MedComm – Oncology最新文献

{"title":"Transforming Growth Factor-Beta Signaling in Cancer: Therapeutic Implications, Challenges, and Pathways to Progress","authors":"Faizah A. Alabi,&nbsp;Izuchukwu F. Okpalanwaka,&nbsp;Adenike Oyegbesan,&nbsp;Ebenezar Okoyeocha,&nbsp;Mariam Oladejo,&nbsp;Sikiru O. Imodoye","doi":"10.1002/mog2.70027","DOIUrl":"https://doi.org/10.1002/mog2.70027","url":null,"abstract":"<p>The transforming growth factor-β (TGF-β) family consists of evolutionarily conserved cytokines that regulate various physiological processes across nearly all tissue and cell types. While TGF-β signaling plays a critical role in immune homeostasis and tissue repair, its dysregulation is implicated in multiple diseases, particularly cancer. Given its dual role in tumor suppression and promotion, TGF-β has emerged as a promising yet challenging therapeutic target. Preclinical studies have demonstrated significant tumor inhibition through TGF-β signaling blockade using diverse classes of inhibitors. However, despite extensive research and clinical trials spanning over two decades, no TGF-β inhibitors have been approved for cancer therapy, underscoring a significant disconnect between preclinical promise and clinical efficacy. This review systematically examines the tumorigenic mechanisms driven by TGF-β and evaluates the therapeutic landscape of anti-TGF-β inhibitors, including receptor kinase inhibitors, neutralizing antibodies, bifunctional ligand traps, integrin-mediated TGF-β therapy, antisense oligonucleotides, TGF-β-targeted vaccines, and various combination strategies. By comparing preclinical and clinical findings, we highlight key challenges and propose novel approaches to improve the translational success of TGF-β-targeted therapies. These insights provide a foundation for optimizing future research and advancing the clinical application of TGF-β inhibitors in oncology.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"4 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144624678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cellular Senescence in Cancer: Mechanisms, Roles in Tumor Progression, and Therapeutic Implications","authors":"Jingrui Yan,&nbsp;Yu Zhang,&nbsp;Guohua Mao,&nbsp;Jun Yu,&nbsp;Tianxing Zhou,&nbsp;Jihui Hao","doi":"10.1002/mog2.70029","DOIUrl":"https://doi.org/10.1002/mog2.70029","url":null,"abstract":"<p>Cellular senescence, a state of irreversible cell cycle arrest accompanied by a senescence-associated secretory phenotype (SASP), plays dual roles in cancer biology. Initially recognized as a tumor-suppressive mechanism by halting the proliferation of damaged cells, senescence paradoxically fosters tumor progression through SASP-mediated immunosuppression and chronic inflammation. Thus, the role of senescent cells in tumors still needs to be further elucidated. Our review comprehensively examines the triggers and molecular pathways of senescence. We also summarized the characteristics and functions of senescent tumor and nontumor cells, delineating the heterogeneous tumor senescence microenvironment. Here, we highlight the functional reprogramming of senescent cells, including enhanced stemness, secretome and metabolome reprogramming, which can sustain tumorigenesis and therapeutic resistance. Furthermore, we discuss emerging therapeutic strategies, notably the “one-two punch” approach to overcome therapy resistance. By integrating recent advances in senescence-targeted therapies, our review underscores the necessity of context-specific strategies to harness senescence's tumor-suppressive effects while mitigating its protumorigenic consequences. These insights provide a roadmap for developing precision therapies and refining biomarker-driven approaches to improve cancer treatment outcomes.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"4 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70029","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144573925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Immune Checkpoints: Basic Signaling Pathways and Clinical Translation in Cancer Therapeutics","authors":"Han Sun,&nbsp;Dan Huang,&nbsp;Huiling Zhang,&nbsp;Mingyuan Dong,&nbsp;Simiao Wang,&nbsp;Man Sun,&nbsp;Jiayi Liu,&nbsp;Yiqi Wang,&nbsp;Xiaojie Qu,&nbsp;Xuefeng Li,&nbsp;Zhaogang Yang","doi":"10.1002/mog2.70030","DOIUrl":"https://doi.org/10.1002/mog2.70030","url":null,"abstract":"<p>Immune checkpoints, the key gatekeepers of immune homeostasis, have become the central targets of modern cancer immunotherapy. These regulatory pathways, composed of co-suppressive and co-stimulatory molecules, enable the immune system to distinguish between self and non-self while preventing excessive tissue damage. However, tumor cells strategically block these protective mechanisms through aberrant expression of checkpoint ligands, creating an immunosuppressive microenvironment that promotes tumor immune evasion and metastatic progression. Yet, immune checkpoint therapy is not universally applied due to its specific mechanisms. This review systematically describes the immune checkpoints that function on various types of immune cells, as well as their molecular structure and functional diversity, and elucidates their role in achieving tumor immune escape. We analyze the clinical translation of immune checkpoint inhibitors (ICIs) and their combination therapies. In addition, we combine preclinical findings with clinical trial data to provide a comprehensive framework for understanding the mechanisms of action and clinical applications of immune checkpoints, as well as to present the challenges in terms of immune-related adverse events of ICIs. This review provides a valuable perspective for developing next-generation immunotherapies and optimizing personalized treatment strategies.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"4 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144573924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phosphatase Dysregulation in Cancer: Signaling Pathways and Therapeutic Opportunities","authors":"Maryam Jama,&nbsp;Michael Overduin,&nbsp;Khaled H. Barakat","doi":"10.1002/mog2.70028","DOIUrl":"https://doi.org/10.1002/mog2.70028","url":null,"abstract":"<p>Phosphatases are increasingly recognized as critical regulators of cancer biology, with important roles in both tumor cells and the tumor immune microenvironment (TIME). These enzymes modulate intracellular signaling pathways that control tumor growth, immune evasion, and metastasis. Although phosphatases were once considered undruggable, recent advances have highlighted their therapeutic potential. Despite growing evidence, phosphatases remain underexplored as drug targets, with no approved therapies to date. This review presents an in-depth overview of phosphatase classification based on catalytic domain similarities and explores their diverse functions as tumor suppressors, oncogenic drivers, or context-dependent regulators. We describe how phosphatases such as PTPN6, PTPN22, and DUSPs regulate key pathways like RAS/MAPK and PI3K/AKT in both tumor and immune cells. Additionally, we discuss the role of phosphatases in shaping the tumor microenvironment through exosome secretion. This review highlights current therapeutic strategies, including small molecules and antibodies, and their synergistic effects with kinase inhibitors and immune checkpoint blockade. By summarizing recent advances, this paper underscores the need for deeper mechanistic insights into phosphatase function in cancer and immunity. Understanding these mechanisms will be key to unlocking their potential as novel therapeutic targets in oncology.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"4 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70028","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144472805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Causal Relationship Between Genetically Proxied Inhibition of HMGCR, NPC1L1, and PCSK9 and Cancers","authors":"Xin Wang,&nbsp;Yiyao Zeng,&nbsp;Zihan Xu,&nbsp;Xiangyue Meng,&nbsp;Jie Chen","doi":"10.1002/mog2.70026","DOIUrl":"https://doi.org/10.1002/mog2.70026","url":null,"abstract":"<p>Cancer remains a significant global health burden, ranking as the second leading cause of death despite considerable medical advances. Increasing evidence links cholesterol metabolism, particularly low-density lipoprotein cholesterol (LDL-C), to cancer risk. Epidemiological studies suggest that elevated LDL-C levels are associated with multiple cancers, including breast, colorectal, and pancreatic cancers [<span>1</span>]. These observations suggest that LDL-C-lowering therapies may have anticancer effects. Although preclinical studies show that statins can inhibit tumor growth and metastasis, the effects of different lipid-lowering agents on cancer risk remain unclear. To investigate this, we conducted a Mendelian randomization (MR) study leveraging genetically proxied LDL-C-lowering drug targets, including HMG-CoA reductase (HMGCR), proprotein convertase subtilisin/kexin type 9 (PCSK9), and Niemann-Pick C1-like 1 (NPC1L1) inhibitors. We examined the associations between these drug targets and 16 different cancer types, as well as overall cancer risk (Figure 1A).</p><p>Figure 1B presented the outcomes of MR analyses investigating the causal effects of genetically proxied lipid-lowering drug targets on 17 different types of cancer, alongside pleiotropy assessments. Funnel plots were used to evaluate heterogeneity. A rigorous instrument selection process yielded between 3 and 60 single nucleotide polymorphisms (SNPs) per target, with all F-statistics &gt; 10, mitigating the risk of weak instrument bias. As for the PCSK9 inhibition (PCSK9i), the fixed-effect inverse-variance weighted (IVW) method clearly demonstrated a protective effect on breast cancer (OR: 0.9124, <i>p</i> = 0.0071, 95%CI: 0.8455–0.9792), which this result was corroborated by the weighted median and the weighted mode method. In addition, it also identified PCSK9i had an obvious protective effect on thyroid cancer (OR: 0.3272, <i>p</i> = 0.0397, 95%CI: 0.0370–0.5915) and brain cancer (OR: 0.9985, <i>p</i> = 1.8786E-07, 95%CI: 0.9980–0.9991), only in the IVW method. More importantly, the PCSK9i retained a strong protective association with overall cancer (OR: 0.9883, <i>p</i> = 5.8596E-11, 95%CI: 0.9848–0.9918). However, PCSK9i showed significant associations with higher risk of oesophageal cancer (OR: 1.0009, <i>p</i> = 0.0028, 95%CI: 1.0003–1.0014) and lung cancer (OR: 1.0328, <i>p</i> = 0.0020, 95%CI: 1.0054–1.2782). Additionally, genetically predicted HMGCR inhibition (HMGCRi) had a positive correlation effect on the risk of breast cancer (OR: 0.8266, <i>p</i> = 0.0001, 95%CI: 0.7300–0.9232), ER+ breast cancer (OR: 0.8281, <i>p</i> = 0.0013, 95%CI: 0.7130–0.9431), serous ovarian cancer (OR: 0.7564, <i>p</i> = 0.0213, 95%CI: 0.5187–0.9941), overall ovarian cancer (OR: 0.5954, <i>p</i> = 2.25081E-05, 95%CI: 0.3555–0.8352), kidney cancer (OR: 0.9883, <i>p</i> = 5.85958E-11, 95% CI: 0.9848–0.9918), brain cancer (OR: 0.9982, <i>p</i> = 0.0168, 95%CI: 0.9967–0.9997) and overall ca","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"4 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70026","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144473049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial Ribosomal Protein Family in Cancers: Mechanistic Insights and Therapeutic Implications","authors":"Qian Chen,&nbsp;Yingli Zhang,&nbsp;Jin-Jian Lu,&nbsp;Ting Li","doi":"10.1002/mog2.70024","DOIUrl":"https://doi.org/10.1002/mog2.70024","url":null,"abstract":"<p>Mitochondria, as the main site for aerobic respiration in cells, are indispensable participants in the reprogrammed metabolic activities of tumor cells. Mitochondrial ribosomal proteins (MRPs), essential components of the mitochondrial ribosome (mitoribosome), play a critical role in maintaining mitochondrial function and regulating oncogenic signaling. Their molecular mechanisms and biological functions make MRPs key regulators of tumorigenesis, drug resistance, and tumor immune escape. MRPs are abnormally expressed in various cancer types and are linked to the prognosis of cancer patients. However, a thorough grasp of the specific mechanisms and a holistic analysis of the relationship between MRPs and different cancers are lacking. This review highlights the specific regulatory roles of MRPs, including MRPS5, MRPS29, MRPL9, MRPL12, MRPL13, MRPL33, MRPL58, and MRPL59, in cancer. Additionally, we examine the potential of MRPs as prospective clinical biomarkers and discuss their relationship with clinical prognosis and treatment response. We further explore the underlying reasons for the diverse functions of MRPs, their implications in cellular signaling and tumor immunity, and consider the prospects for developing MRP inhibitors as therapeutic strategies. Our comprehensive analysis deepens the understanding of MRPs complex biological functions and emphasizes their promising potential as therapeutic targets in cancer treatment.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"4 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70024","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144289297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Foe to Ally: Oncolytic Virus-Driven Xenorejection Ignites Potent Antitumor Immunity","authors":"Yanglin Xu,&nbsp;Bingcheng Chang,&nbsp;Wei He,&nbsp;Jia Liu","doi":"10.1002/mog2.70025","DOIUrl":"https://doi.org/10.1002/mog2.70025","url":null,"abstract":"&lt;p&gt;In a groundbreaking study published in the journal &lt;i&gt;Cell&lt;/i&gt;, Yongxiang Zhao and collaborators designed a recombinant oncolytic virus (NDV-GT) by introducing the porcine α1,3-galactosyltransferase (&lt;i&gt;α1,3GT&lt;/i&gt;) gene into the Newcastle disease virus (NDV). The engineered virus specifically infects tumor cells to express immunogenic αGal epitopes, thereby leveraging xenogeneic rejection mechanisms to activate robust antitumor immune responses (Figure 1) [&lt;span&gt;1&lt;/span&gt;]. The innovative oncolytic virus demonstrates significant safety and preliminary efficacy in a cynomolgus monkey liver cancer model and a clinical trial enrolling 20 patients with refractory cancers.&lt;/p&gt;&lt;p&gt;Oncolytic viruses (OVs) have emerged as a promising and versatile therapeutic modality in cancer immunotherapy, owing to their ability for selective oncolysis and induction of systemic antitumor immunity [&lt;span&gt;2&lt;/span&gt;]. However, inadequate immune priming, limited intra-tumoral dissemination and propagation, and rapid neutralization significantly hinder their therapeutic efficacy and clinical translation [&lt;span&gt;3&lt;/span&gt;]. Moreover, the immunosuppressive tumor microenvironment (TME) markedly suppresses the outcomes of OV-based treatments. Despite advancements in engineered OVs and combinatorial regimens designed to enhance immune activation, clinical response rates remain unsatisfactory, indicating the urgent need for innovative strategies [&lt;span&gt;4&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;Xenogeneic rejection is a hyperacute immune response that occurs when heterologous organs or tissues are transplanted into a recipient of another species. The robust rejection could rapidly destroy xenografts by complement activation and endothelial damage [&lt;span&gt;5&lt;/span&gt;]. The αGal epitope, a unique carbohydrate antigen, is widely present in non-primate mammals (e.g., pigs) and New World monkeys. However, during evolution, the ancestors of Old World monkeys and humans lost the αGal epitopes due to genetic mutations, but evolved anti-Gal antibodies to recognize the epitopes. Thus, when the organs or tissues from non-primate mammals are transplanted into humans, the anti-Gal antibodies quickly bind to αGal epitopes of xenografts, activating hyperacute rejection. Inspired by the hyperacute xenogeneic rejection, a porcine antigen was integrated into the Newcastle disease virus (NDV-GT) to deliver xenogeneic αGal epitopes to tumor cells (Figure 1A). Such recombinant virus camouflages porcine antigens on malignant cells, which would be recognized by the human body as heterologous transplant organs, thereby eliciting tumor-targeted hyperacute rejection analogous to xenograft destruction and converting the “cold” immunosuppressive TME to “hot” (Figure 1B).&lt;/p&gt;&lt;p&gt;The NDV-GT virus specifically and effectively infected different types of cancer cells &lt;i&gt;in vitro&lt;/i&gt; as well as the parent virus, while exhibiting minimal infection in noncancerous cells. Moreover, the infected cancer cells effectively expressed the exogenous gen","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"4 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70025","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144213769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of Adenosine Phosphate Signaling Promotes Antitumor Immunity in Tumor Microenvironment and Facilitate Immunotherapy","authors":"Yantao Xu,&nbsp;Ying Wang,&nbsp;Zixi Jiang,&nbsp;Yi He,&nbsp;Guowei Zhou,&nbsp;Benliang Wei,&nbsp;Jiachen Liu,&nbsp;Xiang Chen","doi":"10.1002/mog2.70022","DOIUrl":"https://doi.org/10.1002/mog2.70022","url":null,"abstract":"<p>Adenosine 5′-triphosphate (ATP) plays a crucial role in intracellular energetic metabolism and functions as a signal transducer in shaping the tumor microenvironment (TME). However, the understanding of the biological functions of adenosine phosphate signaling and its clinical relevance remains limited. Here, we deciphered the multi-omics dysregulation of 15 purinergic P2 receptors (P2Rs) and their clinical relevance. We revealed the presence of 5 ATP signaling subtypes in melanoma, with two distinct functional metaprograms—one metabolic and the other inflammatory. We developed an adenosine phosphate signaling model (APsig) that showed promising prognostic value in melanoma, as well as predictive efficacy of immunotherapy across 1068 tumor samples in 9 independent public cohorts. High APsig was associated with longer overall survival (OS) and improved response to tumor immunotherapy. Additionally, through single-cell and spatial transcriptomic analysis, we explored how APsig promotes antitumor immunity by activating myeloid lineage cells for antigen presentation. Our comprehensive characterization of P2R-mediated adenosine phosphate signaling at both bulk/single-cell and spatial transcriptomic levels highlights its potential as a promising target for developing novel anticancer agents, particularly in combination with immune checkpoint inhibitors.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"4 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144131579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unlocking T-Cell Plasticity in the Tumor Microenvironment: Implications for Cancer Progression and Therapeutic Strategies","authors":"Xiao-Hong Ding,&nbsp;Xue-Pei Li,&nbsp;Fenfang Chen,&nbsp;Han Wang,&nbsp;Yi-Zhou Jiang","doi":"10.1002/mog2.70023","DOIUrl":"https://doi.org/10.1002/mog2.70023","url":null,"abstract":"<p>The tumor microenvironment (TME) is a complex and dynamic ecosystem crucial for cancer development and progression. Within this intricate milieu, T-cells constitute a heterogeneous population and serve as a cornerstone of antitumor immunity. Notably, T-cells can rapidly transition across a wide spectrum of phenotypic and functional states within the disrupted TME. Despite the crucial role of T-cells in cancer immunity, a comprehensive understanding of their plasticity within the TME remains limited. In this review, we delve into the functional plasticity and spatial distribution of T-cells in response to diverse microenvironmental conditions. Additionally, we review the plasticity of T-cell functional states during conventional therapies, highlighting their potential to enhance or limit therapeutic outcomes. Finally, we propose innovative therapeutic approaches that leverage T-cell plasticity to enhance clinical efficacy by regulating the immune response within the TME. By providing insights into the dynamics of T-cell behavior, this review highlights the promising potential of targeting T-cell plasticity as an immuno-sensitizer to refine therapeutic strategies and overcome current challenges in cancer treatment.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"4 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144131580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative Stress in Antigen Processing and Presentation","authors":"Qinxia Chang,&nbsp;Yaying Zhang,&nbsp;Xiaojun Liu,&nbsp;Peng Miao,&nbsp;Wenbing Pu,&nbsp;Shanshan Liu,&nbsp;Jing Zhang,&nbsp;Yuan Tian,&nbsp;Guobo Shen,&nbsp;Na Xie","doi":"10.1002/mog2.70020","DOIUrl":"https://doi.org/10.1002/mog2.70020","url":null,"abstract":"<p>Antigen processing and presentation are fundamental for connecting innate and adaptive immune responses in combating cancers and infections. Reactive oxygen species (ROS), serving as second messengers in various physiological processes, play a vital role in modulating antigen processing and presentation. However, oxidative stress due to an imbalance characterized by excessive accumulation of ROS or inadequate antioxidant defenses can severely impair antigen-specific immune responses, contributing to the pathophysiology of multiple health conditions, notably including various cancers, cancer-associated infections and autoimmune diseases. This review comprehensively investigates the multifaceted effects of ROS on antigen processing and presentation, encompassing immunopeptide generation, the functionality of antigen-presentation machinery (APM), and the interactions of antigen-presenting cells and antigen-specific effector cells. It emphasizes the critical pathophysiological roles of oxidative stress in diseases such as cancers, cancer-associated infections and autoimmune diseases. Moreover, we delve into the therapeutic potential of targeting redox homeostasis to enhance antitumor immune responses. By illuminating the intricate interplay between ROS and immune functionality, this review provides an essential theoretical framework for developing innovative immunotherapy strategies aimed at restoring immune competency and improving clinical outcomes in patients with immune-related diseases.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"4 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143950011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}