CANCER IMMUNOLOGY IMMUNOTHERAPY肿瘤免疫学与免疫治疗
CANCER IMMUNOLOGY IMMUNOTHERAPY(英文缩写 CANCER IMMUNOL IMMUN),ISSN 0340-7004,eISSN 1432-0851,中文译名:肿瘤免疫学与免疫治疗 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 6.630 | Q1 |
| 2022 | 5.800 | Q1 |
| 2023 | 4.600 | Q1 |
| 2024 | 5.100 | Q1 |
| 2025 | 5.800 | Q1 |
CANCER IMMUNOLOGY IMMUNOTHERAPY 最新收录文献
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1. The effect and mechanism of TIPE in promoting M2 polarization through DcR3 in the microenvironment of colorectal cancer.
1. TIPE在结直肠癌微环境中通过DcR3促进M2极化的作用及机制PMID:日期:2026-09-04Elevated expression of tumor necrosis factor α-induced protein 8 (TIPE) is observed in colorectal cancer (CRC) and is known to regulate decoy receptor 3 (DcR3) expression while promoting M2 polarization of macrophages. However, the precise role of DcR3 in macrophage M2 polarization remains to be elucidated. We employed bioinformatic analysis alongside in vitro and in vivo experimental approaches to investigate the regulatory mechanism by which TIPE influences macrophage M2 polarization in CRC. TIPE expression in CRC tissues positively correlates with M2 macrophage markers (CD206, CD163, IL-10). Functionally, TIPE promotes M2 polarization of macrophages by upregulating DcR3. Mechanistically, DcR3 binds to heparan sulfate proteoglycan 2 (HSPG2) in a heparan sulfate (HS)-dependent manner, leading to activation of the protein kinase Bα1 (AKT1) signaling pathway. AKT1 activation not only directly drives M2 polarization but also enhances macrophage chemotaxis and recruitment toward CRC cells by upregulating the chemokine CXCL8. This study reveals a novel mechanism through which TIPE regulates M2 macrophage polarization and function via DcR3, offering new perspectives for the diagnosis and therapeutic targeting of CRC.
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2. Neoadjuvant combined immunotherapy with intratumoral TransCon TLR7/8 Agonist and systemic TransCon IL-2 β/y or pembrolizumab in patients with locally advanced oral cancer-a monocentric experience.
2. 瘤内注射TransCon TLR7/8激动剂联合全身TransCon IL-2 β/y或帕博利珠单抗的新辅助免疫联合治疗用于局部晚期口腔癌患者——单中心经验PMID:日期:2026-09-04Combination immunotherapy has shown encouraging activity across multiple solid tumors. We report the complete and consecutive cohort of patients with locally advanced oral squamous cell carcinoma (OSCC) treated at a single center within the prospective, multicenter, randomized phase 2 BelieveIT-201 trial (ASND0038), evaluating neoadjuvant intratumoral Toll-like receptor (TLR) 7/8 agonist (TransCon TLR7/8 Agonist) therapy combined with systemic immunotherapy. Patients with non-metastatic OSCC treated within the BelieveIT-201 trial (ASND0038) between April and December 2024 were included. Neoadjuvant therapy comprised two cycles of intratumoral TransCon TLR7/8 Agonist combined with either intravenous pembrolizumab or TransCon IL-2 β/γ according to 1:1 randomization, followed by surgical resection. The trial was terminated prematurely by the sponsor for reasons unrelated to safety or efficacy, which limited the cohort to six patients. Clinical, radiographic, pathological responses, and safety were assessed. Immunohistochemical analyses of paired pre- and post-treatment tumor samples evaluated immune cell infiltration (CD3, CD8, CD68, CD163). The individual patient was the unit of analysis, and given the small number of patients all analyses are descriptive; no inferential statistical testing was performed. Progression-free survival (PFS) and overall survival (OS) are reported as absolute event counts. Six patients were treated (median age 63 years; median follow-up 81 weeks). Three patients achieved a major clinical response, two showed partial response, and one had progressive disease. Pathologic evaluation revealed one complete response, one major response, and four non-responses. All patients underwent surgery; postoperative morbidity was substantial, with at least one grade III adverse event in every patient and one postoperative death. All three patients with a major clinical response developed sterile tumor-associated pseudoabscesses in spatial proximity to the injection site. Immunohistochemical analyses revealed remodeling of the tumor immune microenvironment, including increased T-cell infiltration, most pronounced in the tumor center. Within the first year, two of six patients experienced a progression-free survival event (n = 1 progressive disease, n = 1 death). After surgery none of the patients showed disease recurrence. Neoadjuvant intratumoral TransCon TLR7/8 Agonist-based combination immunotherapy was feasible in this small prospective cohort of patients with locally advanced OSCC and was accompanied by consistent remodeling of the tumor immune microenvironment. Because of the limited number of patients and the premature termination of the parent trial, no conclusions on efficacy or on comparative tolerability can be drawn.
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3. Correction: Haemostatic changes during CART cell therapy and risk of complications.
PMID:日期:2026-08-25该文献暂无摘要。
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6. The CREM-IL-15 axis: decoding the persistence-exhaustion paradox in NK cell immunotherapy.
PMID:日期:2026-08-04Natural killer (NK) cells are critical components of the innate immune system, renowned for their ability to recognize and eliminate malignant and infected cells without prior sensitization. NK cell immunotherapy encompasses various approaches, including adoptive transfer of ex vivo expanded NK cells, cytokine stimulation to enhance their activity, and genetic modifications to improve persistence and specificity. CREM is a cAMP-responsive transcription factor that modulates gene expression in response to receptor- and cytokine-driven signaling. Recent evidence now shows that IL-15 and CAR stimulation rapidly induce CREM in activated NK cells. Rafei (Nature 643:1076-1086, 2025) further demonstrated in CAR-NK models that CREM functions as a regulatory checkpoint limiting NK cell cytotoxicity and cytokine production, while its relevance in resting/native NK cells remains to be established. The CREM-IL-15 signaling axis has emerged as a pivotal regulator of NK cell biology, influencing their development, activation, and longevity. IL-15 is a critical cytokine for NK cell survival, proliferation, and functional maturation. Understanding this axis is vital, as it offers insights into mechanisms that sustain NK cell activity and those that lead to functional exhaustion, thereby informing strategies to enhance therapeutic efficacy. A central challenge in NK cell immunotherapy is balancing cellular persistence with functional exhaustion. Persistent NK cell activity is desirable for sustained tumor control; however, prolonged activation often results in cellular exhaustion characterized by diminished cytotoxicity and cytokine production. This paradox hampers the long-term success of NK cell-based treatments. The CREM-IL-15 axis plays a complex role in this dynamic, potentially promoting NK cell survival and persistence while also contributing to exhaustion under certain conditions. Deciphering the molecular underpinnings of this paradox is essential for developing interventions that maintain NK cell functionality over time, thereby improving therapeutic outcomes in cancer patients.
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7. Dual inhibition of tumor cells and tumor-associated neutrophils by anti-CXCR2 antibodies suppresses tumor growth and augments immunotherapy efficacy in ARID1A-deficient pancreatic cancer.
PMID:日期:2026-07-21Pancreatic ductal adenocarcinoma (PDAC) is largely resistant to immune checkpoint blockade (ICB) due to its highly immunosuppressive tumor microenvironment. How to switch the "immune-cold" microenvironment to "immune hot" one is a clinical unmet need. We recently generated a genetically engineered PDAC mouse model (KAR) by combining K-Ras mutation and AT-rich interactive domain-containing protein 1A (ARID1A) inactivation in the pancreas. Compared to the KPC (K-Ras mutation + p53 inactivation) tumors, KAR tumors express higher C-X-C chemokine receptor 2 (CXCR2) and have more CXCR2 neutrophils infiltration. Our previous study demonstrated that activation of CXCR2 by its cognate ligands promotes proliferation and drug resistance in PDAC cells. In addition, increase in tumor-associated neutrophils and high neutrophil-to-lymphocyte ratio are associated with worse prognosis in PDAC patients. Here, we developed a monoclonal antibody against human CXCR2 (huCXCR2-Ab) and tested its therapeutic effect in cells and in animals. Treatment with huCXCR2-Ab inhibited IL-8-induced downstream signaling, and the proliferation of human PDAC cancer cells. In addition, huCXCR2-Ab suppressed PDAC growth in an orthotopic nude mouse model. We next developed a monoclonal antibody against mouse CXCR2 (muCXCR2-Ab) and investigated its immune regulatory effect in vivo. We showed that muCXCR2-Ab reduced tumor burden, increased CD8⁺ T-cell infiltration, and decreased immunosuppressive neutrophils in the KAR mice. Moreover, muCXCR2-Ab augments the therapeutic efficacy of anti-PD-L1. Thus, dual targeting of CXCR2 tumor cells and tumor-associated neutrophils remodels tumor microenvironment and enhances immunotherapy response in ARID1A-deficient PDAC, providing a new strategy for precision therapy of PDAC.
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8. Therapeutic targeting of CD47 using a tri-specific NK cell engager to inhibit multiple myeloma.
PMID:日期:2026-07-20Multiple myeloma (MM), a hematological malignancy, remains an incurable disease due to the development of resistance to the treatment; thus, there is an urgent need for new and effective therapeutic strategies, particularly for patients who do not respond to standard therapies. High levels of Cluster of Differentiation 47 (CD47) expression have been reported in MM and are associated with disease progression. CD47 acts as a cancer immune escape mechanism by binding to SIRPα protein, resulting in inhibiting phagocytosis of macrophages and NK cell activity. Therefore, blocking the CD47 signaling pathway has emerged as a promising strategy for cancer immunotherapy. In this study, we confirmed that MM cells have high CD47 expression. We generated and characterized a tri-specific killer engager targeting CD47, namely TriKE-CD47, that targets both CD47 on MM cells and CD16 on NK cells. Additionally, it incorporates an IL-15 moiety to enhance NK cell proliferation. TriKE-CD47 treatment promoted a remarkable proliferation of NK cells overexpressing CD16 (N6 cells). Co-culturing MM cells with N6 cells, primary NK cells, and monocyte-derived macrophages in the presence of 200 ng of TriKE-CD47 significantly improved NK cytotoxicity and macrophage phagocyte activities against MM cells. Notably, the efficacy of TriKE-CD47 was directly correlated with CD47 expression levels on the target cells reflecting the specificity of TriKE-CD47 to target antigen. Furthermore, TriKE-CD47 effectively suppressed tumor growth in MM xenograft mice models. Taken together, these findings strongly supported that TriKE-CD47 could be a potential therapeutic for MM patients.
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9. Mast cells in tumors: dual roles and therapeutic potential.
PMID:日期:2026-07-19Mast cells (MCs) are tissue-resident immune cells that accumulate in the tumor microenvironment (TME) and display marked functional plasticity. Rather than acting through fixed pro-tumor or anti-tumor phenotypes, tumor-associated MCs acquire functional programs shaped by tumor type, spatial localization, disease stage, and local microenvironmental cues. In this review, we organize these dual roles around cellular crosstalk, mediator release, angiogenic and lymphangiogenic regulation, and extracellular matrix remodeling. Through these interconnected mechanisms, MCs may either promote tumor progression by reinforcing immunosuppression, limiting effector T cell activity, and supporting vascular, lymphatic, and stromal remodeling, or contribute to tumor suppression by promoting tumor cell apoptosis, antigen presentation, cytotoxic immune-cell recruitment, and anti-tumor mediator release. We also examine MC responses to various cancer treatments, including physical treatment modalities, chemotherapy, immunotherapy, targeted therapy, and CAR-based cell therapies, and discuss how these responses may influence therapeutic efficacy and treatment-related toxicity. Furthermore, we highlight emerging MC-targeted strategies that either suppress their chronic pro-tumor secretion or intentionally induce acute anti-tumor degranulation. By deciphering the dual nature of MCs in cancer, this review underscores the potential for reprogramming MCs to improve tumor treatment outcomes.
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10. Preclinical efficacy of iPSC-derived MUC1-targeted CAR-NK cells against esophageal squamous cell carcinoma.
PMID:日期:2026-07-18MUC1 is frequently overexpressed in esophageal squamous cell carcinoma (ESCC), but MUC1-targeted CAR-NK cells remain unexplored in this malignancy. MUC1 expression was assessed by IHC in 90 ESCC specimens, 47 paired adjacent normal tissues, and normal human organs. MUC1-targeted CAR-NK cells were generated from an iPSC platform. Antitumor activity was evaluated against patient-specific ESCC organoids (PSOs), primary ESCC cells, KYSE150 and KYSE140 cells using live/dead staining, CCK-8, and xCELLigence assays. In vivo efficacy was assessed in a KYSE140 xenograft model. MUC1 was expressed in 70% (63/90) of ESCC cases versus 14.9% (7/47) of adjacent normal tissues (P < 0.001), with negligible expression in normal organs. Among MUC1-positive ESCCs, 88.9% and 42.8% showed > 50% and > 80% tumor cell positivity, respectively. iPSC-derived MUC1 CAR-NK cells exhibited > 95% CAR expression across iPSC, progenitor, and mature stages. Compared with controls, MUC1 CAR-NK cells elicited potent, antigen-specific cytotoxicity against MUC1-expressing ESCC PSOs, primary cells, KYSE150, and KYSE140 in vitro and significantly suppressed KYSE140 xenograft growth in vivo. iPSC-derived MUC1-targeted CAR-NK cells exert robust and specific antitumor efficacy against human ESCC, supporting clinical translation of this off-the-shelf cell therapy.