and analyzed by SSP-PCR and SBT-PCR. Results: Eleven WT1 alleles were detected in MM patients, WT1*010 and WT1*012 alleles occupied a higher frequency in MM group (WT1*010: OR=6.13, 95%CI:3.5~10.75, PC<0.000; WT1*012: OR=2.06, 95%CI:1.23~1.44, PC<0.051). STR genotype frequency of WT1*A5 markedly increased (OR=1.62, 95%CI:1.18~2.23, PC<0.05). Genotype frequency of WT1*010/010 also obviously increased (OR=6.28, 95%CI:1.81～21.76, PC<0.05). Conclusion: WT1 allele is highly polymorphic in MM patients and homozygote WT1*010/010 is a susceptible genotype of MM, indicating that the occurrence and development of MM are related to the polymorphism of WT1 gene.
[Abstract] Objective: To analyze the correlation between WT1 gene polymorphism and multiple myeloma (MM) susceptibility in 168 patients. Methods: One hundred and sixty eight MM patients, who were hospitalized in our hospital and Hebei Provincial People's Hospital from January 2013 to December 2017, were researched in this study. There were 121 males (72%) and 47 females(28%) with a median age of 62.4 years old (36~83 years old). Polymorphism of WT1 gene of the samples was detected and analyzed by SSP-PCR and SBT-PCR. Results: Eleven WT1 alleles were detected in MM patients, WT1*010 and WT1*012 alleles occupied a higher frequency in MM group (WT1*010: OR=6.13, 95%CI:3.5~10.75, PC<0.000; WT1*012: OR=2.06, 95%CI:1.23~1.44, PC<0.051). STR genotype frequency of WT1*A5 markedly increased (OR=1.62, 95%CI:1.18~2.23, PC<0.05). Genotype frequency of WT1*010/010 also obviously increased (OR=6.28, 95%CI:1.81～21.76, PC<0.05). Conclusion: WT1 allele is highly polymorphic in MM patients and homozygote WT1*010/010 is a susceptible genotype of MM, indicating that the occurrence and development of MM are related to the polymorphism of WT1 gene.
2019, 26(2):230-235.
DOI: 10.3872/j.issn.1007-385X.2019.02.015
Abstract:
[摘要] 蛋白质酪氨酸磷酸化对细胞的生命活动至关重要，其调控异常与多种疾病的发生密切相关。在酪氨酸磷酸酶家族中，SHP2 是目前唯一被证实的原癌蛋白，参与调控多个癌症相关过程。其活化突变会导致白血病、黑色素瘤、乳腺癌及肺癌的发生。2016 年以来，随着高特异性、可口服的SHP2 新型变构抑制剂成功开发，靶向抑制SHP2 在抑制肿瘤生长以及改善肿瘤耐药性方面逐渐显现出了强大的临床应用潜力，提示SHP2 抑制剂有望成为首个靶向酪氨酸磷酸酶的抗肿瘤靶向药物。
[摘要] 蛋白质酪氨酸磷酸化对细胞的生命活动至关重要，其调控异常与多种疾病的发生密切相关。在酪氨酸磷酸酶家族中，SHP2 是目前唯一被证实的原癌蛋白，参与调控多个癌症相关过程。其活化突变会导致白血病、黑色素瘤、乳腺癌及肺癌的发生。2016 年以来，随着高特异性、可口服的SHP2 新型变构抑制剂成功开发，靶向抑制SHP2 在抑制肿瘤生长以及改善肿瘤耐药性方面逐渐显现出了强大的临床应用潜力，提示SHP2 抑制剂有望成为首个靶向酪氨酸磷酸酶的抗肿瘤靶向药物。
2019, 26(2):236-240.
DOI: 10.3872/j.issn.1007-385X.2019.02.016
Abstract:
[摘要] 外泌体是一种纳米级别的生物膜结构，由机体的多种细胞分泌，广泛分布于唾液、血浆、乳汁等体液中。外泌体中含有蛋白质、mRNA、miRNA、lncRNA、细胞因子、转录因子受体等多种生物活性物质。肿瘤细胞或肿瘤旁细胞分泌的外泌体可将一些肿瘤特有的生物信息转移到邻近细胞，甚至远处细胞，并且通过这种细胞间通信传递肿瘤的特性，从而促进肿瘤的发生发展。本综述旨在着重讨论肿瘤细胞及癌旁细胞分泌的含lncRNA的外泌体对肿瘤微环境，肿瘤的生物学特性的影响，为肿瘤的基础研究及临床诊断治疗提出新的思路。
[摘要] 外泌体是一种纳米级别的生物膜结构，由机体的多种细胞分泌，广泛分布于唾液、血浆、乳汁等体液中。外泌体中含有蛋白质、mRNA、miRNA、lncRNA、细胞因子、转录因子受体等多种生物活性物质。肿瘤细胞或肿瘤旁细胞分泌的外泌体可将一些肿瘤特有的生物信息转移到邻近细胞，甚至远处细胞，并且通过这种细胞间通信传递肿瘤的特性，从而促进肿瘤的发生发展。本综述旨在着重讨论肿瘤细胞及癌旁细胞分泌的含lncRNA的外泌体对肿瘤微环境，肿瘤的生物学特性的影响，为肿瘤的基础研究及临床诊断治疗提出新的思路。
2019, 26(2):241-245.
DOI: 10.3872/j.issn.1007-385X.2019.02.017
Abstract:
[摘要] 目前主要的免疫治疗包括溶瘤病毒、免疫检查点抑制剂、细胞因子、肿瘤疫苗、过继性免疫细胞等。溶瘤病毒是一种很有前景的抗肿瘤新兴制剂，通过选择性杀伤肿瘤细胞、诱导机体产生特异的抗肿瘤免疫反应来实现治疗肿瘤的目的。Talimogene laherparepvec (T-VEC)是第一个被批准用于治疗转移性恶性黑色素瘤的溶瘤病毒。免疫检查点抑制剂以其显著的临床疗效而备受瞩目。免疫检查点抑制剂在许多实体瘤中取得了很好的疗效，包括CTLA-4 及其抑制剂、PD-1 及其抑制剂等。T-VEC与免疫检查点抑制剂抗癌优势互补。溶瘤病毒与联合免疫检查点抑制剂在恶性黑色素瘤的应用包括T-VEC与ipilimumab 联合治疗、T-VEC与pembrolizumab 联合治疗等。通过将溶瘤病毒与免疫检查点抑制剂联合能够显著延长肿瘤患者生存期。本文对两种免疫疗法联合治疗的合理性及两者联合在恶性黑色素瘤中的应用进展作一综述。
[摘要] 目前主要的免疫治疗包括溶瘤病毒、免疫检查点抑制剂、细胞因子、肿瘤疫苗、过继性免疫细胞等。溶瘤病毒是一种很有前景的抗肿瘤新兴制剂，通过选择性杀伤肿瘤细胞、诱导机体产生特异的抗肿瘤免疫反应来实现治疗肿瘤的目的。Talimogene laherparepvec (T-VEC)是第一个被批准用于治疗转移性恶性黑色素瘤的溶瘤病毒。免疫检查点抑制剂以其显著的临床疗效而备受瞩目。免疫检查点抑制剂在许多实体瘤中取得了很好的疗效，包括CTLA-4 及其抑制剂、PD-1 及其抑制剂等。T-VEC与免疫检查点抑制剂抗癌优势互补。溶瘤病毒与联合免疫检查点抑制剂在恶性黑色素瘤的应用包括T-VEC与ipilimumab 联合治疗、T-VEC与pembrolizumab 联合治疗等。通过将溶瘤病毒与免疫检查点抑制剂联合能够显著延长肿瘤患者生存期。本文对两种免疫疗法联合治疗的合理性及两者联合在恶性黑色素瘤中的应用进展作一综述。
2019, 26(2):246-248.
DOI: 10.3872/j.issn.1007-385X.2019.02.018
Abstract:
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.