Cancer letters最新文献

英文中文

Long-term survival case of SCLC transformation after Osimertinib resistance in EGFR-mutant NSCLC: Benefits from chemo-immunotherapy combined with anti-angiogenic therapy followed by Osimertinib rechallenge 表皮生长因子受体突变型 NSCLC 奥希替尼耐药后 SCLC 转化的长期生存案例：化疗免疫疗法联合抗血管生成疗法后奥希替尼再挑战带来的益处

IF 9.1 1区医学 Q1 ONCOLOGY

Cancer letters

Pub Date : 2025-01-23 DOI: 10.1016/j.canlet.2025.217474

Dujiang Liu , Kaibo Ding , Xinyue Li , Zhongsheng Peng , Yanjun Xu

引用次数: 0

Metabolic reprogramming of neutrophils in the tumor microenvironment: Emerging therapeutic targets 肿瘤微环境中中性粒细胞的代谢重编程：新出现的治疗靶点。

IF 9.1 1区医学 Q1 ONCOLOGY

Cancer letters

Pub Date : 2025-01-23 DOI: 10.1016/j.canlet.2025.217466

Shiyun Huang , Jiahao Shi , Jianfeng Shen , Xianqun Fan

Neutrophils are pivotal in the immune system and have been recognized as significant contributors to cancer development and progression. These cells undergo metabolic reprogramming in response to various stimulus, including infections, diseases, and the tumor microenvironment (TME). Under normal conditions, neutrophils primarily rely on aerobic glucose metabolism for energy production. However, within the TME featured by hypoxic and nutrient-deprived conditions, they shift to altered anaerobic glycolysis, lipid metabolism, mitochondrial metabolism and amino acid metabolism to perform their immunosuppressive functions and facilitate tumor progression. Targeting neutrophils within the TME is a promising therapeutic approach. Yet, focusing on their metabolic pathways presents a novel strategy to enhance cancer immunotherapy. This review synthesizes the current understanding of neutrophil metabolic reprogramming in the TME, with an emphasis on the underlying molecular mechanisms and signaling pathways. Studying neutrophil metabolism in the TME poses challenges, such as their short lifespan and the metabolic complexity of the environment, necessitating the development of advanced research methodologies. This review also discusses emerging solutions to these challenges. In conclusion, given their integral role in the TME, targeting the metabolic pathways of neutrophils could offer a promising avenue for cancer therapy.

{"title":"Metabolic reprogramming of neutrophils in the tumor microenvironment: Emerging therapeutic targets","authors":"Shiyun Huang , Jiahao Shi , Jianfeng Shen , Xianqun Fan","doi":"10.1016/j.canlet.2025.217466","DOIUrl":"10.1016/j.canlet.2025.217466","url":null,"abstract":"<div><div>Neutrophils are pivotal in the immune system and have been recognized as significant contributors to cancer development and progression. These cells undergo metabolic reprogramming in response to various stimulus, including infections, diseases, and the tumor microenvironment (TME). Under normal conditions, neutrophils primarily rely on aerobic glucose metabolism for energy production. However, within the TME featured by hypoxic and nutrient-deprived conditions, they shift to altered anaerobic glycolysis, lipid metabolism, mitochondrial metabolism and amino acid metabolism to perform their immunosuppressive functions and facilitate tumor progression. Targeting neutrophils within the TME is a promising therapeutic approach. Yet, focusing on their metabolic pathways presents a novel strategy to enhance cancer immunotherapy. This review synthesizes the current understanding of neutrophil metabolic reprogramming in the TME, with an emphasis on the underlying molecular mechanisms and signaling pathways. Studying neutrophil metabolism in the TME poses challenges, such as their short lifespan and the metabolic complexity of the environment, necessitating the development of advanced research methodologies. This review also discusses emerging solutions to these challenges. In conclusion, given their integral role in the TME, targeting the metabolic pathways of neutrophils could offer a promising avenue for cancer therapy.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"612 ","pages":"Article 217466"},"PeriodicalIF":9.1,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tertiary lymphoid structures as a biomarker in immunotherapy and beyond: Advancing towards clinical application 作为免疫疗法及其他疗法生物标志物的三级淋巴结构：迈向临床应用。

IF 9.1 1区医学 Q1 ONCOLOGY

Cancer letters

Pub Date : 2025-01-23 DOI: 10.1016/j.canlet.2025.217491

Xinyu Cui , Xuanyu Gu , Dongyu Li , Peng Wu , Nan Sun , Chaoqi Zhang , Jie He

Tertiary lymphoid structures (TLSs) are ectopic immune cell clusters formed in nonlymphoid tissues affected by persistent inflammation, such as in cancer and prolonged infections. They have features of the structure and function of secondary lymphoid organs, featuring central CD20⁺ B cells, surrounded by CD3⁺ T cells, CD21⁺ follicular dendritic cells, and CD68⁺ macrophages, with a complex vascular system. TLS formation is governed by lymphotoxin-α1β2, TNF, and chemokines like CCL19, CCL21, and CXCL13, differing from secondary lymphoid organ development in developing later in life at sites of chronic inflammation. Their role in enhancing immune responses, particularly in the context of cancer, makes them a focal point in immunotherapy. This review discusses recent advances in TLS assessment that involves complex gene expression signatures, histological analysis, artificial intelligence, and spatial omics. The presence and maturity of TLS are associated with better outcomes in various cancers, acting as a biomarker for immunotherapy effectiveness. This review explores the structure, formation, and role of TLS in disease prognosis, including their roles in immunotherapy and non-immunotherapy treatments, highlighting a need to develop novel techniques for precise characterization of TLS as well as their significance as predictive biomarkers beyond traditional biomarkers.

{"title":"Tertiary lymphoid structures as a biomarker in immunotherapy and beyond: Advancing towards clinical application","authors":"Xinyu Cui , Xuanyu Gu , Dongyu Li , Peng Wu , Nan Sun , Chaoqi Zhang , Jie He","doi":"10.1016/j.canlet.2025.217491","DOIUrl":"10.1016/j.canlet.2025.217491","url":null,"abstract":"<div><div>Tertiary lymphoid structures (TLSs) are ectopic immune cell clusters formed in nonlymphoid tissues affected by persistent inflammation, such as in cancer and prolonged infections. They have features of the structure and function of secondary lymphoid organs, featuring central CD20<sup>+</sup> B cells, surrounded by CD3<sup>+</sup> T cells, CD21<sup>+</sup> follicular dendritic cells, and CD68<sup>+</sup> macrophages, with a complex vascular system. TLS formation is governed by lymphotoxin-α1β2, TNF, and chemokines like CCL19, CCL21, and CXCL13, differing from secondary lymphoid organ development in developing later in life at sites of chronic inflammation. Their role in enhancing immune responses, particularly in the context of cancer, makes them a focal point in immunotherapy. This review discusses recent advances in TLS assessment that involves complex gene expression signatures, histological analysis, artificial intelligence, and spatial omics. The presence and maturity of TLS are associated with better outcomes in various cancers, acting as a biomarker for immunotherapy effectiveness. This review explores the structure, formation, and role of TLS in disease prognosis, including their roles in immunotherapy and non-immunotherapy treatments, highlighting a need to develop novel techniques for precise characterization of TLS as well as their significance as predictive biomarkers beyond traditional biomarkers.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"613 ","pages":"Article 217491"},"PeriodicalIF":9.1,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CircKIAA0182-YBX1 Axis: A Key Driver of Lung Cancer Progression and Chemoresistance CircKIAA0182 通过与 YBX1 相互作用增强肺癌的进展和化疗耐药性

IF 9.1 1区医学 Q1 ONCOLOGY

Cancer letters

Pub Date : 2025-01-23 DOI: 10.1016/j.canlet.2025.217494

Masha Huang , Jingyi Sun , Qingqing Jiang , Xin Zhao , Hanxue Huang , Mengrong Lei , Shilong Jiang , Fuqiang Yuan , Zhaoqian Liu

Lung cancer, particularly non-small cell lung cancer (NSCLC), remains a leading cause of cancer-related mortality. Resistance to platinum-based chemotherapy, such as cisplatin, significantly limits treatment efficacy. Circular RNAs (circRNAs) have emerged as key regulators of cancer progression and chemotherapy resistance due to their stable structure, which protects them from degradation. In this study, we focus on circKIAA0182, a circRNA identified as highly expressed in cisplatin-resistant NSCLC cells through profiling. We explore its role in cell proliferation, migration, invasion, apoptosis, and cisplatin resistance. Our findings show that circKIAA0182 promotes cisplatin resistance and tumor progression in NSCLC, in vitro and in vivo. Furthermore, we discovered that circKIAA0182 may interact with the RNA-binding protein YBX1, potentially mediating its oncogenic and cisplatin-resistant functions. The biological role of circKIAA0182 presents a promising target for developing therapeutic strategies to overcome NSCLC progression and cisplatin resistance.

{"title":"CircKIAA0182-YBX1 Axis: A Key Driver of Lung Cancer Progression and Chemoresistance","authors":"Masha Huang , Jingyi Sun , Qingqing Jiang , Xin Zhao , Hanxue Huang , Mengrong Lei , Shilong Jiang , Fuqiang Yuan , Zhaoqian Liu","doi":"10.1016/j.canlet.2025.217494","DOIUrl":"10.1016/j.canlet.2025.217494","url":null,"abstract":"<div><div>Lung cancer, particularly non-small cell lung cancer (NSCLC), remains a leading cause of cancer-related mortality. Resistance to platinum-based chemotherapy, such as cisplatin, significantly limits treatment efficacy. Circular RNAs (circRNAs) have emerged as key regulators of cancer progression and chemotherapy resistance due to their stable structure, which protects them from degradation. In this study, we focus on circKIAA0182, a circRNA identified as highly expressed in cisplatin-resistant NSCLC cells through profiling. We explore its role in cell proliferation, migration, invasion, apoptosis, and cisplatin resistance. Our findings show that circKIAA0182 promotes cisplatin resistance and tumor progression in NSCLC, in vitro and in vivo. Furthermore, we discovered that circKIAA0182 may interact with the RNA-binding protein YBX1, potentially mediating its oncogenic and cisplatin-resistant functions. The biological role of circKIAA0182 presents a promising target for developing therapeutic strategies to overcome NSCLC progression and cisplatin resistance.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"612 ","pages":"Article 217494"},"PeriodicalIF":9.1,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dual targeting PPARα and NPC1L1 metabolic vulnerabilities blocks tumorigenesis 双重靶向 PPARα 和 NPC1L1 代谢弱点可阻止肿瘤发生

IF 9.1 1区医学 Q1 ONCOLOGY

Cancer letters

Pub Date : 2025-01-23 DOI: 10.1016/j.canlet.2025.217493

Xiaona You , Xi Hu , Zenghui Sun , Wenwen Xu , Lanlan Liu , Tao Huang , Shenli Yuan , Jilong Yin , Hao Wang , Limei Wang , Juncheng Wang , Wei Xu , Zhiyue Zhang , Yingjie Zhang , Yuchen Fan , Fabao Liu

Dysregulated lipid metabolism is linked to tumor progression. In this study, we identified Niemann-Pick C1-like 1 (NPC1L1) as a downstream effector of PKM2. In breast cancer cells, PKM2 knockout (KO) enhanced NPC1L1 expression while downregulating peroxisome proliferator-activated receptor α (PPARα) signaling pathway. PPARα and nuclear factor-E2 p45-related factor 1/2(Nrf1/2) are transcription factors regulating NPC1L1. In vitro PKM2 KO enhanced recruitment of Nrf1/2 to the NPC1L1 promoter region. Fenofibrate, a PPARα activator, promoted NPC1L1 expression; ezetimibe, an NPC1L1 inhibitor and effective Nrf2 activator, also elevated NPC1L1 expression. Combined administration of fenofibrate and ezetimibe significantly induced cytoplasmic vacuolation, and cell apoptosis. Mechanistically, this combined administration activated inositol required enzyme 1α(IRE1α) and produced the spliced form of X-box binding protein (XBP1s), which in turn enhanced lysine demethylase 6B (KDM6B) transcription. XBP1s interacts with KDM6B to activate genes involved in the unfolded protein response by demethylating di- and tri-methylated lysine 27 of histone H3 (H3K27), consequently increasing H3K27 acetylation levels in breast cancer cell lines. Fenofibrate and ezetimibe synergistically inhibited tumor growth in vivo. Our findings reveal that dual targeting of PPARα and NPC1L1 may represent a novel therapeutic regimen for breast cancer therapy.

{"title":"Dual targeting PPARα and NPC1L1 metabolic vulnerabilities blocks tumorigenesis","authors":"Xiaona You , Xi Hu , Zenghui Sun , Wenwen Xu , Lanlan Liu , Tao Huang , Shenli Yuan , Jilong Yin , Hao Wang , Limei Wang , Juncheng Wang , Wei Xu , Zhiyue Zhang , Yingjie Zhang , Yuchen Fan , Fabao Liu","doi":"10.1016/j.canlet.2025.217493","DOIUrl":"10.1016/j.canlet.2025.217493","url":null,"abstract":"<div><div>Dysregulated lipid metabolism is linked to tumor progression. In this study, we identified Niemann-Pick C1-like 1 (<em>NPC1L1</em>) as a downstream effector of <em>PKM2</em>. In breast cancer cells, <em>PKM2</em> knockout (KO) enhanced <em>NPC1L1</em> expression while downregulating peroxisome proliferator-activated receptor α (PPARα) signaling pathway. PPARα and nuclear factor-E2 p45-related factor 1/2(Nrf1/2) are transcription factors regulating <em>NPC1L1</em>. <em>In vitro PKM2</em> KO enhanced recruitment of Nrf1/2 to the <em>NPC1L1</em> promoter region. Fenofibrate, a PPARα activator, promoted <em>NPC1L1</em> expression; ezetimibe, an <em>NPC1L1</em> inhibitor and effective Nrf2 activator, also elevated <em>NPC1L1</em> expression. Combined administration of fenofibrate and ezetimibe significantly induced cytoplasmic vacuolation, and cell apoptosis. Mechanistically, this combined administration activated inositol required enzyme 1α(IRE1α) and produced the spliced form of X-box binding protein (XBP1s), which in turn enhanced lysine demethylase 6B (KDM6B) transcription. XBP1s interacts with KDM6B to activate genes involved in the unfolded protein response by demethylating di- and tri-methylated lysine 27 of histone H3 (H3K27), consequently increasing H3K27 acetylation levels in breast cancer cell lines. Fenofibrate and ezetimibe synergistically inhibited tumor growth <em>in vivo</em>. Our findings reveal that dual targeting of PPARα and <em>NPC1L1</em> may represent a novel therapeutic regimen for breast cancer therapy.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"612 ","pages":"Article 217493"},"PeriodicalIF":9.1,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

An ER stress and mitochondrial apoptosis Co-inducer for enhanced cancer immunotherapy 增强癌症免疫疗法的ER应激和线粒体凋亡协同诱导剂

IF 9.1 1区医学 Q1 ONCOLOGY

Cancer letters

Pub Date : 2025-01-22 DOI: 10.1016/j.canlet.2025.217485

Guangzhao Xu , Shuzhen Chen , Hekai Yang , Xiaozhe Feng , Fahui Li , Huishuang Zhao , Le Sun , Ping Yan , Yuxi Chen , Guanhong Guo , Wen Sun , Weiguo Song , Zhe-Sheng Chen , Liuya Wei , Wenda Zhong

Though immunogenic cell death (ICD) has garnered significant attention in the realm of anticancer therapies, effectively stimulating strong immune responses with adequate antigen presentation in deep-seated cancers remains challenging. Herein, to promote antigen presentation, an efficient dual-targeted photodynamic ICD inducer is developed. Due to the enhanced spin-orbit coupling and electron structure modulation, the Cy5-I-CF₃ probe showcases exceptional reactive oxygen species (ROS) generation capacity within cancer cells. The Cy5-I-CF₃ also displays the co-targeting ability toward the endoplasmic reticulum (ER) and mitochondria. More importantly, the in-situ ROS generation synergistically facilitates the interaction between ER and mitochondria, thereby invoking a more robust ER stress response through cascade amplification mechanisms, resulting in substantial release of damage-associated molecular patterns (DAMPs) and strong induction of ICD. This augmentation ultimately enhances the endogenous antigen presentation machinery. Adequate antigen presentation promotes the dendritic cell (DC) maturation and infiltration of cytotoxic T lymphocytes (CTLs) to realize efficient immunotherapy. As a result, Cy5-I-CF₃ notably restrains the growth of distant and primary cancers by photodynamic-induced immunotherapy. Our research offers valuable insights for the design of efficacious ICD inducers, advancing the utilization of cancer immunotherapy.

{"title":"An ER stress and mitochondrial apoptosis Co-inducer for enhanced cancer immunotherapy","authors":"Guangzhao Xu , Shuzhen Chen , Hekai Yang , Xiaozhe Feng , Fahui Li , Huishuang Zhao , Le Sun , Ping Yan , Yuxi Chen , Guanhong Guo , Wen Sun , Weiguo Song , Zhe-Sheng Chen , Liuya Wei , Wenda Zhong","doi":"10.1016/j.canlet.2025.217485","DOIUrl":"10.1016/j.canlet.2025.217485","url":null,"abstract":"<div><div>Though immunogenic cell death (ICD) has garnered significant attention in the realm of anticancer therapies, effectively stimulating strong immune responses with adequate antigen presentation in deep-seated cancers remains challenging. Herein, to promote antigen presentation, an efficient dual-targeted photodynamic ICD inducer is developed. Due to the enhanced spin-orbit coupling and electron structure modulation, the Cy5-I-CF<sub>3</sub> probe showcases exceptional reactive oxygen species (ROS) generation capacity within cancer cells. The Cy5-I-CF<sub>3</sub> also displays the co-targeting ability toward the endoplasmic reticulum (ER) and mitochondria. More importantly, the in-situ ROS generation synergistically facilitates the interaction between ER and mitochondria, thereby invoking a more robust ER stress response through cascade amplification mechanisms, resulting in substantial release of damage-associated molecular patterns (DAMPs) and strong induction of ICD. This augmentation ultimately enhances the endogenous antigen presentation machinery. Adequate antigen presentation promotes the dendritic cell (DC) maturation and infiltration of cytotoxic T lymphocytes (CTLs) to realize efficient immunotherapy. As a result, Cy5-I-CF<sub>3</sub> notably restrains the growth of distant and primary cancers by photodynamic-induced immunotherapy. Our research offers valuable insights for the design of efficacious ICD inducers, advancing the utilization of cancer immunotherapy.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"612 ","pages":"Article 217485"},"PeriodicalIF":9.1,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

NEAT1 promotes the perineural invasion of pancreatic cancer via the E2F1/GDNF axis NEAT1 通过 E2F1/GDNF 轴促进胰腺癌的神经周围侵袭

IF 9.1 1区医学 Q1 ONCOLOGY

Cancer letters

Pub Date : 2025-01-22 DOI: 10.1016/j.canlet.2025.217497

Jingtao Gu , Qiqi Wang , Jiantao Mo , Tao Qin , Weikun Qian , Wangxing Duan , Liang Han , Zheng Wang , Qingyong Ma , Jiguang Ma

Pancreatic cancer is characterized by an insidious onset and high degree of malignancy, with a 5-year survival rate of less than 11 %. Perineural invasion (PNI) is one of the pathological features of pancreatic cancer and provides a pathway for distant tumor metastasis, which leads to a poor prognosis. Although NEAT1 promotes the progression of pancreatic cancer, its impact on PNI has not been studied. In this study, we found that NEAT1 facilitates pancreatic cancer metastasis and PNI by regulating E2F1. In vivo experiments showed that NEAT1 promotes PNI in a mouse model. Furthermore, E2F1 is enriched at the promoter region of GDNF and directly participates in its transcriptional regulation. NEAT1 can also recruit P300 to the GDNF promoter region, thereby inducing the H3K27ac modification to further increase chromatin accessibility. This process ultimately facilitates GDNF transcription and tumor innervation, providing a pathway for tumor metastasis.

引用次数: 0

Emerging neuroimmune mechanisms in cancer neuroscience

IF 9.1 1区医学 Q1 ONCOLOGY

Cancer letters

Pub Date : 2025-01-21 DOI: 10.1016/j.canlet.2025.217492

Yingying Huang , Xin Zhou , Jiaqi Liu , Ying Cao , Wei Fu , Jing Yang

It has become increasingly recognized that neural signals can profoundly influence the prognosis of various cancer types. In the past years, we have witnessed “cancer neuroscience,” which primarily focuses on the complex crosstalk between tumors and neural signals, emerging as a new, multidisciplinary direction of biomedical science. This review aims to summarize the current knowledge of this research frontier, with an emphasis on the neuroimmune mechanisms enacted through the reciprocal interactions between tumors and the central or peripheral nervous system. In addition, we wish to highlight several key questions of cancer neuroscience and its neuroimmune action that warrant future research and translational efforts, including novel strategies for manipulating neural signals for antitumor immunotherapies, as well as managing cancer-related neurological or psychiatric complications.

引用次数: 0

Tumor-nerve interactions in cancer regulation and progression

IF 9.1 1区医学 Q1 ONCOLOGY

Cancer letters

Pub Date : 2025-01-20 DOI: 10.1016/j.canlet.2025.217483

Jianyi Zhao , Lilin Cheng , Jian Yang , Feifei Xu , Weixiang Qi , Keman Liao , Li Zhou , Lu Cao , Jiayi Chen , Yingying Lin

Tumor-nerve interactions play a critical role in tumor progression, metastasis, and treatment resistance, redefining our understanding of the tumor microenvironment. This review provides a comprehensive analysis of how the peripheral and central nervous systems contribute to cancer biology, focusing on mechanisms of neural invasion, immune evasion, and tumor adaptation. It has highlighted the emerging potential of repurposing nervous system-targeted drugs originally developed for neurodegenerative and autoimmune diseases as innovative cancer therapies. The review also addresses key challenges, including the limitations of current experimental models and the complexity of translating preclinical findings to clinical applications. By bridging the gap between neuroscience and oncology, this interdisciplinary study aims to discover novel therapeutic strategies to improve outcomes for cancer patients.

引用次数: 0

Local Ablation—Our next hope for pancreatic cancer immunotherapy?

IF 9.1 1区医学 Q1 ONCOLOGY

Cancer letters

Pub Date : 2025-01-20 DOI: 10.1016/j.canlet.2025.217445

Rebekah R. White MD

引用次数: 0

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