MedComm – Oncology最新文献

{"title":"Analysis of reoperational reason of patients with thyroid cancer and strategies for its diagnosis and treatment: A 6-year single-center retrospective study","authors":"Rongli Xie, Yawei Feng, Jiankang Shen, Guohui Xiao, Dan Tan","doi":"10.1002/mog2.70008","DOIUrl":"https://doi.org/10.1002/mog2.70008","url":null,"abstract":"<p>The incidence of thyroid tumors has been increasing in recent years, and the vast majority of new malignant cases are papillary thyroid micro-carcinoma (PTMC).<span><sup>1</sup></span> For patients with PTMC, comprehensive diagnosis and treatment, led by surgery, is the key to clinical cure. Although the lethality of papillary thyroid carcinoma is very low, tumor proliferation mechanism and surgical method after recurrence are still a hot topic of debate.<span><sup>2-4</sup></span> In this paper, thyroid patients admitted from January 2015 to December 2020 were collected. The inclusion criteria were as follows: (1) age from 18 to 80 years old; (2) the first and subsequent surgeries for thyroid were performed in one single center; (3) the postoperative paraffin pathology confirmed thyroid tumor; and (4) the patient's clinical data were complete. In this study, the gender, age, surgical methods, tumor types, maximum diameter of tumor, metastasis of central neck group and lateral lymph nodes, postoperative complications, and length of hospital stay were collected and recorded. For patients with multiple surgeries, the reason for subsequent surgeries and the interval time between surgeries should be additionally recorded.</p><p>A total of 58 patients undergoing thyroid surgeries (1 patient with laparoscopic surgery was excluded) were collected in this study, as shown in Table 1. Fifteen patients in the observation group underwent central lymph node dissection and 26 patients in the lateral lymph node dissection, while only 1 patient in the control group underwent cervical lateral lymph node dissection, and there was a statistically significant difference in the overall surgical method between the two groups (<i>p</i> < 0.01).</p><p>In the control group, 4 cases of benign tumors and 21 cases of papillary carcinoma were confirmed by pathology after the surgery. However, 55 cases of postoperative pathology confirmed malignant tumors in the observation group, including 52 cases of papillary carcinoma, 2 cases of follicular carcinoma, and 1 case of medullary carcinoma. In patients with confirmed papillary carcinoma, the mean tumor size was 1.33 ± 0.14 cm (<i>p</i> < 0.001). The rate of lymph node metastasis in the central group was 27 out of 118 (<i>p</i> < 0.0001) and the rate of lateral lymph node metastasis was 162 out of 241 (<i>p</i> < 0.01), as shown in Table 1.</p><p>The average length of hospital stay in the observation group was 5.64 ± 0.30 days (<i>p</i> < 0.05). There were five cases of adverse reactions (<i>p</i> > 0.05) after the operation, including four cases of hoarseness, one case of choking cough (with hoarseness), and one case of hemorrhage. The average length of hospitalization in the control group was 4.44 ± 0.38 days, and no patients had obvious adverse reactions (Table S1).</p><p>Out of 58 patients who underwent multiple surgeries, 51 patients underwent two surgeries, and 7 patients underwent three surgeries. Am","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143114800","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":"Unraveling the underlying mechanisms of cancer stem cells in therapeutic resistance for optimizing treatment strategies","authors":"Yunhan Tan,&nbsp;Siyuan Qin,&nbsp;Zhe Zhang,&nbsp;Yongen Liu,&nbsp;Li Zhou,&nbsp;Bowen Li,&nbsp;Edouard C. Nice,&nbsp;Yuanyuan Zhang,&nbsp;Jing Jing","doi":"10.1002/mog2.70009","DOIUrl":"https://doi.org/10.1002/mog2.70009","url":null,"abstract":"<p>The success of cancer therapy has been significantly hampered by various mechanisms of therapeutic resistance. Chief among these mechanisms is the presence of clonal heterogeneity within an individual tumor mass. The introduction of the concept of cancer stem cells (CSCs)—a rare and immature subpopulation with tumorigenic potential that contributes to intratumoral heterogeneity—has deepened our understanding of drug resistance. Given the characteristics of CSCs, such as increased drug-efflux activity, enhanced DNA-repair capacity, high metabolic plasticity, adaptability to oxidative stress, and/or upregulated detoxifying aldehyde dehydrogenase (ALDH) enzymes, CSCs have been recognized as a theoretical reservoir for resistant diseases. Implicit in this recognition is the possibility that CSC-targeted therapeutic strategies might offer a breakthrough in overcoming drug resistance in cancer patients. Herein, we summarize the generation of CSCs and our current understanding of the mechanisms underlying CSC-mediated therapeutic resistance. This extended knowledge has progressively been translated into novel anticancer therapeutic strategies and significantly enriched the available options for combination treatments, all of which are anticipated to improve clinical outcomes for patients experiencing CSC-related relapse.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143113766","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 and cellular senescence: Roles in tumor progression and therapeutic opportunities","authors":"Ping Jin,&nbsp;Xu-Dong Feng,&nbsp;Cheng-Shuang Huang,&nbsp;Jia Li,&nbsp;Hui Wang,&nbsp;Xian-Mei Wang,&nbsp;Lei Li,&nbsp;Lan-Qing Ma","doi":"10.1002/mog2.70007","DOIUrl":"https://doi.org/10.1002/mog2.70007","url":null,"abstract":"<p>Oxidative stress results from an imbalance between the production and neutralization of reactive oxygen species. It induces oxidative damage to cellular components including proteins, lipids, nucleic acids, and membranes, therefore intrinsically linking to aging-related diseases such as cancer, cardiovascular disease, and neurological disorders. Emerging evidence suggests that oxidative stress may promote tumor development by influencing various aspects of cellular senescence, such as its onset, pro-inflammatory secretion, and alteration of cellular function and structure. Modulating oxidative stress to target cellular senescence offers a novel strategy for cancer prevention and treatment. However, a thorough grasp of the specific mechanisms at play is lacking. This review will present the association between oxidative stress and cellular senescence and their regulatory role in tumor progression and treatment, with emphasis on senescence-associated secretory phenotype, immunosenescence and therapy-induced senescence. Current agents and strategies that remove side effects of cellular senescence via killing senescent cancer cells or modulating oxidative stress to improve antitumor efficacy will be summarized. This review will help readers better understand the complex relationship between oxidative stress and senescence in cancer, and will also provide a basis for further research in this area.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143119011","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":"Redox regulation of cancer stem cells: Biology and therapeutic implications","authors":"Min Du,&nbsp;Jian Zhang,&nbsp;Max S. Wicha,&nbsp;Ming Luo","doi":"10.1002/mog2.70005","DOIUrl":"https://doi.org/10.1002/mog2.70005","url":null,"abstract":"<p>Cancer stem cells (CSCs) are a small group of tumor cells with the capacity to undergo self-renewal and differentiation. These cells not only initiate and maintain tumor growth, but also confer resistance to current cancer therapies. CSCs display a high degree of plasticity and can be generated under therapeutic stress via dedifferentiation from non-stem-like tumor cells, suggesting the necessity simultaneously targeting CSCs and bulk tumor cells to achieve the best therapeutic effect. Despite the findings that therapeutic stress induces CSC plasticity, the mechanisms underpinning CSC formation and therapeutic resistance are not fully defined. Tumor cells display elevated levels of reactive oxygen species (ROS), contributed by rapid proliferation, enhanced metabolic demands and oncogenic signaling. CSCs achieve redox homeostasis partly by regulating redox-sensitive transcription factors (TFs), including NRF2, HIF-1α, BACH1, NF-kB, FOXOs, AP-1, and others. This review aims to summarize the roles and underlying mechanisms of these TFs in regulation of CSCs and tumor progression from the perspectives of stem cell maintenance, metabolic reprogramming, epithelial–mesenchymal transition (EMT) and angiogenesis. We also discuss the potentials of utilizing specific inhibitors for these TFs in suppressing drug resistance and metastasis by repressing CSC activity, an approach that may provide new targeted therapies for advanced cancer and improve patient outcome.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142861114","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":"CSF@E-Hn: A bone marrow-targeted nanosystem for advanced treatment of hematological malignancies","authors":"Yinyan Jiang,&nbsp;Jianqiao Shentu,&nbsp;Yalu Chen","doi":"10.1002/mog2.70006","DOIUrl":"https://doi.org/10.1002/mog2.70006","url":null,"abstract":"&lt;p&gt;In a recent study published in &lt;i&gt;Nature Nanotechnology&lt;/i&gt;, the research teams of Professor Siwen Li and Professor Yueqing Gu introduced a bispecific bone marrow-targeted nanosystem, CSF@E-Hn, based on hematopoietic stem cell (HSC) nanovesicles (Hn).&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt; The system uses Hn vesicles, decorated with natural killer (NK) cell-activating ligands (aNKG2D) and tumor-targeting antibodies (aPD-L1), encapsulating colony-stimulating factor (CSF) to treat hematological malignancies. Experimental results confirmed the system's therapeutic efficacy in mouse models of acute myelogenous leukemia (AML) and multiple myeloma (MM) and demonstrated its ability to prevent tumor recurrence long-term.&lt;/p&gt;&lt;p&gt;Most malignant hematological tumors arise from uncontrolled clonal expansion of tumor cells within the bone marrow, leading to high mortality and recurrence rates. Although current treatments, including chemotherapy, immunotherapy, and cell therapy, have improved overall survival in patients with hematological malignancies, these strategies still face significant challenges. Targeting bone marrow tumor cells specifically, reducing toxic side effects, and preventing recurrence remain major hurdles due to the lack of effective bone marrow-targeting technologies and the difficulty in reversing the diseased bone marrow microenvironment.&lt;span&gt;&lt;sup&gt;2, 3&lt;/sup&gt;&lt;/span&gt; The unique physiological structure of the bone marrow also acts as a formidable barrier, severely limiting the development of in vivo targeting technologies. In this context, Hn shows great potential for overcoming these challenges. As an ideal carrier, Hn has several advantages: it mirrors the characteristics of parent cells, features a drug-loaded bilayer structure, has a small size, and exhibits low immunogenicity.&lt;span&gt;&lt;sup&gt;4, 5&lt;/sup&gt;&lt;/span&gt; However, how to translate these significant advantages into clinical treatment remains a critical issue in current research.&lt;/p&gt;&lt;p&gt;To address these challenges, the bone marrow-targeted nanosystem CSF@E-Hn, developed by the team of Professor Li and Professor Gu, innovatively fuses nanotechnology with immunotherapy. This system accomplishes precise bone marrow-targeted treatment by capitalizing on the natural bone marrow hematopoietic stem cells and the generation of memory T cells, thus remodeling the bone marrow microenvironment and augmenting the immune response. Additionally, the system possesses excellent biocompatibility and sustained release properties, guaranteeing favorable safety (Figure 1).&lt;/p&gt;&lt;p&gt;The research team conducted a comprehensive evaluation of CSF@E-Hn's performance and efficacy. In vitro experiments demonstrated that the nanosystem, after antibody modification of HSC cells, maintained stable size distribution in phosphate-buffered saline (PBS) and serum. CSF@E-Hn remained stable for up to 14 days under low-temperature storage and thawing at −80°C. When NK cells were isolated from the bone marrow of C57BL/6J mice, CSF@E-Hn eff","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142861158","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":"WNT2 blockade augments antitumor immunity by attenuating myeloid-derived suppressor cells in colorectal cancer","authors":"Cheng Cui,&nbsp;Tian-Tian Zhang,&nbsp;Qian Lin,&nbsp;Tu-Xiong Huang,&nbsp;En-Yu Rao,&nbsp;Ji-Hui Du,&nbsp;Li Fu","doi":"10.1002/mog2.70004","DOIUrl":"https://doi.org/10.1002/mog2.70004","url":null,"abstract":"<p>Colorectal cancer (CRC) ranks as one of the most common malignancies worldwide. Myeloid-derived suppressor cells (MDSCs) represent an immunosuppressive heterogeneous population of immature monocytes and granulocytes constituting a major obstacle for CRC therapy. Previous studies demonstrated that WNT2 is enriched in tumor microenvironment (TME), promoting CRC progression. However, the role of WNT2 in regulating MDSCs to facilitate CRC progression remains largely unexplored. Our analysis of The Cancer Genome Atlas (TCGA) database and blood samples from 50 primary and recurrent CRC patients revealed a positive correlation between WNT2 expression and MDSCs abundance. Treatment with recombinant WNT2 protein significantly enhanced the accumulation and immunosuppressive function of MDSCs in vitro. Conversely, anti-WNT2 monoclonal antibody remarkably reduced the percentage and functional activity of MDSCs in CRC tumor-bearing mice. Mechanistic analyses further demonstrated that WNT2 mediates MDSCs activities through the p38 MAPK/Akt pathway. Collectively, our findings not only highlight the pivotal role of WNT2 in CRC progression by enhancing MDSCs activities within the TME, but also provide evidence that WNT2 levels and MDSCs abundance in peripheral blood could serve as predictive biomarkers for early diagnosis and prognosis of CRC patients.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142859967","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 LAG-3 restores CD8+ T cell effector function through CD94/NKG2-Qa-1b signaling","authors":"Zhiqiang Wang,&nbsp;Mingzhu Yin,&nbsp;Ge Lou","doi":"10.1002/mog2.70003","DOIUrl":"https://doi.org/10.1002/mog2.70003","url":null,"abstract":"&lt;p&gt;A recent study published in &lt;i&gt;Cell&lt;/i&gt; by Ngiow et al. elucidates the synergistic roles of programmed cell death protein 1 (PD-1) and lymphocyte-activation gene 3 (LAG-3) in CD8&lt;sup&gt;+&lt;/sup&gt; T cells.&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt; The authors demonstrate that LAG-3 influences the fate of these cells by sustaining thymocyte selection-associated high mobility group box protein (TOX) expression and modulating the CD94/NKG2-Qa-1b axis in exhausted CD8&lt;sup&gt;+&lt;/sup&gt; T cells. This research enhances our understanding of the intricate mechanisms underlying immune checkpoint blockade and paves the way for novel approaches in cancer immunotherapy.&lt;/p&gt;&lt;p&gt;In chronic viral infections and cancers, CD8&lt;sup&gt;+&lt;/sup&gt; T cells, known as the “warriors” of the immune system, frequently experience exhaustion due to persistent antigenic stimulation. This exhaustion results in impaired proliferation and effector function of exhausted CD8&lt;sup&gt;+&lt;/sup&gt; T cells (Tex), ultimately leading to immune failure. The defining characteristics of Tex include a distinct TOX-driven transcriptional and epigenetic state, along with the sustained expression of various inhibitory receptors (IRs), such as PD-1, LAG-3, and cytotoxic T-lymphocyte antigen-4 (CTLA-4).&lt;span&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/span&gt; Recent advancements in immune checkpoint blockade therapies that target various IRs have significantly improved tumor treatment outcomes. However, only a subset of tumor patients exhibit sustained clinical responses to monotherapy with PD-1/programmed death-ligand 1 (PD-L1) blockade. Consequently, there is a growing interest in exploring the combination of multiple immune receptors to enhance the efficacy of immunotherapeutic approaches. A recent phase III clinical trial, RELATIVITY-047, demonstrated that combining a LAG-3 antibody (relatlimab) and a PD-1 antibody (nivolumab) exhibits enhanced clinical antitumor effects. However, the precise mechanisms by which PD-1 and LAG-3 regulate Tex function, as well as the interconnections between their signaling pathways, remain unclear.&lt;/p&gt;&lt;p&gt;Ngiow et al. investigated the effects of LAG-3 and PD-1 on CD8&lt;sup&gt;+&lt;/sup&gt; T cells at various stages of chronic infection using the Quad transplantation model. Their findings revealed that CD8&lt;sup&gt;+&lt;/sup&gt; T cells lacking PD-1 proliferated significantly faster during the early stages of infection; however, these cells became progressively less sustainable over time. In contrast, cells lacking LAG-3 demonstrated enhanced effector functions, particularly in terms of cytotoxicity and cytokine secretion. This indicates that PD-1 primarily inhibits cell proliferation, while LAG-3 restricts the multifunctionality and killing capacity of effector T cells as they transition into exhausted T cells. The researchers further investigated the mechanism by which LAG-3 influences the differentiation of Tex cells through the regulation of TOX expression. Their findings revealed that LAG-3 deficiency resulted in a significant reduction in TOX expres","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142707993","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":"Pharmacokinetics comparison of aumolertinib, osimertinib, gefitinib and their major metabolites in mouse model and NSCLC patients","authors":"Ran Ren,&nbsp;Jiangang Zhang,&nbsp;Yongpeng He,&nbsp;Xianghua Zeng,&nbsp;Yu Zhou,&nbsp;Luyao Shen,&nbsp;Yongsheng Li,&nbsp;Dairong Li,&nbsp;Huakan Zhao","doi":"10.1002/mog2.70002","DOIUrl":"https://doi.org/10.1002/mog2.70002","url":null,"abstract":"<p>The tyrosine kinase inhibitors (TKIs) of epidermal growth factor receptor (EGFR), such as osimertinib and gefitinib, aumolertinib have been widely used in EGFR mutation-positive non-small cell lung cancer (NSCLC) patients. However, the discrepancy of pharmacokinetic features and distributions in important tissues between these EGFR-TKIs remains obscure. In this study, an ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) method with specificity and accuracy was established. After a single equivalent dose ratio or equal dose gavage, aumolertinib displayed the shortest elimination half-life time (<i>t</i>_1/2), while it showed the largest area under the concentration–time curve in mouse plasma and bone marrow among these 3 EGFR-TKIs. Furthermore, at the time of reaching maximum concentration (<i>t</i>_max) after single equivalent dose ratio gavage, the concentrations of aumolertinib were significantly higher than that of osimertinib and gefitinib in 9 important tissues of mice. Moreover, after single oral administration, aumolertinib displayed the highest concentration in plasma samples from EGFR mutation-positive NSCLC patients. Collectively, our findings manifest that the bioavailability and tissue distribution features of aumolertinib are superior to those of osimertinib and gefitinib, providing a pharmacokinetic basis for the clinical application of aumolertinib and the development of next-generation EGFR-TKIs.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142708332","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":"Epigenetic remodeling under oxidative stress: Mechanisms driving tumor metastasis","authors":"Peilan Peng,&nbsp;Siyuan Qin,&nbsp;Lei Li,&nbsp;Zhijun He,&nbsp;Bowen Li,&nbsp;Edouard C. Nice,&nbsp;Li Zhou,&nbsp;Yunlong Lei","doi":"10.1002/mog2.70000","DOIUrl":"https://doi.org/10.1002/mog2.70000","url":null,"abstract":"<p>Tumor metastasis is a multistep, inefficient process orchestrated by diverse signaling pathways. Compared to primary tumor cells, disseminated tumor cells inevitably encounter higher oxidative stress in foreign environments. The levels of reactive oxygen species (ROS) fluctuate dynamically during different metastatic stages, adding complexity to the regulation of metastatic progression. Numerous studies suggest that epigenetic remodeling, a key reversible mechanism of gene regulation, plays a critical role in responding to oxidative stress and controlling gene expression profiles that drive metastasis. Despite extensive research, a comprehensive understanding of how oxidative stress impacts metastasis through epigenetic modifications remains elusive, such as DNA methylation, histone modification, ncRNAs, and m⁶A modification. Epigenetic therapeutic strategies, such as DNMT inhibitors, HDAC inhibitors (HDACis), and miRNA mimics, have shown promise, yet challenges related to immunogenicity, specificity, and delivery also exist. Furthermore, due to limited understanding, some drugs targeting m⁶A modification have yet to be explored. In this review, we provided an overview of how oxidative stress influences tumor metastatic behavior, summarized the epigenetic mechanisms involved in these processes, and reviewed the latest advancements in epigenetic-targeted therapies, which may pave the way to develop novel strategy for preventing or treating tumor metastasis.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.70000","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142642294","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":"Immunotherapy for gastric cancer: Advances and challenges","authors":"Pei Zhang,&nbsp;Chenyan Zhang,&nbsp;Xiaoying Li,&nbsp;Chen Chang,&nbsp;Cailing Gan,&nbsp;Tinghong Ye,&nbsp;Dan Cao","doi":"10.1002/mog2.92","DOIUrl":"https://doi.org/10.1002/mog2.92","url":null,"abstract":"<p>Gastric cancer (GC) ranks among the leading causes of cancer-related mortality globally. Often, its initial stages manifest subtly, and the infrequency of routine screenings contributes to late diagnoses in many cases. Systemic treatments for GC include chemotherapy, targeted therapy, and immunotherapy, among which immunotherapy is the first-line standard treatment for advanced GC. In recent years, immunotherapy has seen notable advancements, as evidenced by the Food and Drug Administration's approval of drugs such as nivolumab and pembrolizumab for GC treatment. Additionally, several other drugs are currently under rigorous preclinical and clinical investigation. This review aims to shed light on the recent advancements in immunotherapy for GC, particularly emphasizing the insights gained from phase 2/3 clinical trials that assess the efficacy, safety, and promise of various immunotherapeutic modalities, including immune checkpoint inhibitors, CAR-T-cell therapies, and cancer vaccines, in enhancing patient outcomes. Moreover, this review delves into the intricate immunological framework of GC, focusing on the tumor microenvironment, interactions among immune cells, and the roles of immune checkpoints such as PD-L1. We also address the hurdles and prospective paths forward in the realm of immunotherapy for GC, offering fresh viewpoints on potential therapeutic approaches in this evolving domain.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"3 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.92","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142587953","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}