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2025,32(1):1-8, DOI: 10.3872/j.issn.1007-385X.2025.01.001
Abstract:
[Abstract] Chimeric antigen receptor natural killer (CAR-NK) cell therapy, as an emerging cellular immunotherapy strategy, has demonstrated a broader clinical application potential compared to CAR-T cell therapy due to its high safety profile and the unique advantages of 'off-the-shelf ' preparation. This article thoroughly discusses the antitumor mechanisms of CAR-NK cells, elucidating their targeted recognition mechanism, inherent cytotoxic activity, and the latest advancements in optimizing specific receptors to enhance their adaptability within the tumor microenvironment. Additionally, it provides an in-depth analysis of the advantages and challenges of various sources for CAR-NK cells, including peripheral blood, umbilical cord blood, induced pluripotent stem cells (iPSCs), and NK-92 cells, while summarizing their major challenges in the tumor immune microenvironment, such as insufficient persistence, immune suppression, and antigen heterogeneity. Finally, this article presents the therapeutic potential, limitations, and future perspectives of CAR-NK therapy in treating solid tumors, with a focus on its ongoing development and clinical translation.
[Abstract] Chimeric antigen receptor natural killer (CAR-NK) cell therapy, as an emerging cellular immunotherapy strategy, has demonstrated a broader clinical application potential compared to CAR-T cell therapy due to its high safety profile and the unique advantages of 'off-the-shelf ' preparation. This article thoroughly discusses the antitumor mechanisms of CAR-NK cells, elucidating their targeted recognition mechanism, inherent cytotoxic activity, and the latest advancements in optimizing specific receptors to enhance their adaptability within the tumor microenvironment. Additionally, it provides an in-depth analysis of the advantages and challenges of various sources for CAR-NK cells, including peripheral blood, umbilical cord blood, induced pluripotent stem cells (iPSCs), and NK-92 cells, while summarizing their major challenges in the tumor immune microenvironment, such as insufficient persistence, immune suppression, and antigen heterogeneity. Finally, this article presents the therapeutic potential, limitations, and future perspectives of CAR-NK therapy in treating solid tumors, with a focus on its ongoing development and clinical translation.
2025,32(1):9-13, DOI: 10.3872/j.issn.1007-385X.2025.01.002
Abstract:
[Abstract] Since 2017, twelve chimeric antigen receptor gene-modified T lymphocyte (CAR-T cell) products have been approved for the treatment of hematological malignancies, including relapsed/refractory acute B lymphoblastic leukemia (B-ALL), specific subtypes of B cell lymphoma, and multiple myeloma. However, CAR-T cell therapy faces numerous challenges in its clinical application, such as resistance, lengthy production cycles, high individuation and costs in hematological tumors, and tumor heterogeneity/antigen escape, insufficient infiltration capability, immunosuppressive microenvironments, and poor therapeutic response in solid tumors. With the in-depth exploration of tumor immunology and the development of genetic engineering technology, various new strategies have been attempted to enhance the efficacy and generalizability of CAR-T cell therapy. This paper presents a commentary on CAR-T cell therapy, with a focus on key clinical issues and corresponding countermeasures, providing valuable insights for future basic research and clinical transformation of CAR-T cell therapy.
[Abstract] Since 2017, twelve chimeric antigen receptor gene-modified T lymphocyte (CAR-T cell) products have been approved for the treatment of hematological malignancies, including relapsed/refractory acute B lymphoblastic leukemia (B-ALL), specific subtypes of B cell lymphoma, and multiple myeloma. However, CAR-T cell therapy faces numerous challenges in its clinical application, such as resistance, lengthy production cycles, high individuation and costs in hematological tumors, and tumor heterogeneity/antigen escape, insufficient infiltration capability, immunosuppressive microenvironments, and poor therapeutic response in solid tumors. With the in-depth exploration of tumor immunology and the development of genetic engineering technology, various new strategies have been attempted to enhance the efficacy and generalizability of CAR-T cell therapy. This paper presents a commentary on CAR-T cell therapy, with a focus on key clinical issues and corresponding countermeasures, providing valuable insights for future basic research and clinical transformation of CAR-T cell therapy.
2025,32(1):14-23, DOI: 10.3872/j.issn.1007-385X.2025.01.003
Abstract:
[Abstract] Small cell lung cancer (SCLC) is the most aggressive type of lung cancer, accounting for approximately 13% to 15% of all lung cancer cases. Although SCLC patients are highly responsive to chemotherapy and radiotherapy at their initial treatment, they are prone to relapse, leading to a low survival rate. Since 2018, with the success of the IMpower133 and CASPIAN trials, SCLC has entered the era of immunotherapy. Chemotherapy combined with immune checkpoint inhibitors (ICIs) has become the standard firstline treatment for extensive-stage SCLC. Meanwhile, immunotherapy has also achieved preliminary success in limited-stage SCLC. Despite some progress in SCLC immunotherapy, the overall survival benefit remains limited. There is a lack of effective predictive biomarkers, and treatment options for relapsed/refractory SCLC are scarce, posing significant challenges to the future of immunotherapy in SCLC. In this article, the latest clinical research on SCLC immunotherapy, both domestically and internationally, is reviewed, different types of immunotherapeutic agents, biomarkers, and novel immunotherapy targets are analyzed, and the combination strategies and future prospects of SCLC immunotherapy are discussed.
[Abstract] Small cell lung cancer (SCLC) is the most aggressive type of lung cancer, accounting for approximately 13% to 15% of all lung cancer cases. Although SCLC patients are highly responsive to chemotherapy and radiotherapy at their initial treatment, they are prone to relapse, leading to a low survival rate. Since 2018, with the success of the IMpower133 and CASPIAN trials, SCLC has entered the era of immunotherapy. Chemotherapy combined with immune checkpoint inhibitors (ICIs) has become the standard firstline treatment for extensive-stage SCLC. Meanwhile, immunotherapy has also achieved preliminary success in limited-stage SCLC. Despite some progress in SCLC immunotherapy, the overall survival benefit remains limited. There is a lack of effective predictive biomarkers, and treatment options for relapsed/refractory SCLC are scarce, posing significant challenges to the future of immunotherapy in SCLC. In this article, the latest clinical research on SCLC immunotherapy, both domestically and internationally, is reviewed, different types of immunotherapeutic agents, biomarkers, and novel immunotherapy targets are analyzed, and the combination strategies and future prospects of SCLC immunotherapy are discussed.
2025,32(1):24-29, DOI: 10.3872/j.issn.1007-385X.2025.01.004
Abstract:
[Abstract] Immune cell-mediated delivery system employs immune cells as carriers to deliver therapeutic drugs to specific lesion sites by leveraging the innate chemotaxis of these cells. Due to its excellent biocompatibility, low immunogenicity, tissue-specific homing, and ability to cross biological barriers, this approach has emerged as an important strategy for drug delivery and disease treatment. This article systematically discusses the drug delivery strategies of immune cells, the biological characteristics, advantages, and disadvantages of using monocytes, neutrophils, mesenchymal stem cells, and dendritic cells as carrier cells, as well as the latest research progresses on their application in tumor treatment. This review provides valuable insights for further studies on immune cell-mediated drug delivery systems and their clinical transformation.
[Abstract] Immune cell-mediated delivery system employs immune cells as carriers to deliver therapeutic drugs to specific lesion sites by leveraging the innate chemotaxis of these cells. Due to its excellent biocompatibility, low immunogenicity, tissue-specific homing, and ability to cross biological barriers, this approach has emerged as an important strategy for drug delivery and disease treatment. This article systematically discusses the drug delivery strategies of immune cells, the biological characteristics, advantages, and disadvantages of using monocytes, neutrophils, mesenchymal stem cells, and dendritic cells as carrier cells, as well as the latest research progresses on their application in tumor treatment. This review provides valuable insights for further studies on immune cell-mediated drug delivery systems and their clinical transformation.
2025,32(1):30-37, DOI: 10.3872/j.issn.1007-385X.2025.01.005
Abstract:
[Abstract] Thyroid cancer is the most prevalent malignant tumor of the endocrine system, and its incidence has shown a significant upward trend in recent years. Acetylation, an important post-translational protein modification, is involved in regulating gene transcription, cell cycle progression, and invasion ability in various types of thyroid cancers. Additionally, histone deacetylase (HDAC) inhibitors have shown potential in the treatment of thyroid cancer. This article systematically reviews the biological functions and regulatory mechanisms of acetylation in the development and progression of thyroid cancer based on recent literature. Furthermore, it discusses the clinical application prospects of HDAC inhibitors, providing a solid theoretical basis and feasible therapeutic strategies for targeted therapy of thyroid cancer.
[Abstract] Thyroid cancer is the most prevalent malignant tumor of the endocrine system, and its incidence has shown a significant upward trend in recent years. Acetylation, an important post-translational protein modification, is involved in regulating gene transcription, cell cycle progression, and invasion ability in various types of thyroid cancers. Additionally, histone deacetylase (HDAC) inhibitors have shown potential in the treatment of thyroid cancer. This article systematically reviews the biological functions and regulatory mechanisms of acetylation in the development and progression of thyroid cancer based on recent literature. Furthermore, it discusses the clinical application prospects of HDAC inhibitors, providing a solid theoretical basis and feasible therapeutic strategies for targeted therapy of thyroid cancer.
2025,32(1):38-47, DOI: 10.3872/j.issn.1007-385X.2025.01.006
Abstract:
[Abstract] Objective: To investigate the effects of KH-type splicing regulatory protein (KHSRP) targeting and regulating JAK1/ STAT3 signaling axis on the proliferation, migration and invasion of the adenocarcinoma of esophagogastric junction (AEG) cells, as well as the growth of transplanted tumors and lung metastasis. Methods: A total of 64 pairs of AEG tissue and adjacent normal tissue samples, along with clinical data from patients diagnosed at Huaihe Hospital from January 2017 to December 2018 were collected. The expression level of KHSRP in AEG tissues and adjacent normal tissues was observed using immunohistochemical staining. The differential expression of KHSRP in AEG cells (OE-19, TE-7, BIC-1, FLO-1, SK-GT-4, BE-3) and normal esophageal epithelial cells (Het-1A) was detected by qPCR. Lentiviral vectors were used to knockdown and overexpress KHSRP in OE-19, TE-7, FLO-1, and SK-GT-4 cells. The experiment was divided into the following groups:sh-NC group, sh-KHSRP group, Vector group, and KHSRP overexpression group (KHSRP group). The knockdown or overexpression efficiency was detected by qPCR, and the effects of KHSRP knockdown or overexpression on AEG cell proliferation, migration and invasion were evaluated using CCK-8 and Transwell assays, respectively. A mouse xenograft and lung metastasis model was established to observe the effects of KHSRP on tumor growth and metastasis in vivo. The targeted regulation of JAK/STAT signaling pathway by KHSRP was verified by Western blotting. A rescue experiment was conducted to verify whether KHSRP promoted malignant progression of AEG cells through the JAK1/STAT3 signaling pathway. Results: Compared with adjacent normal tissues, the expression level of KHSRP in AEG tissues was significantly increased (P < 0.05 or P < 0.01). Cell function experiments showed that KHSRP overexpression significantly promoted AEG cell proliferation, migration, and invasion in vitro (P < 0.05 or P < 0.01). In vivo animal experiments showed that KHSRP promoted AEG cell xenograft tumor growth and lung metastasis in nude mice (P < 0.05 or P < 0.01). After KHSRP knockdown, the phosphorylation levels of JAK1 and STAT3 in the JAK/STAT signaling pathway were significantly reduced, while overexpression of KHSRP led to the opposite results (P < 0.05 or P < 0.01). Rescue experiment showed that KHSRP could reverse the inhibition of cell proliferation, migration, and invasion caused by JAK1/STAT3 knockdown (P < 0.05 or P < 0.01). Conclusion: KHSRP regulates the malignant progression of AEG cells by activating JAK1/STAT3 signaling axis. KHSRP may become a potential target for the clinical treatment of AEG.
[Abstract] Objective: To investigate the effects of KH-type splicing regulatory protein (KHSRP) targeting and regulating JAK1/ STAT3 signaling axis on the proliferation, migration and invasion of the adenocarcinoma of esophagogastric junction (AEG) cells, as well as the growth of transplanted tumors and lung metastasis. Methods: A total of 64 pairs of AEG tissue and adjacent normal tissue samples, along with clinical data from patients diagnosed at Huaihe Hospital from January 2017 to December 2018 were collected. The expression level of KHSRP in AEG tissues and adjacent normal tissues was observed using immunohistochemical staining. The differential expression of KHSRP in AEG cells (OE-19, TE-7, BIC-1, FLO-1, SK-GT-4, BE-3) and normal esophageal epithelial cells (Het-1A) was detected by qPCR. Lentiviral vectors were used to knockdown and overexpress KHSRP in OE-19, TE-7, FLO-1, and SK-GT-4 cells. The experiment was divided into the following groups:sh-NC group, sh-KHSRP group, Vector group, and KHSRP overexpression group (KHSRP group). The knockdown or overexpression efficiency was detected by qPCR, and the effects of KHSRP knockdown or overexpression on AEG cell proliferation, migration and invasion were evaluated using CCK-8 and Transwell assays, respectively. A mouse xenograft and lung metastasis model was established to observe the effects of KHSRP on tumor growth and metastasis in vivo. The targeted regulation of JAK/STAT signaling pathway by KHSRP was verified by Western blotting. A rescue experiment was conducted to verify whether KHSRP promoted malignant progression of AEG cells through the JAK1/STAT3 signaling pathway. Results: Compared with adjacent normal tissues, the expression level of KHSRP in AEG tissues was significantly increased (P < 0.05 or P < 0.01). Cell function experiments showed that KHSRP overexpression significantly promoted AEG cell proliferation, migration, and invasion in vitro (P < 0.05 or P < 0.01). In vivo animal experiments showed that KHSRP promoted AEG cell xenograft tumor growth and lung metastasis in nude mice (P < 0.05 or P < 0.01). After KHSRP knockdown, the phosphorylation levels of JAK1 and STAT3 in the JAK/STAT signaling pathway were significantly reduced, while overexpression of KHSRP led to the opposite results (P < 0.05 or P < 0.01). Rescue experiment showed that KHSRP could reverse the inhibition of cell proliferation, migration, and invasion caused by JAK1/STAT3 knockdown (P < 0.05 or P < 0.01). Conclusion: KHSRP regulates the malignant progression of AEG cells by activating JAK1/STAT3 signaling axis. KHSRP may become a potential target for the clinical treatment of AEG.
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2012,19(5):550-555, DOI: 10.3872/j.issn.1007-385X.2012.5.018
Abstract:
骨髓增生异常综合征（myelodysplastic syndrome，MDS）的发病机制涉及多阶段、多因素，基因改变与表观遗传修饰可能共同参与了这一过程。DNA甲基化是表观遗传学中一种最为重要的修饰，MDS患者常表现为总体DNA高甲基化。使用DNA甲基转移酶（DNA methyltransferase，DNMT）抑制剂降低总体甲基化水平，在MDS患者中取得了富有成效的临床反应及血液学改善。DNMT抑制剂可分为两类：5-氮杂胞苷(5-azacytidine, 5-Aza-CdR)、地西他滨（5-Aza-2-deoxycytidine, decitabine）等核苷和核苷衍生物类抑制剂，它们可提高MDS患者的临床完全反应率、部分反应率及血液学改善，但缓解率、疗效尚不够令人满意；肼苯哒嗪等非核苷类抑制剂。非核苷类抑制剂与丙戊酸镁联合应用治疗MDS获得成功，为MDS去甲基化治疗药物的研究开启了一种新思路。
骨髓增生异常综合征（myelodysplastic syndrome，MDS）的发病机制涉及多阶段、多因素，基因改变与表观遗传修饰可能共同参与了这一过程。DNA甲基化是表观遗传学中一种最为重要的修饰，MDS患者常表现为总体DNA高甲基化。使用DNA甲基转移酶（DNA methyltransferase，DNMT）抑制剂降低总体甲基化水平，在MDS患者中取得了富有成效的临床反应及血液学改善。DNMT抑制剂可分为两类：5-氮杂胞苷(5-azacytidine, 5-Aza-CdR)、地西他滨（5-Aza-2-deoxycytidine, decitabine）等核苷和核苷衍生物类抑制剂，它们可提高MDS患者的临床完全反应率、部分反应率及血液学改善，但缓解率、疗效尚不够令人满意；肼苯哒嗪等非核苷类抑制剂。非核苷类抑制剂与丙戊酸镁联合应用治疗MDS获得成功，为MDS去甲基化治疗药物的研究开启了一种新思路。
2016,23(2):149-160, DOI: 10.3872/j.issn.1007-385X.2016.02.001
Abstract:
Immunocyte therapy for tumor has drawn a great attention in recent years due to its significant effect. Immunocytes, including T cell, NK cell and DCs, play a key role in immune responses of anti-tumors and immunotherapy of tumors. Among them, the techique of chimeric antigen receptor (CAR) modified-T cell (CAR-T) and inhibitor therapy which reverses CTLA-4 and PD-1/PD-L1 and so on immune checkpoints of tumor immune suppressive function have respectively achieved exciting results in therapies of blood tumors, melanoma and other solid tumors. How to further improve the efficacy, to increase adaptive tumor diseases and to control immune related adverse reactions of the therapy could become the focus of future research. NK cell will also take advantages of CAR technique and inhibitors of immune checkpoints to further strengthen its role in the tumor therapy. How to enhance the curative effect of DCs as the first therapeutic tumor vaccine approved by FDA based on its confirmed safe and non-toxic side effects could become a hot point. In this paper, problems that need to be solved in the field were further analyzed and prospected with combination of recent advances in the immunocyte-therapy for tumor.
Immunocyte therapy for tumor has drawn a great attention in recent years due to its significant effect. Immunocytes, including T cell, NK cell and DCs, play a key role in immune responses of anti-tumors and immunotherapy of tumors. Among them, the techique of chimeric antigen receptor (CAR) modified-T cell (CAR-T) and inhibitor therapy which reverses CTLA-4 and PD-1/PD-L1 and so on immune checkpoints of tumor immune suppressive function have respectively achieved exciting results in therapies of blood tumors, melanoma and other solid tumors. How to further improve the efficacy, to increase adaptive tumor diseases and to control immune related adverse reactions of the therapy could become the focus of future research. NK cell will also take advantages of CAR technique and inhibitors of immune checkpoints to further strengthen its role in the tumor therapy. How to enhance the curative effect of DCs as the first therapeutic tumor vaccine approved by FDA based on its confirmed safe and non-toxic side effects could become a hot point. In this paper, problems that need to be solved in the field were further analyzed and prospected with combination of recent advances in the immunocyte-therapy for tumor.
2018,25(1):23-27, DOI: 10.3872/j.issn.1007-385X.2018.01.004
Abstract:
Prostate cancer has become one of the most common malignant diseases in Chinese male. Hormonal therapy is an important and effective way to treat prostate cancer (especially advanced prostate cancer); however, some disputes merged from the clinical application are still to be solved. It seems crucial to unify the understanding and implement overall management to get satisfied effect in hormonal therapy of prostate cancer. According to guidelines and clinical trials in both domestic and overseas, we make a summary of series of problems that appeared in hormonal therapy of prostate cancer, such as treatment opportunity, treatment strategy, patients choose, prognosis and follow-up etc.
Prostate cancer has become one of the most common malignant diseases in Chinese male. Hormonal therapy is an important and effective way to treat prostate cancer (especially advanced prostate cancer); however, some disputes merged from the clinical application are still to be solved. It seems crucial to unify the understanding and implement overall management to get satisfied effect in hormonal therapy of prostate cancer. According to guidelines and clinical trials in both domestic and overseas, we make a summary of series of problems that appeared in hormonal therapy of prostate cancer, such as treatment opportunity, treatment strategy, patients choose, prognosis and follow-up etc.
2010,17(1):57-61, DOI: 10.3872/j.issn.1007-385X.2010.1.011
Abstract:
Objective: To prepare poly DL lactide poly (PELA) microspheres encapsulating recombinant tissue inhibitors of metalloproteinase 1 (TIMP 1) adenovirus, and to investigate their effects on the proliferation of hepatocellular carcinoma HepG2 cells. Methods:The microsphere was constructed by encapsulating recombinant adenovirus containing TIMP 1 in biodegradable PELA. The diameter of the microsphere, quantity of virus encapsulated, loading rate, and releasing kinetics were measured. HepG2 cells were infected with the microspheres; the infection efficiency was examined by fluorescent microscope; and the ultrastructure was observed by TEM. The expression of TIMP 1 mRNA in HepG2 cells was examined by semi quantitative RT PCR, and the proliferation of HepG2 cells was detected by MTT assay. Results:The microsphere encapsulating recombinant TIMP 1 adenovirus was successfully constructed, with its diameter, entrapment efficiency, and virus loading rate being 1.965, 60.0%, and 10.5×108/mg, respectively. About 60% of the viruses were released within 120 h, and the total releasing time was longer than 240 h. Infection with rAdTIMP 1 PELA microsphere efficiently induced TIMP 1 expression in HepG2 cells, and significantly inhibited the proliferation of HepG2 cells, with the inhibitory rate being 47%. Conclusion:PELA microsphere encapsulating recombinant TIMP 1 adenovirus can markedly inhibit the proliferation of HepG2 cells, which provides an experimental basis for the combining macromolecular chemistry and gene therapy for treatment of hepatocellular carcinoma.
Objective: To prepare poly DL lactide poly (PELA) microspheres encapsulating recombinant tissue inhibitors of metalloproteinase 1 (TIMP 1) adenovirus, and to investigate their effects on the proliferation of hepatocellular carcinoma HepG2 cells. Methods:The microsphere was constructed by encapsulating recombinant adenovirus containing TIMP 1 in biodegradable PELA. The diameter of the microsphere, quantity of virus encapsulated, loading rate, and releasing kinetics were measured. HepG2 cells were infected with the microspheres; the infection efficiency was examined by fluorescent microscope; and the ultrastructure was observed by TEM. The expression of TIMP 1 mRNA in HepG2 cells was examined by semi quantitative RT PCR, and the proliferation of HepG2 cells was detected by MTT assay. Results:The microsphere encapsulating recombinant TIMP 1 adenovirus was successfully constructed, with its diameter, entrapment efficiency, and virus loading rate being 1.965, 60.0%, and 10.5×108/mg, respectively. About 60% of the viruses were released within 120 h, and the total releasing time was longer than 240 h. Infection with rAdTIMP 1 PELA microsphere efficiently induced TIMP 1 expression in HepG2 cells, and significantly inhibited the proliferation of HepG2 cells, with the inhibitory rate being 47%. Conclusion:PELA microsphere encapsulating recombinant TIMP 1 adenovirus can markedly inhibit the proliferation of HepG2 cells, which provides an experimental basis for the combining macromolecular chemistry and gene therapy for treatment of hepatocellular carcinoma.
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
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.