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Volume 25,Issue 11,2018 Table of Contents
2018, 25(11):1089-1093.
DOI: 10.3872/j.issn.1007-385X.2018.11.001
Abstract:
[Abstract] Advanced gastric cancer is one of cancer types with poor prognosis in East Asia and China. Treatment strategies are especially limited in patients with advanced gastric cancer due to the lack of potent efficacy and serious toxicity. In 2017, immune checkpoint inhibitors targeting programmed cell death protein-1 (PD-1) or programmed death ligand-1 (PD-L1) have been approved by FDA for treating advanced gastric or gastroesophageal junction cancer (GC/GEJC) as a third-line option. However, immune checkpoint inhibitors have not been used in the first or second-line setting for advanced gastric cancer. Presently, many clinical trials are undergoing to determine the efficacy of combined therapy including checkpoint inhibitor plus chemotherapy, dual combinations with two immune checkpoint inhibitors, to enhance anticancer activity of immune checkpoint inhibitors and expand targeted patients. Furthermore, areas for further study include the development and validation of novel biomarkers to predict patients who are most likely to respond to treatment and characterization of outcomes with immune checkpoint inhibitors in different defined disease subgroups.
[Abstract] Advanced gastric cancer is one of cancer types with poor prognosis in East Asia and China. Treatment strategies are especially limited in patients with advanced gastric cancer due to the lack of potent efficacy and serious toxicity. In 2017, immune checkpoint inhibitors targeting programmed cell death protein-1 (PD-1) or programmed death ligand-1 (PD-L1) have been approved by FDA for treating advanced gastric or gastroesophageal junction cancer (GC/GEJC) as a third-line option. However, immune checkpoint inhibitors have not been used in the first or second-line setting for advanced gastric cancer. Presently, many clinical trials are undergoing to determine the efficacy of combined therapy including checkpoint inhibitor plus chemotherapy, dual combinations with two immune checkpoint inhibitors, to enhance anticancer activity of immune checkpoint inhibitors and expand targeted patients. Furthermore, areas for further study include the development and validation of novel biomarkers to predict patients who are most likely to respond to treatment and characterization of outcomes with immune checkpoint inhibitors in different defined disease subgroups.
2018, 25(11):1094-1098.
DOI: 10.3872/j.issn.1007-385X.2018.11.002
Abstract:
[Abstract] Gastric cancer (GC) is one of the malignant tumors with the highest morbidity and mortality in China, and conventional therapies such as surgery, chemotherapy and radiotherapy have limited curative effect on it. GC is highly heterogeneous. With the research on GC deepening into a molecular level and the rapid development of immunotherapy, individualized immunotherapy has become the most promising technology in the field of GC therapy. Several molecular classifications have been put forward in recent years,accurately as well as comprehensively depicting the genomic and molecular characteristics of GC. Moreover, molecular classifications also provided molecular immunological information of GC, which gave implications for the screening of benefit population and treatment decision-making. Based on the several existing GC molecular classifications, this review discussed the guiding significance of molecular classifications on the development and application of GC individualized immunotherapy.
[Abstract] Gastric cancer (GC) is one of the malignant tumors with the highest morbidity and mortality in China, and conventional therapies such as surgery, chemotherapy and radiotherapy have limited curative effect on it. GC is highly heterogeneous. With the research on GC deepening into a molecular level and the rapid development of immunotherapy, individualized immunotherapy has become the most promising technology in the field of GC therapy. Several molecular classifications have been put forward in recent years,accurately as well as comprehensively depicting the genomic and molecular characteristics of GC. Moreover, molecular classifications also provided molecular immunological information of GC, which gave implications for the screening of benefit population and treatment decision-making. Based on the several existing GC molecular classifications, this review discussed the guiding significance of molecular classifications on the development and application of GC individualized immunotherapy.
2018, 25(11):1099-1103.
DOI: 10.3872/j.issn.1007-385X.2018.11.003
Abstract:
[Abstract] Precision medicine is defined as an approach to personalized diagnosis and treatment, based on the omics information of patients.Standardized specimen collection is the basis of molecular pathology diagnosis, which also is the prerequisite for precision medicine.Endoscopic biopsy is an important approach to obtain specimen in gastrointestinal tumors. Here, after summarizing the molecular basis of gastric cancer related to precision medicine, we propose problems involved in the endoscopic specimen collection, and make recommendations accordingly.
[Abstract] Precision medicine is defined as an approach to personalized diagnosis and treatment, based on the omics information of patients.Standardized specimen collection is the basis of molecular pathology diagnosis, which also is the prerequisite for precision medicine.Endoscopic biopsy is an important approach to obtain specimen in gastrointestinal tumors. Here, after summarizing the molecular basis of gastric cancer related to precision medicine, we propose problems involved in the endoscopic specimen collection, and make recommendations accordingly.
2018, 25(11):1104-1112.
DOI: 10.3872/j.issn.1007-385X.2018.11.004
Abstract:
Objective: To investigate the molecular mechanism of lncRNA FOXD2-AS1 participating in apatinib resistance in gastric cancer cells by regulating miR-185-5p/CCND2 axis. Methods: The gastri cancer tissues and corresponding paracancerous tissues of 25 patients with gastric cancer were collected from April 2016 to December 2017 in the Fifth People’s Hospital of Wuxi City. The expressions of FOXD2-AS1, miR-185-5p, and cyclin D2 (CCND2) in gastric cancer tissues or cell lines were examined by quantitative realtime polymerase chain reaction (qRT-PCR). CCK-8 assay, Transwell assay and Annexin V-FITC/PI double staining flow cytometry assay were applied to assess the sensitivity of gastric cancer cells to apatinib. The interaction between FOXD2-AS1, miR-185-5p and CCND2 was explored by dual luciferase reporter gene assay, which was then confirmed by qRT-PCR, and Western blotting. Results:FOXD2-AS1 was highly expressed in gastric cancer tissues and apatinib-resistant gastric cancer cells. Over-expression of FOXD2-AS1 promoted apatinib-resistance of MGC-803/AP cells. Dual luciferase reporter gene assay confirmed that FOXD2-AS1 directly interacted with miR-185-5p and suppressed its expression. miR-185-5p significantly abolished the promotion effect of FOXD2-AS1 on apatinibresistance via inhibiting cell proliferation, invasion and promoting apoptosis of gastric MGC-803/AP cells. miR-185-5p could negatively regulate CCND2 expression; and FOXD2-AS1 promoted the cell proliferation, invasion and inhibited apoptosis of MGC-803/AP cells via down-regulating the inhibition effect of miR-185-5p on CCND2, thus further enhanced the apatinib-resistance of gastric cancer cells. Conclusion: FOXD2-AS1 induced apatinib-resistance of gastric cancer cells by regulating miR-185-5p/CCND2 axis.
Objective: To investigate the molecular mechanism of lncRNA FOXD2-AS1 participating in apatinib resistance in gastric cancer cells by regulating miR-185-5p/CCND2 axis. Methods: The gastri cancer tissues and corresponding paracancerous tissues of 25 patients with gastric cancer were collected from April 2016 to December 2017 in the Fifth People’s Hospital of Wuxi City. The expressions of FOXD2-AS1, miR-185-5p, and cyclin D2 (CCND2) in gastric cancer tissues or cell lines were examined by quantitative realtime polymerase chain reaction (qRT-PCR). CCK-8 assay, Transwell assay and Annexin V-FITC/PI double staining flow cytometry assay were applied to assess the sensitivity of gastric cancer cells to apatinib. The interaction between FOXD2-AS1, miR-185-5p and CCND2 was explored by dual luciferase reporter gene assay, which was then confirmed by qRT-PCR, and Western blotting. Results:FOXD2-AS1 was highly expressed in gastric cancer tissues and apatinib-resistant gastric cancer cells. Over-expression of FOXD2-AS1 promoted apatinib-resistance of MGC-803/AP cells. Dual luciferase reporter gene assay confirmed that FOXD2-AS1 directly interacted with miR-185-5p and suppressed its expression. miR-185-5p significantly abolished the promotion effect of FOXD2-AS1 on apatinibresistance via inhibiting cell proliferation, invasion and promoting apoptosis of gastric MGC-803/AP cells. miR-185-5p could negatively regulate CCND2 expression; and FOXD2-AS1 promoted the cell proliferation, invasion and inhibited apoptosis of MGC-803/AP cells via down-regulating the inhibition effect of miR-185-5p on CCND2, thus further enhanced the apatinib-resistance of gastric cancer cells. Conclusion: FOXD2-AS1 induced apatinib-resistance of gastric cancer cells by regulating miR-185-5p/CCND2 axis.
2018, 25(11):1105-1118.
DOI: 10.3872/j.issn.1007-385X.2018.11.005
Abstract:
Objective: To explore the target relationship between miR-138-5p and TCF3, and its effect on invasion and migration of human grastric cancer SGC-7901 cells. Methods: After being transfected with miR-138-5p mimic, the relative mRNA expression of miR-138-5p and TCF3 in SGC-7901 cells was detected by qRT-PCR. Bioinformatics methods were used to predict the targeted matching relationship between miR-138-5p and TCF3 gene, which was then verified by the luciferase reporter gene system. After transfecting normal gastric cancer cells and TCF3 high expression gastric cancer cells with miR-138-5p mimic, Western blotting was performed to detect the protein expressions of TCF3, N-cadherin, Vimentin, Slug and E-cadherin; Transwell assay and scratch assay were used to detect the invasion and migration ability of gastric cancer cells, respectively. Results: Over-expression of miR-138-5p inhibited the expression of TCF3 mRNA. Bioinformatics software predicted that miR-138-5p and TCF3 mRNA had targeted binding areas.miR-138-5p mimics reduced the luciferase activity of TCF3 wild-type plasmids, without affecting the luciferase activity of TCF3 mutant-type plasmids. miR-138-5p inhibited the expression of TCF3 protein, and attenuated the promotion effect of TCF3 over-expression on the invasion and migration of SGC-7901 cells, in the meanwhile, down-regulated the protein expressions of N-cadherin, Vimentin and Slug proteins, and up-regulated the protein expression of E-cadherin. Conclusion: miR-138-5p directly regulates the expression of TCF3 and affects the invasion and migration of gastric cancer SGC-7901 cells.
Objective: To explore the target relationship between miR-138-5p and TCF3, and its effect on invasion and migration of human grastric cancer SGC-7901 cells. Methods: After being transfected with miR-138-5p mimic, the relative mRNA expression of miR-138-5p and TCF3 in SGC-7901 cells was detected by qRT-PCR. Bioinformatics methods were used to predict the targeted matching relationship between miR-138-5p and TCF3 gene, which was then verified by the luciferase reporter gene system. After transfecting normal gastric cancer cells and TCF3 high expression gastric cancer cells with miR-138-5p mimic, Western blotting was performed to detect the protein expressions of TCF3, N-cadherin, Vimentin, Slug and E-cadherin; Transwell assay and scratch assay were used to detect the invasion and migration ability of gastric cancer cells, respectively. Results: Over-expression of miR-138-5p inhibited the expression of TCF3 mRNA. Bioinformatics software predicted that miR-138-5p and TCF3 mRNA had targeted binding areas.miR-138-5p mimics reduced the luciferase activity of TCF3 wild-type plasmids, without affecting the luciferase activity of TCF3 mutant-type plasmids. miR-138-5p inhibited the expression of TCF3 protein, and attenuated the promotion effect of TCF3 over-expression on the invasion and migration of SGC-7901 cells, in the meanwhile, down-regulated the protein expressions of N-cadherin, Vimentin and Slug proteins, and up-regulated the protein expression of E-cadherin. Conclusion: miR-138-5p directly regulates the expression of TCF3 and affects the invasion and migration of gastric cancer SGC-7901 cells.
2018, 25(11):1119-1124.
DOI: 10.3872/j.issn.1007-385X.2018.11.006
Abstract:
Objective: To investigate the effects of nuclear factor 5 of activated T cells (NFAT5) on proliferation and apoptosis of human gastric cancer MGC803 cells and to explore the possible mechanisms. Methods: Three siRNAs targeting NFAT5 gene (siRNA2567,siRNA2714 and siRNA4562) and one negative control siRNA were designed and chemically synthesized before transfected into human gastric cancer cell line MGC803 by liposome. Real-time PCR was used to detect the changes of NFAT5 mRNA expression in MGC803 cells to further pick out the siRNA that most effectively inhibit the expression of NFAT5. Further, Real-time PCR and Western blotting assay were carried out to test mRNA and protein levels of NFAT5 and S100A4 in cells 48 h after NFAT5-siRNA transfection.Then, CCK-8 assay and FCM assay were used to detect the influence of silencing NFAT5 on cell proliferation and apoptosis, respectively.Results: siRNA2567 was the most effective siRNA that significantly inhibited the expression of NFAT5 mRNA (P<0.01),and thus was validated as NFAT5-siRNA. Real-time PCR and Western blotting assay confirmed that both mRNA and protein levels of NFAT5 and S100A4 were down-regulated in cells 48 h after NFAT5-siRNA transfection. Compared with NC-siRNA group, the proliferation ability of MGC803 cells in the NFAT5-siRNA group was significantly down-regulated at 72 h and 96 h (P<0.01). And FCM assay showed that compared with NC-siRNA group, cell apoptosis rate of NFAT5-siRNA group was significantly increased from (2.7±0.2)% to (7.9±0.2)%, (P<0.01) 48 h after NFAT5-siRNA transfection. Conclusion: NFAT5-siRNA transfection can silence NFAT5 gene expression in gastric cancer MGC803 cells effectively. NFAT5 may inhibit proliferation and promote cell apoptosis of gastric cancer cells possibly through regulating S100A4 expression.
Objective: To investigate the effects of nuclear factor 5 of activated T cells (NFAT5) on proliferation and apoptosis of human gastric cancer MGC803 cells and to explore the possible mechanisms. Methods: Three siRNAs targeting NFAT5 gene (siRNA2567,siRNA2714 and siRNA4562) and one negative control siRNA were designed and chemically synthesized before transfected into human gastric cancer cell line MGC803 by liposome. Real-time PCR was used to detect the changes of NFAT5 mRNA expression in MGC803 cells to further pick out the siRNA that most effectively inhibit the expression of NFAT5. Further, Real-time PCR and Western blotting assay were carried out to test mRNA and protein levels of NFAT5 and S100A4 in cells 48 h after NFAT5-siRNA transfection.Then, CCK-8 assay and FCM assay were used to detect the influence of silencing NFAT5 on cell proliferation and apoptosis, respectively.Results: siRNA2567 was the most effective siRNA that significantly inhibited the expression of NFAT5 mRNA (P<0.01),and thus was validated as NFAT5-siRNA. Real-time PCR and Western blotting assay confirmed that both mRNA and protein levels of NFAT5 and S100A4 were down-regulated in cells 48 h after NFAT5-siRNA transfection. Compared with NC-siRNA group, the proliferation ability of MGC803 cells in the NFAT5-siRNA group was significantly down-regulated at 72 h and 96 h (P<0.01). And FCM assay showed that compared with NC-siRNA group, cell apoptosis rate of NFAT5-siRNA group was significantly increased from (2.7±0.2)% to (7.9±0.2)%, (P<0.01) 48 h after NFAT5-siRNA transfection. Conclusion: NFAT5-siRNA transfection can silence NFAT5 gene expression in gastric cancer MGC803 cells effectively. NFAT5 may inhibit proliferation and promote cell apoptosis of gastric cancer cells possibly through regulating S100A4 expression.
2018, 25(11):1125-1130.
DOI: 10.3872/j.issn.1007-385X.2018.11.007
Abstract:
Objective: To investigate the effect of Caveolin-1(Cav-1) protein on the malignant biological behaviors of NCI-N87 gastric cancer cells, and further to analyze the possible molecular mechanisms. Methods: NCI-N87 cell line that stably expressing Cav-1 was constructed; MTT assay, colony formation assay and wound healing assay were used to examine the effect of Cav-1 on the malignant biological behaviors of gastric cancer cells; Western bloting was used to detect the effect of Cav-1 protein on Her-2 activation as well as the ERK and Akt signaling pathway under the induction with EGF ligand. Results: Over-expression of Cav-1 significantly inhibited the proliferation and migration of NCI-N87 cells. With the stimulation of EGF ligand, Cav-1 over-expression significantly inhibited the tyrosine phosphorylation level of Her-2 and the ratio of P-ERK/ERK as well as P-AKT/AKT. Conclusion: The over-expression of Cav-1 could significantly inhibit Her-2 tyrosine phosphorylation, and may inhibit the proliferation and migration of NCI-N87 cells via the down-stream MAPK and PI3K/Akt signaling pathway.
Objective: To investigate the effect of Caveolin-1(Cav-1) protein on the malignant biological behaviors of NCI-N87 gastric cancer cells, and further to analyze the possible molecular mechanisms. Methods: NCI-N87 cell line that stably expressing Cav-1 was constructed; MTT assay, colony formation assay and wound healing assay were used to examine the effect of Cav-1 on the malignant biological behaviors of gastric cancer cells; Western bloting was used to detect the effect of Cav-1 protein on Her-2 activation as well as the ERK and Akt signaling pathway under the induction with EGF ligand. Results: Over-expression of Cav-1 significantly inhibited the proliferation and migration of NCI-N87 cells. With the stimulation of EGF ligand, Cav-1 over-expression significantly inhibited the tyrosine phosphorylation level of Her-2 and the ratio of P-ERK/ERK as well as P-AKT/AKT. Conclusion: The over-expression of Cav-1 could significantly inhibit Her-2 tyrosine phosphorylation, and may inhibit the proliferation and migration of NCI-N87 cells via the down-stream MAPK and PI3K/Akt signaling pathway.
GAO Shile
,
LU Donghui
,
LIU Meiqin
,
WANG Chong
,
WEI Lei
,
XU Peng
,
LIU Yan
,
TANG Zhengzhong
,
HU Zongtao
2018, 25(11):1131-1134.
DOI: 10.3872/j.issn.1007-385X.2018.11.008
Abstract:
Objective: To observe the short-term efficacy and toxicity of apatinib monotherapy as well as docetaxel plus cisplatin in advanced gastric cancer. Method: According to inclusion and exclusion criteria, 108 patients with advanced gastric cancer in the 105th Hospital of PLA were selected. According to random table grouping method, there were 54 cases in group A and 54 cases in group B.Patients in group A received continuous oral administration of apatinib alone, while group B received docetaxel plus cisplatin chemotherapy,with 3 weeks as a cycle and 4 cycles for a course. The efficacy and side effects were evaluated 3 months later. Results: In group A, there were 4 cases of CR, 25 cases of PR, 18 cases of SD and 7 cases of PD; the ORR was 53.7% and DCR was 87%. In group B, there were 2 cases of CR, 19 cases of PR, 21 cases of SD and 12 cases of PD; the ORR was 38.9% and DCR was 77.8%. The ORR and DCR in group A were significantly better than those in group B (P<0.05). The main adverse reactions were gastrointestinal reaction,myelosuppression, hypertension and hand-foot syndrome, all of which were grade 1 to 2; The incidence of bone marrow suppression and gastrointestinal reaction in group A was lower than that in group B (P<0.05), while the incidence of hand-foot syndrome and hypertension in group B was lower than that in group A (P<0.01). Conclusion：The short-term efficacy of targeted therapy of apatinib alone was better than that of docetaxel combined with cisplatin chemotherapy, and the toxicity and side effects of both regimens were controllable; Apatinib can be used as the primary regimen for the treatment of advanced gastric cancer.
Objective: To observe the short-term efficacy and toxicity of apatinib monotherapy as well as docetaxel plus cisplatin in advanced gastric cancer. Method: According to inclusion and exclusion criteria, 108 patients with advanced gastric cancer in the 105th Hospital of PLA were selected. According to random table grouping method, there were 54 cases in group A and 54 cases in group B.Patients in group A received continuous oral administration of apatinib alone, while group B received docetaxel plus cisplatin chemotherapy,with 3 weeks as a cycle and 4 cycles for a course. The efficacy and side effects were evaluated 3 months later. Results: In group A, there were 4 cases of CR, 25 cases of PR, 18 cases of SD and 7 cases of PD; the ORR was 53.7% and DCR was 87%. In group B, there were 2 cases of CR, 19 cases of PR, 21 cases of SD and 12 cases of PD; the ORR was 38.9% and DCR was 77.8%. The ORR and DCR in group A were significantly better than those in group B (P<0.05). The main adverse reactions were gastrointestinal reaction,myelosuppression, hypertension and hand-foot syndrome, all of which were grade 1 to 2; The incidence of bone marrow suppression and gastrointestinal reaction in group A was lower than that in group B (P<0.05), while the incidence of hand-foot syndrome and hypertension in group B was lower than that in group A (P<0.01). Conclusion：The short-term efficacy of targeted therapy of apatinib alone was better than that of docetaxel combined with cisplatin chemotherapy, and the toxicity and side effects of both regimens were controllable; Apatinib can be used as the primary regimen for the treatment of advanced gastric cancer.
2018, 25(11):1135-1139.
DOI: 10.3872/j.issn.1007-385X.2018.11.009
Abstract:
Objective: To observe the clinical efficacy of apatinib combined with chemotherapy for advanced gastric cancer as secondline and above treatment, and to analyze the survival of patients. Methods: Seventy-two patients with advanced gastric cancer that treated at Department of Oncology, the First Affiliated Hospital of Zhengzhou University from March 2016 to April 2017 were included in this study according to the inclusion and exclusion criteria; patients were randomly divided into chemotherapy group, apatinib group,apatinib combined with chemotherapy group. And the clinical efficacy and the survival of patients were investigated. Results: For chemotherapy group, apatinib group, apatinib combined with chemotherapy group, the disease control rate (DCR) and objective response rate (ORR) were 48.3%, 61.1%,72.0% (P>0.05) and 13.8%, 16.7%, 28.0%(P>0.05), respectively; and the incidence rate of adverse reaction at grade three-four was 17.1%, 16.8% and 24.0% (P>0.05), respectively. Compared with the chemotherapy group (93 d), the median progress-free survival (mPFS) time in the apatinib group and apatinib combined with chemotherapy group was 117 d (P=0.128) and 160 d (P=0.001). Furthermore, univariate and multivariate analyses showed that TNM staging (P=0.036), ascites (P=0.041) and treatment regimen (P=0.001) were the independent factors affecting PFS. Conclusion: As the second-line or above treatment in advanced gastric cancer, compared with single chemotherapy and single apatinib group, apatinib combined with chemotherapy displays more satisfactory achievement in remission rate, accompanied by controllable adverse reactions and considerable survival benefit.
Objective: To observe the clinical efficacy of apatinib combined with chemotherapy for advanced gastric cancer as secondline and above treatment, and to analyze the survival of patients. Methods: Seventy-two patients with advanced gastric cancer that treated at Department of Oncology, the First Affiliated Hospital of Zhengzhou University from March 2016 to April 2017 were included in this study according to the inclusion and exclusion criteria; patients were randomly divided into chemotherapy group, apatinib group,apatinib combined with chemotherapy group. And the clinical efficacy and the survival of patients were investigated. Results: For chemotherapy group, apatinib group, apatinib combined with chemotherapy group, the disease control rate (DCR) and objective response rate (ORR) were 48.3%, 61.1%,72.0% (P>0.05) and 13.8%, 16.7%, 28.0%(P>0.05), respectively; and the incidence rate of adverse reaction at grade three-four was 17.1%, 16.8% and 24.0% (P>0.05), respectively. Compared with the chemotherapy group (93 d), the median progress-free survival (mPFS) time in the apatinib group and apatinib combined with chemotherapy group was 117 d (P=0.128) and 160 d (P=0.001). Furthermore, univariate and multivariate analyses showed that TNM staging (P=0.036), ascites (P=0.041) and treatment regimen (P=0.001) were the independent factors affecting PFS. Conclusion: As the second-line or above treatment in advanced gastric cancer, compared with single chemotherapy and single apatinib group, apatinib combined with chemotherapy displays more satisfactory achievement in remission rate, accompanied by controllable adverse reactions and considerable survival benefit.
2018, 25(11):1140-1147.
DOI: 10.3872/j.issn.1007-385X.2018.11.010
Abstract:
Objective: To investigate the mechanism of miR-29c modulating apatinib resistance of gastric cancer tissues and cells MGC-803 via regulating TNRC18. Methods: A total of 39 gastric cancer patients with complete clinical data, who were treated in the Central Hospital of Wuhan from Feb. 2015 to Oct. 2017, were collected for this study. The expression of miR-29c was detected by qRTPCR in gastric cancer tissues and cell lines. The effect of miR-29c over-expression/knockdown on the proliferation, invasion and apoptosis of MGC-803/AP cells in vitro was measured by CCK-8 assay, Transwell and Annexin V-FITC/PI double staining flow cytometry assay. Western blotting was used to detect the regulation of miR-29c on TNRC18. Moreover, the relationship between miR-29c and TNRC18 was examined by dual luciferase reporter gene assay. Results: qRT-PCR revealed that miR-29c was low expressed in gastric cancer cell lines and gastric cancer tissues from patients resistant to apatinib. Moreover, dual luciferase reporter gene assay confirmed that miR-29c directly binds to the 3′ UTR of TNRC18 mRNA to suppress its expression in MGC-803/AP cells. Furthermore, miR-29c inhibited the apatinib resistance in gastric cancer MGC-803/AP cells via inhibiting cell proliferation, invasion and promoting cell apoptosis by targeted down-regulating TNRC18. Additionally, in vivo experiment also confirmed that miR-29c modulated apatinib-resistance in gastric cancer cells by targeted inhibiting TNRC18. Conclusion: miR-29c/TNRC18 axis plays a certain role in the resistance of gastric cancer tissues and MGC-803/AP cells to apatinib, and over-expression of miR-29c may reverse the resistance of MGC-803/AP cells to apatinib.
Objective: To investigate the mechanism of miR-29c modulating apatinib resistance of gastric cancer tissues and cells MGC-803 via regulating TNRC18. Methods: A total of 39 gastric cancer patients with complete clinical data, who were treated in the Central Hospital of Wuhan from Feb. 2015 to Oct. 2017, were collected for this study. The expression of miR-29c was detected by qRTPCR in gastric cancer tissues and cell lines. The effect of miR-29c over-expression/knockdown on the proliferation, invasion and apoptosis of MGC-803/AP cells in vitro was measured by CCK-8 assay, Transwell and Annexin V-FITC/PI double staining flow cytometry assay. Western blotting was used to detect the regulation of miR-29c on TNRC18. Moreover, the relationship between miR-29c and TNRC18 was examined by dual luciferase reporter gene assay. Results: qRT-PCR revealed that miR-29c was low expressed in gastric cancer cell lines and gastric cancer tissues from patients resistant to apatinib. Moreover, dual luciferase reporter gene assay confirmed that miR-29c directly binds to the 3′ UTR of TNRC18 mRNA to suppress its expression in MGC-803/AP cells. Furthermore, miR-29c inhibited the apatinib resistance in gastric cancer MGC-803/AP cells via inhibiting cell proliferation, invasion and promoting cell apoptosis by targeted down-regulating TNRC18. Additionally, in vivo experiment also confirmed that miR-29c modulated apatinib-resistance in gastric cancer cells by targeted inhibiting TNRC18. Conclusion: miR-29c/TNRC18 axis plays a certain role in the resistance of gastric cancer tissues and MGC-803/AP cells to apatinib, and over-expression of miR-29c may reverse the resistance of MGC-803/AP cells to apatinib.
2018, 25(11):1148-1153.
DOI: 10.3872/j.issn.1007-385X.2018.11.011
Abstract:
Objective: To assess the association between interleukin-17 (IL-17) gene rs763780 polymorphism and susceptibility of gastric cancer using Meta-analysis. Methods: A comprehensive search was performed on PubMed, EMBASE, the Cochrane Library, Web of Science, Wanfang Database, Chinese Biomedical Literature Database, Chinese Science and Technology Academic Journal and Chinese Journal Full-text Database from their inception to December 2017 to identify relevant case-control studies on association between interleukin-17 (IL-17) gene rs763780 polymorphism and susceptibility of gastric cancer. Meta-analysis was performed using STATA 12.0 software. Results: A total of 10 case-control studies were included in this Meta-analysis, involving 3 892 gastric cancer cases and 4 627 controls. The results showed that there was association between IL-17 rs763780 polymorphism and gastric cancer risk in allele genetic model (C vs T: OR=1.90, 95% CI=1.73-2.08), additive model (CC vs TT: OR=1.76, 95% CI=1.45-2.14), codominant model (CC vs CT: OR =1.26, 95% CI=1.13-1.42), dominant model (CC vs CT+TT: OR=1.93, 95% CI=1.65-2.26) and recessive model (TT vs CT+CC: OR=1.67, 95% CI=1.38-2.03). Conclusion: IL-17 rs763780 polymorphism increases the risk of gastric cancer.
Objective: To assess the association between interleukin-17 (IL-17) gene rs763780 polymorphism and susceptibility of gastric cancer using Meta-analysis. Methods: A comprehensive search was performed on PubMed, EMBASE, the Cochrane Library, Web of Science, Wanfang Database, Chinese Biomedical Literature Database, Chinese Science and Technology Academic Journal and Chinese Journal Full-text Database from their inception to December 2017 to identify relevant case-control studies on association between interleukin-17 (IL-17) gene rs763780 polymorphism and susceptibility of gastric cancer. Meta-analysis was performed using STATA 12.0 software. Results: A total of 10 case-control studies were included in this Meta-analysis, involving 3 892 gastric cancer cases and 4 627 controls. The results showed that there was association between IL-17 rs763780 polymorphism and gastric cancer risk in allele genetic model (C vs T: OR=1.90, 95% CI=1.73-2.08), additive model (CC vs TT: OR=1.76, 95% CI=1.45-2.14), codominant model (CC vs CT: OR =1.26, 95% CI=1.13-1.42), dominant model (CC vs CT+TT: OR=1.93, 95% CI=1.65-2.26) and recessive model (TT vs CT+CC: OR=1.67, 95% CI=1.38-2.03). Conclusion: IL-17 rs763780 polymorphism increases the risk of gastric cancer.
2018, 25(11):1154-1158.
DOI: 10.3872/j.issn.1007-385X.2018.11.012
Abstract:
[摘要] 外泌体通过胞内体内陷形成多泡体再与质膜融合后释放，其内含有蛋白质、脂质、核酸等生物活性物质。外泌体通过与受体细胞融合，将其内含的生物活性物质作为信号分子传递给受体细胞，从而介导细胞间信号交流。胃癌细胞分泌大量的外泌体，可影响周围细胞的功能，在调控胃癌的生物学行为中发挥重要作用。外泌体在胃癌相关研究中取得较多新进展，包括对胃癌的生长、转移、免疫逃避、耐药性等生物学行为的影响及相关机制，以及作为药物载体在胃癌靶向治疗中的临床应用。
[摘要] 外泌体通过胞内体内陷形成多泡体再与质膜融合后释放，其内含有蛋白质、脂质、核酸等生物活性物质。外泌体通过与受体细胞融合，将其内含的生物活性物质作为信号分子传递给受体细胞，从而介导细胞间信号交流。胃癌细胞分泌大量的外泌体，可影响周围细胞的功能，在调控胃癌的生物学行为中发挥重要作用。外泌体在胃癌相关研究中取得较多新进展，包括对胃癌的生长、转移、免疫逃避、耐药性等生物学行为的影响及相关机制，以及作为药物载体在胃癌靶向治疗中的临床应用。
LI Shanzhi
,
CHEN Shuang
,
ZHAO Jin
,
LI Yiquan
,
ZHU Yilong
,
LI Wenjie
,
YIN Xunzhe
,
CUI Yingli
,
WANG Jing
,
LIU Xing
,
LI Xiao
,
JIN Ningyi
2018, 25(11):1159-1165.
DOI: 10.3872/j.issn.1007-385X.2018.11.013
Abstract:
Objective: To explore the difference in the proliferation inhibition of doxorubicin and dual specific oncolytic adenoviruses (Ad-VT, Ad-T, Ad-VP3 and d-Mock) on breast cancer cells and normal mammary cells. Methods: The proliferation inhibition rates of doxorubicin and recombinant adenovirus(Ad-VT, Ad-T, Ad-VP3and Mock) on breast cancer cells were detected through WST-1 experiment,and the effects of two drugs on the inhibitory rates of normal mammary epithelial cells were also detected. Moreover, the apoptosis rates of doxorubicin and oncolytic adenoviruses on breast cancer cells and normal mammary epithelial cells were evaluated by Annexin V flow cytometry, Hoechst and JC-1 staining, and the difference in the apoptosis rates were also compared. Results: All the re-combinant adenovirus could effectively suppress the proliferation of breast cancer cells (P<0.05 or P<0.01), the inhibition effects followed the order of Ad-VT>Ad-T>Ad-VP3>Ad-MOCK, and the inhibition effect was positively correlated with time. Doxorubicin could also effectively suppress the proliferation of breast cancer cells (P<0.05 or P<0.01), and the inhibition effect was markedly enhanced with the increases in does and time. However, doxorubicin also showed strong inhibition effect on the normal mammary epithelial cells,and the inhibition rate achieved 80% under 72 h and 5 ug/ml doxorubicin, while that of oncolytic adenovirus Ad-VT on MCF-10A was 20% at 72 h. The apoptosis effects of oncolytic adenoviruses-induced breast cancer cellwere increased with time, and the apoptosis rate efficiency followed the order of Ad-VT>Ad-T>Ad-VP3>Ad-MOCK, but they displayed low ability to induce normal mammary cell apoptosis. The apoptosis effects of doxorubicin-induced breast cancer cell were similar to that of the normal mammary epithelial cell (P<0.05 or P<0.01), which followed the dose of 0.05<0.5<5 μg/ml. Conclusion: Dual specific oncolytic adenoviruses can effectively suppress the proliferation of breast cancer cells, but they have low inhibition on normal mammary cells, which have displayed superior safety and provide a new method for the biotherapy of tumor.
Objective: To explore the difference in the proliferation inhibition of doxorubicin and dual specific oncolytic adenoviruses (Ad-VT, Ad-T, Ad-VP3 and d-Mock) on breast cancer cells and normal mammary cells. Methods: The proliferation inhibition rates of doxorubicin and recombinant adenovirus(Ad-VT, Ad-T, Ad-VP3and Mock) on breast cancer cells were detected through WST-1 experiment,and the effects of two drugs on the inhibitory rates of normal mammary epithelial cells were also detected. Moreover, the apoptosis rates of doxorubicin and oncolytic adenoviruses on breast cancer cells and normal mammary epithelial cells were evaluated by Annexin V flow cytometry, Hoechst and JC-1 staining, and the difference in the apoptosis rates were also compared. Results: All the re-combinant adenovirus could effectively suppress the proliferation of breast cancer cells (P<0.05 or P<0.01), the inhibition effects followed the order of Ad-VT>Ad-T>Ad-VP3>Ad-MOCK, and the inhibition effect was positively correlated with time. Doxorubicin could also effectively suppress the proliferation of breast cancer cells (P<0.05 or P<0.01), and the inhibition effect was markedly enhanced with the increases in does and time. However, doxorubicin also showed strong inhibition effect on the normal mammary epithelial cells,and the inhibition rate achieved 80% under 72 h and 5 ug/ml doxorubicin, while that of oncolytic adenovirus Ad-VT on MCF-10A was 20% at 72 h. The apoptosis effects of oncolytic adenoviruses-induced breast cancer cellwere increased with time, and the apoptosis rate efficiency followed the order of Ad-VT>Ad-T>Ad-VP3>Ad-MOCK, but they displayed low ability to induce normal mammary cell apoptosis. The apoptosis effects of doxorubicin-induced breast cancer cell were similar to that of the normal mammary epithelial cell (P<0.05 or P<0.01), which followed the dose of 0.05<0.5<5 μg/ml. Conclusion: Dual specific oncolytic adenoviruses can effectively suppress the proliferation of breast cancer cells, but they have low inhibition on normal mammary cells, which have displayed superior safety and provide a new method for the biotherapy of tumor.
2018, 25(11):1166-1170.
DOI: 10.3872/j.issn.1007-385X.2018.11.014
Abstract:
Objective: To investigate the role of LncRNA RP11-513G11.1 in the chemoresistance and evaluation of prognosis in small cell lung cancer (SCLC). Methods: From June 2012 to June 2017，98 cases of SCLC tissue, 30 cases of paracancerous tissue and 30 cases of normal lung tissue were performed by surgery, puncture biopsy or bronchoscopic biopsy from the Affiliated Hospital of Southwest Medical University. QRT-PCR was used to detect the expression of LncRNA RP11-513G11.1 in SCLC tissue, paracancerous tissue,normal lung tissue and SCLC sensitive cell strain H69, drug resistance cell strain H69AR. All patients received EP regimen (etoposide+cisplatin). According to their chemosensitivity, they were divided into chemosensitivity group and drug resistance group. The expression of LncRNA RP11-513G11.1 in two groups was detected. The relationship between RP11-513G11.1 expression and prognosis,survival time and risk factors of OS in patients were analyzed. Results: The expression of LncRNA RP11-513G11.1 in H69AR chemoresistant cells (13.790±2.830) was significantly higher than that in H69AR chemosensitive cells (1.080±0.090) (P<0.01),the expression level of LncRNA RP11-513G11.1 in SCLC tissues (8.558±1.130) was significantly higher than that in adjacent tissues (1.188±0.090) and normal lung tissues (1.636±0.150) (all P<0.01), the expression of RP11-513G11.1 in chemoresistant patients was significantly higher than that in chemosensitive patients (4.974±0.313) (P<0.01). The expression of RP11-513G11.1 was not related to gender and age,but was related to disease stage, lymph node metastasis, distant metastasis and chemotherapy resistance in SCLC patients (all P<0.05);High expression RP11-513G11.1 patients was shorter PFS [(12.59 ±2.08) months] and OS [(24.98 ±1.56) months] than those with low expression [(25.47 ± 1.23) months] and [(39.03 ± 2.67) months] (P<0.01). Univariate and multivariate analysis showed that RP11-513G11.1 expression, disease stage and distant metastasis were independent prognostic risk factors for SCLC patients (all P<0.05).Conclusion: LncRNA RP11-513G11.1 may be a potential biomarker of chemosensitivity and prognosis in SCLC patients.
Objective: To investigate the role of LncRNA RP11-513G11.1 in the chemoresistance and evaluation of prognosis in small cell lung cancer (SCLC). Methods: From June 2012 to June 2017，98 cases of SCLC tissue, 30 cases of paracancerous tissue and 30 cases of normal lung tissue were performed by surgery, puncture biopsy or bronchoscopic biopsy from the Affiliated Hospital of Southwest Medical University. QRT-PCR was used to detect the expression of LncRNA RP11-513G11.1 in SCLC tissue, paracancerous tissue,normal lung tissue and SCLC sensitive cell strain H69, drug resistance cell strain H69AR. All patients received EP regimen (etoposide+cisplatin). According to their chemosensitivity, they were divided into chemosensitivity group and drug resistance group. The expression of LncRNA RP11-513G11.1 in two groups was detected. The relationship between RP11-513G11.1 expression and prognosis,survival time and risk factors of OS in patients were analyzed. Results: The expression of LncRNA RP11-513G11.1 in H69AR chemoresistant cells (13.790±2.830) was significantly higher than that in H69AR chemosensitive cells (1.080±0.090) (P<0.01),the expression level of LncRNA RP11-513G11.1 in SCLC tissues (8.558±1.130) was significantly higher than that in adjacent tissues (1.188±0.090) and normal lung tissues (1.636±0.150) (all P<0.01), the expression of RP11-513G11.1 in chemoresistant patients was significantly higher than that in chemosensitive patients (4.974±0.313) (P<0.01). The expression of RP11-513G11.1 was not related to gender and age,but was related to disease stage, lymph node metastasis, distant metastasis and chemotherapy resistance in SCLC patients (all P<0.05);High expression RP11-513G11.1 patients was shorter PFS [(12.59 ±2.08) months] and OS [(24.98 ±1.56) months] than those with low expression [(25.47 ± 1.23) months] and [(39.03 ± 2.67) months] (P<0.01). Univariate and multivariate analysis showed that RP11-513G11.1 expression, disease stage and distant metastasis were independent prognostic risk factors for SCLC patients (all P<0.05).Conclusion: LncRNA RP11-513G11.1 may be a potential biomarker of chemosensitivity and prognosis in SCLC patients.
2018, 25(11):1171-1175.
DOI: 10.3872/j.issn.1007-385X.2018.11.015
Abstract:
Objective: To study the expression of HOXA10 gene in endometrial carcinoma and its effect on the apoptosis, migration and invasion of Ishikawa cells. Methods: Twenty-one cases of endometrial carcinoma tissue samples and 25 cases of normal endometrial tissue samples from patients treated at the Department of Obstetrics and Gynecology, Nanjing Drum Tower Hospital from 2012 to 2013 were collected for this study. The mRNA and protein expressions of HOXA10 in endometrial carcinoma and normal endometrial tissues were separately tested by Realtime-qPCR (qRT-PCR) and Western blotting. Ishikawa cells were infected with adenovirus-flag-HOXA10 at different multiplicity (5, 10, 20 MOI), and infected by adenovirus-flag-lacz (20 MOI) as control; And the cell apoptosis was tested by Flow Cytometry. Ishikawa cells were transfected with 50 nmol/L si-HOXA10 plasmids and 50 nmol/L si-NC plasmids, as down-regulation group and down-regulation control group, respectively. Ishikawa cells were infected with 20 MOI adenovirus-flag-HOXA10 and 20 MOI adenovirus-flag-lacz, as up-regulation group and up-regulation control group, respectively. The ability of migration and invasion was detected by transwell assay. Results: The results of qRT-PCR and Western blotting showed that the expressions of HOXA10 mRNA and protein in endometrial carcinoma samples were both significantly lower than normal samples [mRNA: (0.56±0.14)vs (1.36±0.33), P<0.01; protein: (1.01±0.25) vs (2.10±0.71), P<0.001]. After the up-regulation of HOXA10 gene in Ishikawa cell line, the cell apoptosis rate in ad-flag-HOXA10 groups (5, 10, 20 MOI) was significantly raised, and most of which was in the early apoptosis [(50.92±8.79)%, (55.17±4.07)%, (76.10±3.65)% vs (7.74 ± 0.15)%, all P<0.01]. The number of migrated cells was markedly up-regulated in si-HOXA10 group [(248±25) vs (135±15), P<0.01] but markedly down-regulated in ad-flag-HOXA10 group [(50±6) vs (100±13), P<0.01]. The number of invasive cells was markedly up-regulated in si-HOXA10 group [(131±18) vs (66±9), P<0.01] but markedly down-regulated in ad-flag-HOXA10 group [(34±8) vs (60±4), P<0.01]. Conclusions: Both mRNA and protein expressions of HOXA10 were down-regulated in endometrial carcinoma samples than in normal endometrium. Up-regulation of HOXA10 gene in Ishikawa cell line can promote cell apoptosis and inhibit cell migration and invasion.
Objective: To study the expression of HOXA10 gene in endometrial carcinoma and its effect on the apoptosis, migration and invasion of Ishikawa cells. Methods: Twenty-one cases of endometrial carcinoma tissue samples and 25 cases of normal endometrial tissue samples from patients treated at the Department of Obstetrics and Gynecology, Nanjing Drum Tower Hospital from 2012 to 2013 were collected for this study. The mRNA and protein expressions of HOXA10 in endometrial carcinoma and normal endometrial tissues were separately tested by Realtime-qPCR (qRT-PCR) and Western blotting. Ishikawa cells were infected with adenovirus-flag-HOXA10 at different multiplicity (5, 10, 20 MOI), and infected by adenovirus-flag-lacz (20 MOI) as control; And the cell apoptosis was tested by Flow Cytometry. Ishikawa cells were transfected with 50 nmol/L si-HOXA10 plasmids and 50 nmol/L si-NC plasmids, as down-regulation group and down-regulation control group, respectively. Ishikawa cells were infected with 20 MOI adenovirus-flag-HOXA10 and 20 MOI adenovirus-flag-lacz, as up-regulation group and up-regulation control group, respectively. The ability of migration and invasion was detected by transwell assay. Results: The results of qRT-PCR and Western blotting showed that the expressions of HOXA10 mRNA and protein in endometrial carcinoma samples were both significantly lower than normal samples [mRNA: (0.56±0.14)vs (1.36±0.33), P<0.01; protein: (1.01±0.25) vs (2.10±0.71), P<0.001]. After the up-regulation of HOXA10 gene in Ishikawa cell line, the cell apoptosis rate in ad-flag-HOXA10 groups (5, 10, 20 MOI) was significantly raised, and most of which was in the early apoptosis [(50.92±8.79)%, (55.17±4.07)%, (76.10±3.65)% vs (7.74 ± 0.15)%, all P<0.01]. The number of migrated cells was markedly up-regulated in si-HOXA10 group [(248±25) vs (135±15), P<0.01] but markedly down-regulated in ad-flag-HOXA10 group [(50±6) vs (100±13), P<0.01]. The number of invasive cells was markedly up-regulated in si-HOXA10 group [(131±18) vs (66±9), P<0.01] but markedly down-regulated in ad-flag-HOXA10 group [(34±8) vs (60±4), P<0.01]. Conclusions: Both mRNA and protein expressions of HOXA10 were down-regulated in endometrial carcinoma samples than in normal endometrium. Up-regulation of HOXA10 gene in Ishikawa cell line can promote cell apoptosis and inhibit cell migration and invasion.
2018, 25(11):1176-1179.
DOI: 10.3872/j.issn.1007-385X.2018.11.016
Abstract:
Objective: To compare the safety and efficacy of bevacizumab plus cisplatin and cisplatin alone in the treatment of malignant pleural effusion of lung cancer patients. Methods: From November 2014 to November 2017, 27 patients diagnosed with lung cancer complicated with malignant pleural effusion at the department of Oncology, the Central Hospital of Huludao, were enrolled in this study. Fourteen patients received bevacizumab plus cisplatin and thirteen patients received cisplatin alone. The clinical efficacy and adverse reactions were compared between the two groups. Results: There was no significant difference in the general condition between the two groups before treatment(P>0.05). The bevacizumab group had better short-term efficacy than the cisplatin group and the difference was statistically significant(92.9% vs 61.5%, P<0.05). The main adverse reactions during the treatment were bone marrow suppression and gastrointestinal discomfort, etc. The incidence of adverse reactions was similar between the two groups, with no statistically significant difference(P>0.05). Conclusion: Compared with cisplatin alone, bevacizumab combined with cisplatin has better shortterm efficacy in the treatment of lung cancer patients with malignant pleural effusion. The adverse reactions were quite similar.
Objective: To compare the safety and efficacy of bevacizumab plus cisplatin and cisplatin alone in the treatment of malignant pleural effusion of lung cancer patients. Methods: From November 2014 to November 2017, 27 patients diagnosed with lung cancer complicated with malignant pleural effusion at the department of Oncology, the Central Hospital of Huludao, were enrolled in this study. Fourteen patients received bevacizumab plus cisplatin and thirteen patients received cisplatin alone. The clinical efficacy and adverse reactions were compared between the two groups. Results: There was no significant difference in the general condition between the two groups before treatment(P>0.05). The bevacizumab group had better short-term efficacy than the cisplatin group and the difference was statistically significant(92.9% vs 61.5%, P<0.05). The main adverse reactions during the treatment were bone marrow suppression and gastrointestinal discomfort, etc. The incidence of adverse reactions was similar between the two groups, with no statistically significant difference(P>0.05). Conclusion: Compared with cisplatin alone, bevacizumab combined with cisplatin has better shortterm efficacy in the treatment of lung cancer patients with malignant pleural effusion. The adverse reactions were quite similar.
2018, 25(11):1180-1184.
DOI: 10.3872/j.issn.1007-385X.2018.11.017
Abstract:
[摘要] 肿瘤是由肿瘤细胞及其周围基质细胞和非细胞组分构成的复合体，肿瘤的发生发展是肿瘤细胞与其微环境相互促进、共同演化的一个动态过程，肿瘤微环境在肿瘤的生长转移过程中发挥至关重要的作用。肿瘤相关成纤维细胞（cancer associated fibroblasts, CAFs），作为肿瘤微环境中最主要的组成成分之一，能够分泌多种细胞因子，从而促进肿瘤血管生成，诱导肿瘤细胞发生上皮间质转化，打破组织细胞之间的稳态，使微环境更有利于肿瘤生长。CAFs对乳腺癌、肝癌、胃癌、结直肠癌、卵巢癌、肺癌等多种常见癌有促进作用。本文就近年来CAFs对肿瘤的发生发展、耐药及其他方面的影响及作用机制加以讨论，以期为癌症的治疗提供新的思路。
[摘要] 肿瘤是由肿瘤细胞及其周围基质细胞和非细胞组分构成的复合体，肿瘤的发生发展是肿瘤细胞与其微环境相互促进、共同演化的一个动态过程，肿瘤微环境在肿瘤的生长转移过程中发挥至关重要的作用。肿瘤相关成纤维细胞（cancer associated fibroblasts, CAFs），作为肿瘤微环境中最主要的组成成分之一，能够分泌多种细胞因子，从而促进肿瘤血管生成，诱导肿瘤细胞发生上皮间质转化，打破组织细胞之间的稳态，使微环境更有利于肿瘤生长。CAFs对乳腺癌、肝癌、胃癌、结直肠癌、卵巢癌、肺癌等多种常见癌有促进作用。本文就近年来CAFs对肿瘤的发生发展、耐药及其他方面的影响及作用机制加以讨论，以期为癌症的治疗提供新的思路。
2018, 25(11):1185-1190.
DOI: 10.3872/j.issn.1007-385X.2018.11.018
Abstract:
[摘要] 肝细胞癌（hepatocellular carcinoma，HCC）是全球发病率和死亡率较高的恶性肿瘤之一。菌群平衡对于维持肠道和全身态的代谢与免疫非常重要，肠道微生物与肝细胞癌的形成密切相关。肠漏、菌群失衡、微生物代谢物及免疫抑制是导致肝细胞癌形成的主要机制。肠漏及微生物相关模式分子-Toll样受体促进肝细胞癌的发生发展；菌群失衡及菌群移位除了能引起晚期肝病的感染性并发症之外，还能使肝脏中产生慢性炎症；肠道菌群及代谢物还可影响细胞的分化；肠道菌群及代谢产物介导的免疫抑制也可促进肝细胞癌的发生。可通过靶向肠道菌群，如使用抗生素杀灭有害菌群，使用益生菌调节菌群平衡，使用药物改善肠漏，使用药物拮抗TLR等策略来抑制肝细胞癌的发生。肠道微生物稳态与肝癌的研究进展为有效预防和治疗肝癌提出了新的策略。
[摘要] 肝细胞癌（hepatocellular carcinoma，HCC）是全球发病率和死亡率较高的恶性肿瘤之一。菌群平衡对于维持肠道和全身态的代谢与免疫非常重要，肠道微生物与肝细胞癌的形成密切相关。肠漏、菌群失衡、微生物代谢物及免疫抑制是导致肝细胞癌形成的主要机制。肠漏及微生物相关模式分子-Toll样受体促进肝细胞癌的发生发展；菌群失衡及菌群移位除了能引起晚期肝病的感染性并发症之外，还能使肝脏中产生慢性炎症；肠道菌群及代谢物还可影响细胞的分化；肠道菌群及代谢产物介导的免疫抑制也可促进肝细胞癌的发生。可通过靶向肠道菌群，如使用抗生素杀灭有害菌群，使用益生菌调节菌群平衡，使用药物改善肠漏，使用药物拮抗TLR等策略来抑制肝细胞癌的发生。肠道微生物稳态与肝癌的研究进展为有效预防和治疗肝癌提出了新的策略。
2018, 25(11):1191-1199.
DOI: 10.3872/j.issn.1007-385X.2018.11.019
Abstract:
[摘要] LL-37 是人体内发现的唯一一种Cathelicidin 类抗菌肽，由其前体hCAP-18 经丝氨酸蛋白酶3 剪切后产生。研究发现，LL-37 可在卵巢癌、肺癌、恶性黑色素瘤、皮肤鳞状细胞癌、前列腺癌等肿瘤中发挥促癌作用；而在胃癌、结直肠癌、白血病等肿瘤中发挥抑癌作用。本文就LL-37 在这些恶性肿瘤发生发展过程中所起的作用作一综述。
[摘要] LL-37 是人体内发现的唯一一种Cathelicidin 类抗菌肽，由其前体hCAP-18 经丝氨酸蛋白酶3 剪切后产生。研究发现，LL-37 可在卵巢癌、肺癌、恶性黑色素瘤、皮肤鳞状细胞癌、前列腺癌等肿瘤中发挥促癌作用；而在胃癌、结直肠癌、白血病等肿瘤中发挥抑癌作用。本文就LL-37 在这些恶性肿瘤发生发展过程中所起的作用作一综述。
2018, 25(11):1200-1204.
DOI: 10.3872/j.issn.1007-385X.2018.11.020
Abstract:
[摘要] 人表皮生长因子受体2（human epidermal growth factor receptor 2，HER2）阳性乳腺癌侵袭性高，预后差。随着抗HER2药物的不断出现及广泛应用，HER2 阳性乳腺癌患者的预后出现了非常显著的改善。10 年随访结果证实1 年曲妥珠单抗辅助治疗可以显著降低疾病复发风险；对于术后的高危人群，曲妥珠单抗联合帕妥珠单抗或者曲妥珠单抗序贯来那替尼可以进一步减少复发。5 年随访结果表明帕妥珠单抗+曲妥珠单抗为基础的新辅助治疗可使病理完全缓解（pathological complete response，pCR）转化为长期生存获益；白蛋白紫杉醇代替普通紫杉醇与抗HER2 药物联用可以进一步提高pCR率；而抗HER2 药物联合内分泌治疗尚不能达到与联合化疗在新辅助治疗中疗效，即使联合CDK4/6 抑制剂，对于pCR的提高依然有限。曲妥珠单抗+帕妥珠单抗联合紫杉类药物是晚期HER2 阳性乳腺癌的标准一线方案；对于老年、体弱的患者，节拍环磷酰胺可以作为紫杉类药物的替代品；拉帕替尼+曲妥珠单抗联合内分泌治疗可以作为HER2 阳性伴激素受体阳性的选择，疗效优于曲妥珠单抗联合内分泌治疗；T-DM1 无论是作为二线治疗还是三线及以后的治疗均提高了患者生存获益，是治疗晚期、耐药HER2阳性乳腺癌的首选。
[摘要] 人表皮生长因子受体2（human epidermal growth factor receptor 2，HER2）阳性乳腺癌侵袭性高，预后差。随着抗HER2药物的不断出现及广泛应用，HER2 阳性乳腺癌患者的预后出现了非常显著的改善。10 年随访结果证实1 年曲妥珠单抗辅助治疗可以显著降低疾病复发风险；对于术后的高危人群，曲妥珠单抗联合帕妥珠单抗或者曲妥珠单抗序贯来那替尼可以进一步减少复发。5 年随访结果表明帕妥珠单抗+曲妥珠单抗为基础的新辅助治疗可使病理完全缓解（pathological complete response，pCR）转化为长期生存获益；白蛋白紫杉醇代替普通紫杉醇与抗HER2 药物联用可以进一步提高pCR率；而抗HER2 药物联合内分泌治疗尚不能达到与联合化疗在新辅助治疗中疗效，即使联合CDK4/6 抑制剂，对于pCR的提高依然有限。曲妥珠单抗+帕妥珠单抗联合紫杉类药物是晚期HER2 阳性乳腺癌的标准一线方案；对于老年、体弱的患者，节拍环磷酰胺可以作为紫杉类药物的替代品；拉帕替尼+曲妥珠单抗联合内分泌治疗可以作为HER2 阳性伴激素受体阳性的选择，疗效优于曲妥珠单抗联合内分泌治疗；T-DM1 无论是作为二线治疗还是三线及以后的治疗均提高了患者生存获益，是治疗晚期、耐药HER2阳性乳腺癌的首选。
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Supported by:Beijing E-Tiller Technology Development Co., Ltd.
Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.