Drug Resistance Updates最新文献

{"title":"Circulating tumor cells with increasing aneuploidy predict inferior prognosis and therapeutic resistance in small cell lung cancer","authors":"Zhongpeng Xie ,&nbsp;Yanxia Wang ,&nbsp;Tingfei Chen ,&nbsp;Wei Fan ,&nbsp;Lihong Wei ,&nbsp;Bixia Liu ,&nbsp;Xiaohua Situ ,&nbsp;Qinru Zhan ,&nbsp;Tongze Fu ,&nbsp;Tian Tian ,&nbsp;Shuhua Li ,&nbsp;Qiong He ,&nbsp;Jianwen Zhou ,&nbsp;Huipin Wang ,&nbsp;Juan Du ,&nbsp;Hsian-Rong Tseng ,&nbsp;Yiyan Lei ,&nbsp;Ke-Jing Tang ,&nbsp;Zunfu Ke","doi":"10.1016/j.drup.2024.101117","DOIUrl":"https://doi.org/10.1016/j.drup.2024.101117","url":null,"abstract":"<div><h3>Aims</h3><p>Treatment resistance commonly emerges in small cell lung cancer (SCLC), necessitating the development of novel and effective biomarkers to dynamically assess therapeutic efficacy. This study aims to evaluate the clinical utility of aneuploid circulating tumor cells (CTCs) for risk stratification and treatment response monitoring.</p></div><div><h3>Methods</h3><p>A total of 126 SCLC patients (two cohorts) from two independent cancer centers were recruited as the study subjects. Blood samples were collected from these patients and aneuploid CTCs were detected. Aneuploid CTC count (ACC) and aneuploid CTC score (ACS), were used to predict progression-free survival (PFS) and overall survival (OS). The performance of the ACC and the ACS was evaluated by calculating the area under the receiver operating characteristic (ROC) curve (AUC).</p></div><div><h3>Results</h3><p>Compared to ACC, ACS exhibited superior predictive power for PFS and OS in these 126 patients. Moreover, both univariate and multivariate analyses revealed that ACS was an independent prognostic factor. Dynamic ACS changes reflected treatment response, which is more precise than ACC changes. ACS can be used to assess chemotherapy resistance and is more sensitive than radiological examination (with a median lead time of 2.8 months; P &lt; 0.001). When patients had high ACS levels (&gt; 1.115) at baseline, the combination of immunotherapy and chemotherapy resulted in longer PFS (median PFS, 7.7 months; <em>P</em> = 0.007) and OS (median OS, 16.3 months; <em>P</em> = 0.033) than chemotherapy alone (median PFS, 4.9 months; median OS, 13.6 months).</p></div><div><h3>Conclusions</h3><p>ACS could be used as a biomarker for risk stratification, treatment response monitoring, and individualized therapeutic intervention in SCLC patients.</p></div>","PeriodicalId":51022,"journal":{"name":"Drug Resistance Updates","volume":"76 ","pages":"Article 101117"},"PeriodicalIF":15.8,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141594932","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}

{"title":"Mechanisms of sensitivity and resistance to CDK4/CDK6 inhibitors in hormone receptor-positive breast cancer treatment","authors":"Antonino Glaviano ,&nbsp;Seth A. Wander ,&nbsp;Richard D. Baird ,&nbsp;Kenneth C.-H. Yap ,&nbsp;Hiu Yan Lam ,&nbsp;Masakazu Toi ,&nbsp;Daniela Carbone ,&nbsp;Birgit Geoerger ,&nbsp;Violeta Serra ,&nbsp;Robert H. Jones ,&nbsp;Joanne Ngeow ,&nbsp;Eneda Toska ,&nbsp;Justin Stebbing ,&nbsp;Karen Crasta ,&nbsp;Richard S. Finn ,&nbsp;Patrizia Diana ,&nbsp;Karla Vuina ,&nbsp;Robertus A.M. de Bruin ,&nbsp;Uttam Surana ,&nbsp;Aditya Bardia ,&nbsp;Alan Prem Kumar","doi":"10.1016/j.drup.2024.101103","DOIUrl":"10.1016/j.drup.2024.101103","url":null,"abstract":"<div><p>Cell cycle dysregulation is a hallmark of cancer that promotes eccessive cell division. Cyclin-dependent kinase 4 (CDK4) and cyclin-dependent kinase 6 (CDK6) are key molecules in the G1-to-S phase cell cycle transition and are crucial for the onset, survival, and progression of breast cancer (BC). Small-molecule CDK4/CDK6 inhibitors (CDK4/6i) block phosphorylation of tumor suppressor Rb and thus restrain susceptible BC cells in G1 phase. Three CDK4/6i are approved for the first-line treatment of patients with advanced/metastatic hormone receptor-positive (HR⁺)/human epidermal growth factor receptor 2-negative (HER2^-) BC in combination with endocrine therapy (ET). Though this has improved the clinical outcomes for survival of BC patients, there is no established standard next-line treatment to tackle drug resistance. Recent studies suggest that CDK4/6i can modulate other distinct effects in both BC and breast stromal compartments, which may provide new insights into aspects of their clinical activity. This review describes the biochemistry of the CDK4/6-Rb-E2F pathway in HR⁺ BC, then discusses how CDK4/6i can trigger other effects in BC/breast stromal compartments, and finally outlines the mechanisms of CDK4/6i resistance that have emerged in recent preclinical studies and clinical cohorts, emphasizing the impact of these findings on novel therapeutic opportunities in BC.</p></div>","PeriodicalId":51022,"journal":{"name":"Drug Resistance Updates","volume":"76 ","pages":"Article 101103"},"PeriodicalIF":15.8,"publicationDate":"2024-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S136876462400061X/pdfft?md5=9dae70a41ea2429e508ee1587c59783f&pid=1-s2.0-S136876462400061X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141463858","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}

{"title":"Intercellular adhesion molecule-1 suppresses TMZ chemosensitivity in acquired TMZ-resistant gliomas by increasing assembly of ABCB1 on the membrane","authors":"Xin Zhang ,&nbsp;Yingying Tan ,&nbsp;Tao Li ,&nbsp;Dashan Tan ,&nbsp;Bin Fu ,&nbsp;Mengdi Yang ,&nbsp;Yaxin Chen ,&nbsp;Mengran Cao ,&nbsp;Chenyuan Xuan ,&nbsp;Qianming Du ,&nbsp;Rong Hu ,&nbsp;Qing Wang","doi":"10.1016/j.drup.2024.101112","DOIUrl":"10.1016/j.drup.2024.101112","url":null,"abstract":"<div><h3>Aims</h3><p>Despite aggressive treatment, the recurrence of glioma is an inevitable occurrence, leading to unsatisfactory clinical outcomes. A plausible explanation for this phenomenon is the phenotypic alterations that glioma cells undergo aggressive therapies, such as TMZ-therapy. However, the underlying mechanisms behind these changes are not well understood.</p></div><div><h3>Methods</h3><p>The TMZ chemotherapy resistance model was employed to assess the expression of intercellular adhesion molecule-1 (ICAM1) in both in vitro and in vivo settings. The potential role of ICAM1 in regulating TMZ chemotherapy resistance was investigated through knockout and overexpression techniques. Furthermore, the mechanism underlying ICAM1-mediated TMZ chemotherapy resistance was examined using diverse molecular biological methods, and the lipid raft protein was subsequently isolated to investigate the cellular subcomponents where ICAM1 operates.</p></div><div><h3>Results</h3><p>Acquired TMZ resistant (TMZ-R) glioma models heightened production of intercellular adhesion molecule-1 (ICAM1) in TMZ-R glioma cells. Additionally, we observed a significant suppression of TMZ-R glioma proliferation upon inhibition of ICAM1, which was attributed to the enhanced intracellular accumulation of TMZ. Our findings provide evidence supporting the role of ICAM1, a proinflammatory marker, in promoting the expression of ABCB1 on the cell membrane of TMZ-resistant cells. We have elucidated the mechanistic pathway by which ICAM1 modulates phosphorylated moesin, leading to an increase in ABCB1 expression on the membrane. Furthermore, our research has revealed that the regulation of moesin by ICAM1 was instrumental in facilitating the assembly of ABCB1 exclusively on the lipid raft of the membrane.</p></div><div><h3>Conclusions</h3><p>Our findings suggest that ICAM1 is an important mediator in TMZ-resistant gliomas and targeting ICAM1 may provide a new strategy for enhancing the efficacy of TMZ therapy against glioma.</p></div>","PeriodicalId":51022,"journal":{"name":"Drug Resistance Updates","volume":"76 ","pages":"Article 101112"},"PeriodicalIF":15.8,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1368764624000700/pdfft?md5=0d7967e1f48378679a6226daad3cb472&pid=1-s2.0-S1368764624000700-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141460568","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}

{"title":"Cancer plasticity in therapy resistance: Mechanisms and novel strategies","authors":"Xing Niu ,&nbsp;Wenjing Liu ,&nbsp;Yinling Zhang ,&nbsp;Jing Liu ,&nbsp;Jianjun Zhang ,&nbsp;Bo Li ,&nbsp;Yue Qiu ,&nbsp;Peng Zhao ,&nbsp;Zhongmiao Wang ,&nbsp;Zhe Wang","doi":"10.1016/j.drup.2024.101114","DOIUrl":"10.1016/j.drup.2024.101114","url":null,"abstract":"<div><p>Therapy resistance poses a significant obstacle to effective cancer treatment. Recent insights into cell plasticity as a new paradigm for understanding resistance to treatment: as cancer progresses, cancer cells experience phenotypic and molecular alterations, corporately known as cell plasticity. These alterations are caused by microenvironment factors, stochastic genetic and epigenetic changes, and/or selective pressure engendered by treatment, resulting in tumor heterogeneity and therapy resistance. Increasing evidence suggests that cancer cells display remarkable intrinsic plasticity and reversibly adapt to dynamic microenvironment conditions. Dynamic interactions between cell states and with the surrounding microenvironment form a flexible tumor ecosystem, which is able to quickly adapt to external pressure, especially treatment. Here, this review delineates the formation of cancer cell plasticity (CCP) as well as its manipulation of cancer escape from treatment. Furthermore, the intrinsic and extrinsic mechanisms driving CCP that promote the development of therapy resistance is summarized. Novel treatment strategies, e.g., inhibiting or reversing CCP is also proposed. Moreover, the review discusses the multiple lines of ongoing clinical trials globally aimed at ameliorating therapy resistance. Such advances provide directions for the development of new treatment modalities and combination therapies against CCP in the context of therapy resistance.</p></div>","PeriodicalId":51022,"journal":{"name":"Drug Resistance Updates","volume":"76 ","pages":"Article 101114"},"PeriodicalIF":15.8,"publicationDate":"2024-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141460567","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}

{"title":"Corrigendum to: “Circumventing drug resistance in gastric cancer: A spatial multi-omics exploration of chemo and immuno-therapeutic response dynamics” [Drug Resist Updates 74 (2024) 101080]","authors":"","doi":"10.1016/j.drup.2024.101101","DOIUrl":"10.1016/j.drup.2024.101101","url":null,"abstract":"","PeriodicalId":51022,"journal":{"name":"Drug Resistance Updates","volume":"76 ","pages":"Article 101101"},"PeriodicalIF":15.8,"publicationDate":"2024-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1368764624000591/pdfft?md5=2ead238e638e281ff287d547daeddbdc&pid=1-s2.0-S1368764624000591-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141428221","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}

{"title":"Surface chemistry engineered selenium nanoparticles as bactericidal and immuno-modulating dual-functional agents for combating methicillin-resistant Staphylococcus aureus Infection","authors":"Qingyue Bu ,&nbsp;Dan Jiang ,&nbsp;Yangyang Yu,&nbsp;Yunqing Deng,&nbsp;Tianfeng Chen,&nbsp;Ligeng Xu","doi":"10.1016/j.drup.2024.101102","DOIUrl":"10.1016/j.drup.2024.101102","url":null,"abstract":"<div><p>Because of the extremely complexed microenvironment of drug-resistant bacterial infection, nanomaterials with both bactericidal and immuno-modulating activities are undoubtedly the ideal modality for overcoming drug resistance. Herein, we precisely engineered the surface chemistry of selenium nanoparticles (SeNPs) using neutral (polyvinylpyrrolidone-PVP), anionic (letinan-LET) and cationic (chitosan-CS) surfactants. It was found that surface chemistry greatly influenced the bioactivities of functionalized SeNPs, their interactions with methicillin-resistant Staphylococcus aureus (MRSA), immune cells and metabolisms. LET-functionalized SeNPs with distinct metabolisms exhibited the best inhibitory efficacy compared to other kinds of SeNPs against MRSA through inducing robust ROS generation and damaging bacterial cell wall. Meanwhile, only LET-SeNPs could effectively activate natural kill (NK) cells, and enhance the phagocytic capability of macrophages and its killing activity against bacteria. Furthermore, <em>in vivo</em> studies suggested that LET-SeNPs treatment highly effectively combated MRSA infection and promoted wound healing by triggering much more mouse NK cells, CD8⁺ and CD4⁺ T lymphocytes infiltrating into the infected area at the early stage to efficiently eliminate MRSA in the mouse model. This study demonstrates that the novel functionalized SeNP with dual functions could serve as an effective antibacterial agent and could guide the development of next generation antibacterial agents.</p></div>","PeriodicalId":51022,"journal":{"name":"Drug Resistance Updates","volume":"76 ","pages":"Article 101102"},"PeriodicalIF":15.8,"publicationDate":"2024-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141463785","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}

{"title":"LncRNA DYNLRB2-AS1 promotes gemcitabine resistance of nasopharyngeal carcinoma by inhibiting the ubiquitination degradation of DHX9 protein","authors":"Kai-Lin Chen ,&nbsp;Sai-Wei Huang ,&nbsp;Ji-Jin Yao ,&nbsp;Shi-Wei He ,&nbsp;Sha Gong ,&nbsp;Xi-Rong Tan ,&nbsp;Ye-Lin Liang ,&nbsp;Jun-Yan Li ,&nbsp;Sheng-Yan Huang ,&nbsp;Ying-Qin Li ,&nbsp;Yin Zhao ,&nbsp;Han Qiao ,&nbsp;Sha Xu ,&nbsp;Shengbing Zang ,&nbsp;Jun Ma ,&nbsp;Na Liu","doi":"10.1016/j.drup.2024.101111","DOIUrl":"10.1016/j.drup.2024.101111","url":null,"abstract":"<div><p>Gemcitabine (GEM) based induction chemotherapy is a standard treatment for locoregionally advanced nasopharyngeal carcinoma (NPC). However, approximately 15 % of patients are still resistant to GEM-containing chemotherapy, which leads to treatment failure. Nevertheless, the underlying mechanisms of GEM resistance remain poorly understood. Herein, based on a microarray analysis, we identified 221 dysregulated lncRNAs, of which, DYNLRB2-AS1 was one of the most upregulated lncRNAs in GEM-resistance NPC cell lines. DYNLRB2-AS1 was shown to function as contain an oncogenic lncRNA that promoted NPC GEM resistance, cell proliferation, but inhibited cell apoptosis. Mechanistically, DYNLRB2-AS1 could directly bind to the DHX9 protein and prevent its interaction with the E3 ubiquitin ligase PRPF19, and thus blocking PRPF19-mediated DHX9 degradation, which ultimately facilitated the repair of DNA damage in the presence of GEM. Clinically, higher DYNLRB2-AS1 expression indicated an unfavourable overall survival of NPC patients who received induction chemotherapy. Overall, this study identified the oncogenic lncRNA DYNLRB2-AS1 as an independent prognostic biomarker for patients with locally advanced NPC and as a potential therapeutic target for overcoming GEM chemoresistance in NPC.</p></div>","PeriodicalId":51022,"journal":{"name":"Drug Resistance Updates","volume":"76 ","pages":"Article 101111"},"PeriodicalIF":15.8,"publicationDate":"2024-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141403928","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}

{"title":"Lansoprazole (LPZ) reverses multidrug resistance (MDR) in cancer through impeding ATP-binding cassette (ABC) transporter-mediated chemotherapeutic drug efflux and lysosomal sequestration","authors":"Ning Ji ,&nbsp;Hui Li ,&nbsp;Yixuan Zhang ,&nbsp;Yuelin Li ,&nbsp;Peiyu Wang ,&nbsp;Xin Chen ,&nbsp;Yi-Nan Liu ,&nbsp;Jing-Quan Wang ,&nbsp;Yuqi Yang ,&nbsp;Zhe-Sheng Chen ,&nbsp;Yueguo Li ,&nbsp;Ran Wang ,&nbsp;Dexin Kong","doi":"10.1016/j.drup.2024.101100","DOIUrl":"10.1016/j.drup.2024.101100","url":null,"abstract":"<div><h3>Aims</h3><p>Lansoprazole is one of the many proton pump inhibitors (PPIs) that acts more strongly with ABCB1 and ABCG2. The present study is to investigate the potential of lansoprazole on reversal of ABCB1/G2-mediated MDR in cancer, <em>in vitro</em> and <em>in vivo</em>.</p></div><div><h3>Methods</h3><p>Reversal studies and combination evaluation were conducted to determine the synergistic anti-MDR effects on lansoprazole. Lysosomal staining was used to determination of lansoprazole on ABCB1-mediated lysosomal sequestration. Substrate accumulation and efflux assays, ATPase activity, and molecular docking were conducted to evaluate lansoprazole on ABCB1/G2 functions. Western blot and immunofluorescence were used to detect lansoprazole on ABCB1/G2 expression and subcellular localization. MDR nude mice models were established to evaluate the effects of lansoprazole on MDR <em>in vivo</em>.</p></div><div><h3>Results</h3><p>Lansoprazole attenuated ABCB1/G2-mediated MDR and exhibited synergistic effects with substrate drugs in MDR cells. <em>In vivo</em> experiments demonstrated that lansoprazole attenuated ABCB1/G2-mediated MDR and exhibited synergistic effects that augmented the sensitivity of substrate anticancer drugs in ABCB1/G2-mediated settings without obvious toxicity. Lansoprazole impeded lysosomal sequestration mediated by ABCB1, leading to a substantial increase in intracellular accumulation of substrate drugs. The effects of lansoprazole were not attributable to downregulation or alterations in subcellular localization of ABCB1/G2. Lansoprazole promoted the ATPase activity of ABCB1/G2 and competitively bound to the substrate-binding region of ABCB1/G2.</p></div><div><h3>Conclusions</h3><p>These findings present novel therapeutic avenues whereby the combination of lansoprazole and chemotherapeutic agents mitigates MDR mediated by ABCB1/G2 overexpression.</p></div>","PeriodicalId":51022,"journal":{"name":"Drug Resistance Updates","volume":"76 ","pages":"Article 101100"},"PeriodicalIF":24.3,"publicationDate":"2024-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141276541","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}

{"title":"Targeting anoikis resistance as a strategy for cancer therapy","authors":"Yumin Wang ,&nbsp;Sihang Cheng ,&nbsp;Joshua S. Fleishman ,&nbsp;Jichao Chen ,&nbsp;Hailin Tang ,&nbsp;Zhe-Sheng Chen ,&nbsp;Wenkuan Chen ,&nbsp;Mingchao Ding","doi":"10.1016/j.drup.2024.101099","DOIUrl":"10.1016/j.drup.2024.101099","url":null,"abstract":"<div><p>Anoikis, known as matrix detachment-induced apoptosis or detachment-induced cell death, is crucial for tissue development and homeostasis. Cancer cells develop means to evade anoikis, e.g. anoikis resistance, thereby allowing for cells to survive under anchorage-independent conditions. Uncovering the mechanisms of anoikis resistance will provide details about cancer metastasis, and potential strategies against cancer cell dissemination and metastasis. Here, we summarize the principal elements and core molecular mechanisms of anoikis and anoikis resistance. We discuss the latest progress of how anoikis and anoikis resistance are regulated in cancers. Furthermore, we summarize emerging data on selective compounds and nanomedicines, explaining how inhibiting anoikis resistance can serve as a meaningful treatment modality against cancers. Finally, we discuss the key limitations of this therapeutic paradigm and possible strategies to overcome them. In this review, we suggest that pharmacological modulation of anoikis and anoikis resistance by bioactive compounds could surmount anoikis resistance, highlighting a promising therapeutic regimen that could be used to overcome anoikis resistance in cancers.</p></div>","PeriodicalId":51022,"journal":{"name":"Drug Resistance Updates","volume":"75 ","pages":"Article 101099"},"PeriodicalIF":24.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141232016","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}

{"title":"Application of biomimetic nanovaccines in cancer immunotherapy: A useful strategy to help combat immunotherapy resistance","authors":"Zhijie Xu ,&nbsp;Haiyan Zhou ,&nbsp;Tongfei Li ,&nbsp;Qiaoli Yi ,&nbsp;Abhimanyu Thakur ,&nbsp;Kui Zhang ,&nbsp;Xuelei Ma ,&nbsp;Jiang-Jiang Qin ,&nbsp;Yuanliang Yan","doi":"10.1016/j.drup.2024.101098","DOIUrl":"https://doi.org/10.1016/j.drup.2024.101098","url":null,"abstract":"<div><p>Breakthroughs in actual clinical applications have begun through vaccine-based cancer immunotherapy, which uses the body's immune system, both humoral and cellular, to attack malignant cells and fight diseases. However, conventional vaccine approaches still face multiple challenges eliciting effective antigen-specific immune responses, resulting in immunotherapy resistance. In recent years, biomimetic nanovaccines have emerged as a promising alternative to conventional vaccine approaches by incorporating the natural structure of various biological entities, such as cells, viruses, and bacteria. Biomimetic nanovaccines offer the benefit of targeted antigen-presenting cell (APC) delivery, improved antigen/adjuvant loading, and biocompatibility, thereby improving the sensitivity of immunotherapy. This review presents a comprehensive overview of several kinds of biomimetic nanovaccines in anticancer immune response, including cell membrane-coated nanovaccines, self-assembling protein-based nanovaccines, extracellular vesicle-based nanovaccines, natural ligand-modified nanovaccines, artificial antigen-presenting cells-based nanovaccines and liposome-based nanovaccines. We also discuss the perspectives and challenges associated with the clinical translation of emerging biomimetic nanovaccine platforms for sensitizing cancer cells to immunotherapy.</p></div>","PeriodicalId":51022,"journal":{"name":"Drug Resistance Updates","volume":"75 ","pages":"Article 101098"},"PeriodicalIF":24.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141244735","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}