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Volume 31,Issue 8,2024 Table of Contents
2024, 31(8):743-751.
DOI: 10.3872/j.issn.1007-385X.2024.08.001
Abstract:
Immunotherapy has emerged as a groundbreaking approach that has revolutionized tumor treatment and revitalized research in tumor immunology. At the forefront of this innovation is immune-organoid, which has become an indispensable tool in tumor immunology research. These models excel in reconstructing the tumor immune microenvironment, faithfully mimicking the response mechanisms and interactions of immune cells. Consequently, they have garnered widespread adoption in tumor immunology research. The innovative immune-organoid models encompass two primary categories: those derived from immune organs and those involving co-cultures of tumor organoids with immune cells. These models offer a versatile platform with applications spanning diverse domains, including the elucidation of tumorigenesis mechanisms, drug screening processes, the acceleration of cancer vaccine development, and the guidance of personalized therapeutic strategies. In this review, we provide a comprehensive summary of the current culture methods and status of immune-organoid. We also explore the wide application of immune-organoid in tumor immunology, while addressing the challenges they face and offering insights into future directions for this promising technology.
Immunotherapy has emerged as a groundbreaking approach that has revolutionized tumor treatment and revitalized research in tumor immunology. At the forefront of this innovation is immune-organoid, which has become an indispensable tool in tumor immunology research. These models excel in reconstructing the tumor immune microenvironment, faithfully mimicking the response mechanisms and interactions of immune cells. Consequently, they have garnered widespread adoption in tumor immunology research. The innovative immune-organoid models encompass two primary categories: those derived from immune organs and those involving co-cultures of tumor organoids with immune cells. These models offer a versatile platform with applications spanning diverse domains, including the elucidation of tumorigenesis mechanisms, drug screening processes, the acceleration of cancer vaccine development, and the guidance of personalized therapeutic strategies. In this review, we provide a comprehensive summary of the current culture methods and status of immune-organoid. We also explore the wide application of immune-organoid in tumor immunology, while addressing the challenges they face and offering insights into future directions for this promising technology.
2024, 31(8):752-758.
DOI: 10.3872/j.issn.1007-385X.2024.08.002
Abstract:
With the rapid development of precision medicine, extracellular vesicles (EVs) have shown tremendous potential in the diagnosis and therapeutic applications of diseases such as tumors. Drug-Loaded Microparticles Immunotherapy is an innovative cancer immunotherapy technology originating in China. It utilizes tumor-derived microparticles as carriers, encapsulating or loading commonly used clinical small molecule chemotherapeutic drugs. This approach achieves effective tumor destruction through mechanisms such as targeted drug delivery, activation of neutrophils, reversal of macrophages polarization, and enhancement of tumor antigen presentation. Over more than a decade of research into anti-tumor mechanisms, preclinical assessments, and clinical trials, this technology has successfully transitioned to clinical application and received clinical approval. To further advance the standardized and scientific application of Drug-Loaded Microparticles Immunotherapy, Committee for Tumor Immunology & Biotherapy of Chinese Society for Immunology and the Society of Cancer Biotherapy of China Anti-Cancer Association jointly organized technical and clinical experts in the fields of extracellular vesicles and tumor immunotherapy. After multiple rounds of discussions and revisions, they collaboratively drafted the“ Expert Consensus on Clinical Application of Drug-Loaded Microparticles Immunotherapy”. This consensus introduces the research and practical application of the therapy in cancer treatment, addresses existing challenges, and outlines future development directions. Its primary goal is to offer guidance and insights for the optimal clinical use of this innovative therapeutic approach.
With the rapid development of precision medicine, extracellular vesicles (EVs) have shown tremendous potential in the diagnosis and therapeutic applications of diseases such as tumors. Drug-Loaded Microparticles Immunotherapy is an innovative cancer immunotherapy technology originating in China. It utilizes tumor-derived microparticles as carriers, encapsulating or loading commonly used clinical small molecule chemotherapeutic drugs. This approach achieves effective tumor destruction through mechanisms such as targeted drug delivery, activation of neutrophils, reversal of macrophages polarization, and enhancement of tumor antigen presentation. Over more than a decade of research into anti-tumor mechanisms, preclinical assessments, and clinical trials, this technology has successfully transitioned to clinical application and received clinical approval. To further advance the standardized and scientific application of Drug-Loaded Microparticles Immunotherapy, Committee for Tumor Immunology & Biotherapy of Chinese Society for Immunology and the Society of Cancer Biotherapy of China Anti-Cancer Association jointly organized technical and clinical experts in the fields of extracellular vesicles and tumor immunotherapy. After multiple rounds of discussions and revisions, they collaboratively drafted the“ Expert Consensus on Clinical Application of Drug-Loaded Microparticles Immunotherapy”. This consensus introduces the research and practical application of the therapy in cancer treatment, addresses existing challenges, and outlines future development directions. Its primary goal is to offer guidance and insights for the optimal clinical use of this innovative therapeutic approach.
2024, 31(8):759-768.
DOI: 10.3872/j.issn.1007-385X.2024.08.003
Abstract:
Objective: To preliminarily explore the potential mechanisms by which lymphocyte antigen 6 complex, locus E (Ly6E) regulates tumor immune microenvironment (TIME) in breast cancer 4T1 cells using single-cell RNA transcription sequencing technology (scRNA-seq). Methods: A mouse breast cancer 4T1 cell line with Ly6e gene knockout (Ly6E-KO) was constructed by CRISPR-Cas9 technology. The in vitro proliferation and in vivo growth capabilities of Ly6E-KO cells were compared to those of the wide type 4T1 cells (Ly6E-WT). CD45-positive cells from both types of tumor tissues were sorted by flow cytometry and analyzed using scRNA-seq. The sequencing results were first screened for differentially expressed gene profiles using the Seurat software package and annotated based on marker genes. Then, Cellchat and Monocle2 software were used to analyze the cell-to-cell interactions and the evolutionary trajectories of specific immune cells. Results: Compared with Ly6E-WT, Ly6E-KO cells showed no significant difference in in vitro proliferation capability but demonstrated significantly reduced in vivo growth capability (PConclusion: Ly6e gene knockout in tumor cells can enhance the anti-tumor immune response by increasing DC activation and infiltration in TIME.
Objective: To preliminarily explore the potential mechanisms by which lymphocyte antigen 6 complex, locus E (Ly6E) regulates tumor immune microenvironment (TIME) in breast cancer 4T1 cells using single-cell RNA transcription sequencing technology (scRNA-seq). Methods: A mouse breast cancer 4T1 cell line with Ly6e gene knockout (Ly6E-KO) was constructed by CRISPR-Cas9 technology. The in vitro proliferation and in vivo growth capabilities of Ly6E-KO cells were compared to those of the wide type 4T1 cells (Ly6E-WT). CD45-positive cells from both types of tumor tissues were sorted by flow cytometry and analyzed using scRNA-seq. The sequencing results were first screened for differentially expressed gene profiles using the Seurat software package and annotated based on marker genes. Then, Cellchat and Monocle2 software were used to analyze the cell-to-cell interactions and the evolutionary trajectories of specific immune cells. Results: Compared with Ly6E-WT, Ly6E-KO cells showed no significant difference in in vitro proliferation capability but demonstrated significantly reduced in vivo growth capability (PConclusion: Ly6e gene knockout in tumor cells can enhance the anti-tumor immune response by increasing DC activation and infiltration in TIME.
2024, 31(8):769-776.
DOI: 10.3872/j.issn.1007-385X.2024.08.004
Abstract:
Objective: To elucidate the molecular mechanism by which Porphyromonas gingivalis (Pg) induces epithelialmesenchymal transition (EMT) in esophageal squamous cell carcinoma (ESCC) cells. Methods: KEGG was used to identify the biological pathways enriched by Pg-induced differentially expressed genes in ESCC. WB and/or immunofluorescence (IF) were used to detect the changes in the expression of glycoprotein-A repetitions predominant protein (GARP), TGF-β, pSMAD/SMAD, Snail, Oct4 and EMT-related molecules in Pg-induced ESCC cells. ELISA was used to measure changes in TGF-β1 level. Immunohistochemistry was used to detect the expression of GARP and TGF- β1 in ESCC tissues. The tumorigenic effect of Pg on ESCC was verified by Transwell assays and animal experiments. Results: Pg activated multiple signaling pathways, such as TGF-β, Hippo, and PI3K/Akt. Pginfection stimulated an increased secretion of total TGF- β1 and active TFG- β1 in ESCC cells (PPPg. The protein levels of TGF-β1 and GARP in ESCC tissues with high Pg abundance were higher than those in ESCC tissues with low Pg abundance. The abundance of Pg was positively correlated with the protein expression of TGF-β1 and GARP (P=0.001 5). Conclusion: Pg activates the TGF-β/Smad axis through GARP to promote the occurrence of EMT in ESCC cells, thereby facilitating the migration, invasion and growth of ESCC cells. Pg clearance or TGF-β signaling blockade can reverse these Pg-induced promotive effects on ESCC.
Objective: To elucidate the molecular mechanism by which Porphyromonas gingivalis (Pg) induces epithelialmesenchymal transition (EMT) in esophageal squamous cell carcinoma (ESCC) cells. Methods: KEGG was used to identify the biological pathways enriched by Pg-induced differentially expressed genes in ESCC. WB and/or immunofluorescence (IF) were used to detect the changes in the expression of glycoprotein-A repetitions predominant protein (GARP), TGF-β, pSMAD/SMAD, Snail, Oct4 and EMT-related molecules in Pg-induced ESCC cells. ELISA was used to measure changes in TGF-β1 level. Immunohistochemistry was used to detect the expression of GARP and TGF- β1 in ESCC tissues. The tumorigenic effect of Pg on ESCC was verified by Transwell assays and animal experiments. Results: Pg activated multiple signaling pathways, such as TGF-β, Hippo, and PI3K/Akt. Pginfection stimulated an increased secretion of total TGF- β1 and active TFG- β1 in ESCC cells (PPPg. The protein levels of TGF-β1 and GARP in ESCC tissues with high Pg abundance were higher than those in ESCC tissues with low Pg abundance. The abundance of Pg was positively correlated with the protein expression of TGF-β1 and GARP (P=0.001 5). Conclusion: Pg activates the TGF-β/Smad axis through GARP to promote the occurrence of EMT in ESCC cells, thereby facilitating the migration, invasion and growth of ESCC cells. Pg clearance or TGF-β signaling blockade can reverse these Pg-induced promotive effects on ESCC.
2024, 31(8):777-785.
DOI: 10.3872/j.issn.1007-385X.2024.08.005
Abstract:
Objective：To prepare and characterize CD8 antibody-conjugated CPI-444 (C) -loaded nanoparticles (CNP/α CD8) and investigate their effects on CD8+ T cell activation, proliferation, and anti-tumor activity. Methods：Nanoparticles encapsulating the adenosine A2A receptor(A2AR) antagonist CPI-444 (C) or the fluorescent dye Coumarin-6 (C6) were prepared using the double emulsion solvent evaporation method and EDC/NHS chemistry for antibody conjugation, resulting in CNP/αCD8 and C6NP/αCD8. The morphology and size of the nanoparticles were characterized by scanning electron microscopy and NanoPlus particle size analyzer. Drug loading and release profiles were determined using liquid chromatography-tandem mass spectrometry (LC-MS/MS) and centrifugation. The internalization of C6NP/αCD8 by CD8+ T cells were examined by flow cytometry and fluorescence microscopy. The effects of CNP/αCD8 on the proliferation, activation, cytotoxicity, and tumor killing ability of CD8+ T cells were examined by flow cytometry, ELISA, and lactate dehydrogenase (LDH) assay. Results: The CNP/αCD8 nanoparticles were spherical with an average diameter of about 150 nm, effectively encapsulating CPI-444 and conjugating CD8 antibodies, with a drug encapsulation efficiency and a CD8 antibody conjugation efficiency of approximately 60% and 53.4%, respectively. The nanoparticles exhibited good stability and were efficiently internalized by CD8+ T cells, inhibiting A2AR expression. Biological function assays showed that CNP/αCD8 enhanced CD8+ T cell proliferation, promoted T cell activation, cytokine secretion, granzyme B, and perforin production, and improved the tumorkilling ability of CD8+ T cells. Conclusion：CNP/αCD8 nanoparticles can significantly enhance the immune functions of CD8+ T cells, likely by inhibiting A2AR expression.
Objective：To prepare and characterize CD8 antibody-conjugated CPI-444 (C) -loaded nanoparticles (CNP/α CD8) and investigate their effects on CD8+ T cell activation, proliferation, and anti-tumor activity. Methods：Nanoparticles encapsulating the adenosine A2A receptor(A2AR) antagonist CPI-444 (C) or the fluorescent dye Coumarin-6 (C6) were prepared using the double emulsion solvent evaporation method and EDC/NHS chemistry for antibody conjugation, resulting in CNP/αCD8 and C6NP/αCD8. The morphology and size of the nanoparticles were characterized by scanning electron microscopy and NanoPlus particle size analyzer. Drug loading and release profiles were determined using liquid chromatography-tandem mass spectrometry (LC-MS/MS) and centrifugation. The internalization of C6NP/αCD8 by CD8+ T cells were examined by flow cytometry and fluorescence microscopy. The effects of CNP/αCD8 on the proliferation, activation, cytotoxicity, and tumor killing ability of CD8+ T cells were examined by flow cytometry, ELISA, and lactate dehydrogenase (LDH) assay. Results: The CNP/αCD8 nanoparticles were spherical with an average diameter of about 150 nm, effectively encapsulating CPI-444 and conjugating CD8 antibodies, with a drug encapsulation efficiency and a CD8 antibody conjugation efficiency of approximately 60% and 53.4%, respectively. The nanoparticles exhibited good stability and were efficiently internalized by CD8+ T cells, inhibiting A2AR expression. Biological function assays showed that CNP/αCD8 enhanced CD8+ T cell proliferation, promoted T cell activation, cytokine secretion, granzyme B, and perforin production, and improved the tumorkilling ability of CD8+ T cells. Conclusion：CNP/αCD8 nanoparticles can significantly enhance the immune functions of CD8+ T cells, likely by inhibiting A2AR expression.
2024, 31(8):786-795.
DOI: 10.3872/j.issn.1007-385X.2024.08.006
Abstract:
Objective: To investigate the impact of peroxisomal membrane protein 4 (PXMP4) on the migration, invasion, and epithelial-mesenchymal transition (EMT) of hepatocellular carcinoma (HCC) cells. Methods: A total of 38 pairs of HCC and paracancerous tissue samples were collected from the Department of Pathology, the Third Affiliated Hospital of Xinxiang Medical College from January 2018 to December 2022. Bioinformatics and immunohistochemistry were used to analyze PXMP4 expression in HCC tissues and its correlation with clinicopathological features of HCC patients. PXMP4 was silenced in HCCLM3 and MHCC97H cells and overexpressed in Huh7 and MHCC97L cells. The silencing/overexpression efficiency was verified by WB assay and qPCR. CCK-8 assay, wound healing assay, and Transwell invasion assay were used to detect the effects of PXMP4 interference or overexpression on the proliferation, migration, and invasion abilities of HCC cells. WB assay was used to detect the protein expression of N-cadherin, E-cadherin, vimentin, extracellular signal-regulated kinase (ERK), and p-ERK in HCC cells with PXMP4 interference/ overexpression or 0, 5, 10, and 20 μmol/L U0126 treatment. Results: Bioinformatics and immunohistochemistry showed that PXMP4 was highly expressed in HCC tissues (PPPPConclusion: PXMP4 is highly expressed in HCC tissues and is closely related to HCC cell differentiation. PXMP4 promotes EMT in HCC cells by activating the ERK1/2 signaling pathway.
Objective: To investigate the impact of peroxisomal membrane protein 4 (PXMP4) on the migration, invasion, and epithelial-mesenchymal transition (EMT) of hepatocellular carcinoma (HCC) cells. Methods: A total of 38 pairs of HCC and paracancerous tissue samples were collected from the Department of Pathology, the Third Affiliated Hospital of Xinxiang Medical College from January 2018 to December 2022. Bioinformatics and immunohistochemistry were used to analyze PXMP4 expression in HCC tissues and its correlation with clinicopathological features of HCC patients. PXMP4 was silenced in HCCLM3 and MHCC97H cells and overexpressed in Huh7 and MHCC97L cells. The silencing/overexpression efficiency was verified by WB assay and qPCR. CCK-8 assay, wound healing assay, and Transwell invasion assay were used to detect the effects of PXMP4 interference or overexpression on the proliferation, migration, and invasion abilities of HCC cells. WB assay was used to detect the protein expression of N-cadherin, E-cadherin, vimentin, extracellular signal-regulated kinase (ERK), and p-ERK in HCC cells with PXMP4 interference/ overexpression or 0, 5, 10, and 20 μmol/L U0126 treatment. Results: Bioinformatics and immunohistochemistry showed that PXMP4 was highly expressed in HCC tissues (PPPPConclusion: PXMP4 is highly expressed in HCC tissues and is closely related to HCC cell differentiation. PXMP4 promotes EMT in HCC cells by activating the ERK1/2 signaling pathway.
2024, 31(8):796-802.
DOI: 10.3872/j.issn.1007-385X.2024.08.007
Abstract:
Objective: To explore the effects of astilbin (AST) on the proliferation, migration and vasculogenic mimicry (VM) formation in breast cancer cells by regulating the hypoxia-inducible factor-1α (HIF-1α)/vascular endothelial growth factor (VEGF) axis. Methods: Breast cancer cells (MCF-7 and MDA-MB-231) were treated with AST at different concentrations (0, 5, 25, 50, 100, 150, 200, 300 μmol/L), and the cell viability was detected using the CKK-8 assay. The MCF-7 and MDA-MB-231 cells were divided into control group, low-dose AST (AST-L), medium-dose AST (AST-M), high-dose AST (AST-H), and AST-H+DMOG (HIF-1α/VEGF pathway activator) groups. The effect of AST on cell proliferation was detected by EdU assay, the influence on apoptosis was detected using flow cytometry, the migration and invasion abilities of cells were examined using Transwell chamber assay, and the VM formation was analyzed using Matrigel tube formation assay. The expression of HIF-1α, VEGF, VE-cadherin, E-cadherin, N-cadherin and MMP-2 was detected by WB assay. Results: Compared with 0 μmol/L AST, the viability of cells treated with 5, 25, 50, 100, 150, 200, and 300 μmol/L AST decreased obviously, which was in a dose-dependent manner (P protein expression of HIF-1α, VEGF, VE-cadherin, N-cadherin, and MMP-2, while the apoptosis rate and E-cadherin protein expression obviously increased (all PPConclusion: AST can inhibit the proliferation, migration, invasion, and VM formation of breast cancer cells and promote apoptosis, which may be related to the inhibition of the HIF-1α/VEGF signaling pathway.
Objective: To explore the effects of astilbin (AST) on the proliferation, migration and vasculogenic mimicry (VM) formation in breast cancer cells by regulating the hypoxia-inducible factor-1α (HIF-1α)/vascular endothelial growth factor (VEGF) axis. Methods: Breast cancer cells (MCF-7 and MDA-MB-231) were treated with AST at different concentrations (0, 5, 25, 50, 100, 150, 200, 300 μmol/L), and the cell viability was detected using the CKK-8 assay. The MCF-7 and MDA-MB-231 cells were divided into control group, low-dose AST (AST-L), medium-dose AST (AST-M), high-dose AST (AST-H), and AST-H+DMOG (HIF-1α/VEGF pathway activator) groups. The effect of AST on cell proliferation was detected by EdU assay, the influence on apoptosis was detected using flow cytometry, the migration and invasion abilities of cells were examined using Transwell chamber assay, and the VM formation was analyzed using Matrigel tube formation assay. The expression of HIF-1α, VEGF, VE-cadherin, E-cadherin, N-cadherin and MMP-2 was detected by WB assay. Results: Compared with 0 μmol/L AST, the viability of cells treated with 5, 25, 50, 100, 150, 200, and 300 μmol/L AST decreased obviously, which was in a dose-dependent manner (P protein expression of HIF-1α, VEGF, VE-cadherin, N-cadherin, and MMP-2, while the apoptosis rate and E-cadherin protein expression obviously increased (all PPConclusion: AST can inhibit the proliferation, migration, invasion, and VM formation of breast cancer cells and promote apoptosis, which may be related to the inhibition of the HIF-1α/VEGF signaling pathway.
2024, 31(8):803-814.
DOI: 10.3872/j.issn.1007-385X.2024.08.008
Abstract:
Objective: To explore angiogenesis-related immune genes (ARIGs) in ovarian cancer using the bioinformatics method, investigate their relationship with ovarian cancer prognosis, and elucidate potential differences in tumor microenvironment and immunotherapy response among patients with different prognosis, so as to provide new therapeutic targets for ovarian cancer patients. Methods: Transcriptome and survival data for ovarian cancer were downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases, respectively. The differentially expressed genes were analyzed using R software, and the correlation between ARIGs and immune-related genes was identified by the Pearson correlation coefficient, leading to the selection of differentially expressed ARIGs. A prognostic model was constructed by LASSO regression analysis, and the clinical features and risk scores were evaluated through COX analysis. Patients were divided into a high-risk group and a low-risk group. Single sample gene set enrichment analysis (ssGSEA) and tumor immune dysfunction and exclusion (TIDE) were used to analyze the correlation between the prognostic risk model and immune invasion and immunotherapy response. Finally, 85 pairs of tumor tissues and fallopian tube tissues of ovarian cancer patients who were surgically treated in the Fourth Hospital of Hebei Medical University from May 2015 to May 2016 were collected. The expression of five differentially expressed ARIGs in ovarian cancer tissues was verified by qPCR and WB, and their relationship with clinicopathological features of ovarian cancer patients was analyzed. The biological function of these ARIGs in ovarian cancer cells was preliminarily explored. Results: A total of 142 differentially expressed ARIGs were screened by bioinformatics analysis. Lasso and Cox regression analyses identified five genes (PTGER3, SCTR, IGHG1, HSPA8, IGF2) as prognostic genes, and a prognostic risk model was constructed. Patients in the high-risk group had a worse prognosis. Moreover, significant differences were observed in immune cell infiltration and immunotherapy response between patients with different risk scores. Finally, qPCR and WB verified that these 5 genes were highly expressed in ovarian cancer tissues, with HSPA8 being the most highly expressed. High HSPA8 expression was positively correlated with advanced FIGO stage, poor histological grade, lymph node metastasis and peritoneal metastasis in ovarian cancer patients (all P<0.001). Cell function experiments confirmed that HSPA8 could promote the proliferation, migration, and invasion of ovarian cancer cells(P<0.01). Conclusion: The five differentially expressed ARIGs can effectively predict the prognosis of ovarian cancer patients and are related to immune cell infiltration and immunotherapy efficacy. Preliminary evidence suggests that these genes play a pro-carcinogenic role in ovary cancer.
Objective: To explore angiogenesis-related immune genes (ARIGs) in ovarian cancer using the bioinformatics method, investigate their relationship with ovarian cancer prognosis, and elucidate potential differences in tumor microenvironment and immunotherapy response among patients with different prognosis, so as to provide new therapeutic targets for ovarian cancer patients. Methods: Transcriptome and survival data for ovarian cancer were downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases, respectively. The differentially expressed genes were analyzed using R software, and the correlation between ARIGs and immune-related genes was identified by the Pearson correlation coefficient, leading to the selection of differentially expressed ARIGs. A prognostic model was constructed by LASSO regression analysis, and the clinical features and risk scores were evaluated through COX analysis. Patients were divided into a high-risk group and a low-risk group. Single sample gene set enrichment analysis (ssGSEA) and tumor immune dysfunction and exclusion (TIDE) were used to analyze the correlation between the prognostic risk model and immune invasion and immunotherapy response. Finally, 85 pairs of tumor tissues and fallopian tube tissues of ovarian cancer patients who were surgically treated in the Fourth Hospital of Hebei Medical University from May 2015 to May 2016 were collected. The expression of five differentially expressed ARIGs in ovarian cancer tissues was verified by qPCR and WB, and their relationship with clinicopathological features of ovarian cancer patients was analyzed. The biological function of these ARIGs in ovarian cancer cells was preliminarily explored. Results: A total of 142 differentially expressed ARIGs were screened by bioinformatics analysis. Lasso and Cox regression analyses identified five genes (PTGER3, SCTR, IGHG1, HSPA8, IGF2) as prognostic genes, and a prognostic risk model was constructed. Patients in the high-risk group had a worse prognosis. Moreover, significant differences were observed in immune cell infiltration and immunotherapy response between patients with different risk scores. Finally, qPCR and WB verified that these 5 genes were highly expressed in ovarian cancer tissues, with HSPA8 being the most highly expressed. High HSPA8 expression was positively correlated with advanced FIGO stage, poor histological grade, lymph node metastasis and peritoneal metastasis in ovarian cancer patients (all P<0.001). Cell function experiments confirmed that HSPA8 could promote the proliferation, migration, and invasion of ovarian cancer cells(P<0.01). Conclusion: The five differentially expressed ARIGs can effectively predict the prognosis of ovarian cancer patients and are related to immune cell infiltration and immunotherapy efficacy. Preliminary evidence suggests that these genes play a pro-carcinogenic role in ovary cancer.
9 Clinical efficacy of DC combined with CIK in treating locally advanced or advanced pancreatic cancer
SHU Yan
,
HE Yuan
,
ZHANG Yan
,
SHI Ruifang
,
WANG Jing
,
WANG Ruixuan
,
WANG Zhongda
,
ZHU Yue
,
WANG Jing
,
YAO Lu
,
FU Gongbo
,
LEI Zengjie
,
JIA Shaochang
,
JIANG Longwei
,
ZHOU Xiaoxian
2024, 31(8):815-820.
DOI: 10.3872/j.issn.1007-385X.2024.08.009
Abstract:
Objective: To evaluate the clinical efficacy of dendritic cells (DC) combined with cytokine-induced killer cells (CIK) in the treatment of locally advanced or advanced pancreatic cancer. Methods: A retrospective analysis was conducted on the clinical data of 156 patients with locally advanced or advanced pancreatic cancer who underwent autologous DC combined with CIK treatment in the Oncology Department of the Eastern Theater Command General Hospital from November 2011 to December 2023. Changes in serum tumor markers, lymphocyte subsets, cytokine levels, adverse reactions, short-term efficacy, and long-term efficacy before and after treatment were statistically analyzed. Results: Among the 156 pancreatic cancer patients, 92 underwent imaging examinations before and after treatment, with results showing no CR (complete remission), no PR (partial remission), 42 cases of SD (stable disease), and 50 cases of PD (progressive disease). The objective remission rate (ORR) was 0%, and the disease control rate (DCR) was 45.65%. There was no significant difference in peripheral blood CA199 levels before and after treatment, but 19 patients showed a reduction of more than 20% after treatment. No statistical differences were observed in CD3+ , CD4+ , CD8+ , CD56+ , CD25+ peripheral blood lymphocyte subsets levels and CD4+ /CD8+ T cell ratio before and after treatment (all P>0.05). However, the average levels of IL-2 and IFN-γ in peripheral blood of patients were significantly increased after treatment (all PP>0.05). The median overall survival (mOS) of the 156 patients was 8.53 months, with 1-year, 2-year, and 3-year cumulative survival rates of 39%, 15%, and 15%, respectively. No 5-year survival data were available for follow-up. No severe adverse reactions occurred during the treatment. Conclusion: DC-CIK therapy can induce anti-tumor immune responses in patients with locally advanced and advanced pancreatic cancer, achieving certain objective efficacy and potentially prolonging patient survival.
Objective: To evaluate the clinical efficacy of dendritic cells (DC) combined with cytokine-induced killer cells (CIK) in the treatment of locally advanced or advanced pancreatic cancer. Methods: A retrospective analysis was conducted on the clinical data of 156 patients with locally advanced or advanced pancreatic cancer who underwent autologous DC combined with CIK treatment in the Oncology Department of the Eastern Theater Command General Hospital from November 2011 to December 2023. Changes in serum tumor markers, lymphocyte subsets, cytokine levels, adverse reactions, short-term efficacy, and long-term efficacy before and after treatment were statistically analyzed. Results: Among the 156 pancreatic cancer patients, 92 underwent imaging examinations before and after treatment, with results showing no CR (complete remission), no PR (partial remission), 42 cases of SD (stable disease), and 50 cases of PD (progressive disease). The objective remission rate (ORR) was 0%, and the disease control rate (DCR) was 45.65%. There was no significant difference in peripheral blood CA199 levels before and after treatment, but 19 patients showed a reduction of more than 20% after treatment. No statistical differences were observed in CD3+ , CD4+ , CD8+ , CD56+ , CD25+ peripheral blood lymphocyte subsets levels and CD4+ /CD8+ T cell ratio before and after treatment (all P>0.05). However, the average levels of IL-2 and IFN-γ in peripheral blood of patients were significantly increased after treatment (all PP>0.05). The median overall survival (mOS) of the 156 patients was 8.53 months, with 1-year, 2-year, and 3-year cumulative survival rates of 39%, 15%, and 15%, respectively. No 5-year survival data were available for follow-up. No severe adverse reactions occurred during the treatment. Conclusion: DC-CIK therapy can induce anti-tumor immune responses in patients with locally advanced and advanced pancreatic cancer, achieving certain objective efficacy and potentially prolonging patient survival.
2024, 31(8):821-826.
DOI: 10.3872/j.issn.1007-385X.2024.08.010
Abstract:
T细胞受体（TCR）序列可作为分辨T细胞特异性的唯一标签，因其多样性的特征，在特定时间内个体循环系统中所有 TCR构成的TCR组库可以反映个体的抗肿瘤免疫状态。单细胞TCR测序技术能够在单细胞水平上检测编码TCR双链的基因序 列和表达量等信息，包括获得TCR的α链和β链的配对信息，从而在细胞水平上更为准确地探索TCR组库的异质性，还可结合其 他技术将TCR序列与基因组、转录组、蛋白质组等多组学信息成套配对，精准展现细胞水平上的多角度信息。因该技术具有高通 量、高分辨率的优势而被广泛应用于肿瘤免疫治疗相关研究，为探索TME中T细胞功能、发展T细胞受体工程化T细胞（TCR-T） 疗法、预测免疫检查点抑制剂（ICI）疗效等提供重要依据，成为重要的筛选工具，期待该技术的发展使更多肿瘤患者受益。
T细胞受体（TCR）序列可作为分辨T细胞特异性的唯一标签，因其多样性的特征，在特定时间内个体循环系统中所有 TCR构成的TCR组库可以反映个体的抗肿瘤免疫状态。单细胞TCR测序技术能够在单细胞水平上检测编码TCR双链的基因序 列和表达量等信息，包括获得TCR的α链和β链的配对信息，从而在细胞水平上更为准确地探索TCR组库的异质性，还可结合其 他技术将TCR序列与基因组、转录组、蛋白质组等多组学信息成套配对，精准展现细胞水平上的多角度信息。因该技术具有高通 量、高分辨率的优势而被广泛应用于肿瘤免疫治疗相关研究，为探索TME中T细胞功能、发展T细胞受体工程化T细胞（TCR-T） 疗法、预测免疫检查点抑制剂（ICI）疗效等提供重要依据，成为重要的筛选工具，期待该技术的发展使更多肿瘤患者受益。
2024, 31(8):827-832.
DOI: 10.3872/j.issn.1007-385X.2024.08.011
Abstract:
白细胞介素-24（IL-24）是一种具有显著抗肿瘤活性的细胞因子，可诱导肿瘤细胞凋亡、抑制肿瘤细胞增殖和减少肿瘤 血管生成，其通过p38 MAPK、PI3K和JAK/STAT等多种信号通路调节细胞周期、细胞代谢等关键过程，并有效抑制肿瘤发生、发 展。IL-24独特的抗肿瘤机制和临床应用潜力使其受到广泛关注。然而，IL-24的肿瘤靶向性、毒副作用、递送效率和剂量控制等 问题限制了其在临床中的广泛应用。为提高IL-24的治疗效率和靶向性，研究人员通过基因工程改造和溶瘤病毒载体递送等方 式优化和增强其治疗效果。此外，IL-24与放化疗等抗肿瘤手段联合可显著提高治疗效果并减少不良反应，提供了更为安全有效 的癌症治疗方案。
白细胞介素-24（IL-24）是一种具有显著抗肿瘤活性的细胞因子，可诱导肿瘤细胞凋亡、抑制肿瘤细胞增殖和减少肿瘤 血管生成，其通过p38 MAPK、PI3K和JAK/STAT等多种信号通路调节细胞周期、细胞代谢等关键过程，并有效抑制肿瘤发生、发 展。IL-24独特的抗肿瘤机制和临床应用潜力使其受到广泛关注。然而，IL-24的肿瘤靶向性、毒副作用、递送效率和剂量控制等 问题限制了其在临床中的广泛应用。为提高IL-24的治疗效率和靶向性，研究人员通过基因工程改造和溶瘤病毒载体递送等方 式优化和增强其治疗效果。此外，IL-24与放化疗等抗肿瘤手段联合可显著提高治疗效果并减少不良反应，提供了更为安全有效 的癌症治疗方案。
2024, 31(8):833-837.
DOI: 10.3872/j.issn.1007-385X.2024.08.012
Abstract:
胃癌的发病率及死亡率均较高，其治疗方式一般以手术为主，并辅以放化疗。目前，联合化疗仍是治疗胃癌患者的重 要方式，应用白蛋白纳米技术制备的白蛋白结合型紫杉醇联合替吉奥在提高胃癌患者疾病缓解率和延长生存期等方面展现出优 势。该联合治疗方案具有安全性较高，能有效改善患者的生活质量，在胃癌患者的治疗中显示出良好的临床应用前景。但目前 相关研究还相对有限，仍需进一步的临床试验数据验证其疗效和安全性。笔者阐述了白蛋白结合型紫杉醇联合替吉奥在胃癌治 疗中的应用现状、临床研究及安全性分析，为胃癌的临床治疗提供了一定的指导意义。
胃癌的发病率及死亡率均较高，其治疗方式一般以手术为主，并辅以放化疗。目前，联合化疗仍是治疗胃癌患者的重 要方式，应用白蛋白纳米技术制备的白蛋白结合型紫杉醇联合替吉奥在提高胃癌患者疾病缓解率和延长生存期等方面展现出优 势。该联合治疗方案具有安全性较高，能有效改善患者的生活质量，在胃癌患者的治疗中显示出良好的临床应用前景。但目前 相关研究还相对有限，仍需进一步的临床试验数据验证其疗效和安全性。笔者阐述了白蛋白结合型紫杉醇联合替吉奥在胃癌治 疗中的应用现状、临床研究及安全性分析，为胃癌的临床治疗提供了一定的指导意义。
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- 《中国肿瘤生物治疗杂志》
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.