Clinical and translational discovery最新文献

{"title":"Research progress on fusion genes in tumours","authors":"Yinyi Chang,&nbsp;Zitong Zhao,&nbsp;Yongmei Song","doi":"10.1002/ctd2.352","DOIUrl":"https://doi.org/10.1002/ctd2.352","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The concept of gene fusion describes the process of fusing two genes into one, which is closely linked to tumour occurrence and development and may even be the direct cause of some tumours. Due to their tumour-specific expression and ability to drive tumour occurrence and development, there is great potential for fusion genes to be used as diagnostic markers and targets for specific types of tumours.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Main body</h3>\u0000 \u0000 <p>Although many fusion genes have been detected so far, they mainly focus on a small number of highly recurrent fusion genes detected in patients' tumours. There are few studies on the functional mechanism and clinical relevance of rare gene fusions. Our review discusses the generation mechanisms, detection methods, biological functions, and mechanisms of action of fusion genes. Additionally, we discuss the clinical significance of fusion gene detection in some tumour types.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The function mechanism research of rare gene fusion is very necessary, and more functions of fusion genes independent of unfused/normal genes can be explored in future studies. There is still a long way to go in implementing precision tumour therapy targeting gene fusion.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72605,"journal":{"name":"Clinical and translational discovery","volume":"4 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ctd2.352","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141967546","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":"High-fat diet effects on brain mitochondrial complex I activity and protein lipoxidation: implications for translational medicine","authors":"Vetriselvan Subramaniyan,&nbsp;Ainil Hawa Jansi,&nbsp;Harshini Muruganantham","doi":"10.1002/ctd2.354","DOIUrl":"https://doi.org/10.1002/ctd2.354","url":null,"abstract":"<p>Recent research has highlighted the significant effects of high-fat diets (HFDs) on brain health, particularly focusing on mitochondrial complex I activity and protein lipoxidation. Mitochondrial complex I, the first enzyme of the electron transport chain, is crucial for oxidative phosphorylation and adenosine triphosphate (ATP) production. In individuals consuming an HFD, complex I activity notably increases, initially appearing beneficial due to enhanced energy production. However, this upregulation is linked to elevated reactive oxygen species (ROS) production, leading to oxidative stress and mitochondrial dysfunction. Over the past 5 years, studies have associated this imbalance with neurodegenerative conditions and cognitive decline in obese individuals.<span>¹</span></p><p>The brain's energy demands are met primarily through oxidative phosphorylation, with mitochondrial complex I playing a pivotal role. In the context of an HFD, complex I activity is upregulated, ostensibly to meet increased energy requirements. However, this heightened activity has a significant downside. Increased complex I activity is closely associated with ROS production, chemically reactive molecules containing oxygen. While ROS are normal byproducts of cellular metabolism, excessive ROS production can overwhelm the cell's antioxidant defences, leading to oxidative stress (Figure 1).<span>^{2, 3}</span></p><p>Oxidative stress is a critical factor in the pathogenesis of neurodegenerative diseases. It damages cellular components, including lipids, proteins and DNA, disrupting normal cellular functions and leading to cell death. In the brain, which has a high metabolic rate and limited regenerative capacity, oxidative stress is particularly detrimental. Studies have shown that in obese individuals, the brain exhibits higher levels of oxidative damage, correlated with cognitive impairments and increased risk of neurodegenerative disorders such as Alzheimer's disease. Lipoxidation, the oxidative modification of proteins by lipid peroxidation products, is another significant consequence of a HFD. Lipid peroxidation is a process where ROS attack polyunsaturated fatty acids in cell membranes, resulting in the formation of reactive lipid aldehydes. These aldehydes can covalently modify proteins, forming advanced lipoxidation end-products (ALEs). ALEs accumulate in neural tissues and alter protein structure and function, leading to impaired cellular processes and neuronal damage.<span>^{4, 5}</span></p><p>The brain's synaptic function is particularly vulnerable to lipoxidation. Synaptic proteins are essential for neurotransmission, and their modification by ALEs can disrupt signal transduction, leading to synaptic dysfunction, cognitive deficits and neurodegenerative changes. Recent studies have provided evidence that the increased ROS production due to elevated complex I activity accelerates lipid peroxidation, thereby enhancing protein lipoxidati","PeriodicalId":72605,"journal":{"name":"Clinical and translational discovery","volume":"4 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ctd2.354","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141967344","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":"Cross-sectional analysis of pharmaceutical industry payments to board-certified breast cancer specialists in Japan","authors":"Anju Murayama,&nbsp;Kenichi Higuchi,&nbsp;Hinari Kugo","doi":"10.1002/ctd2.331","DOIUrl":"https://doi.org/10.1002/ctd2.331","url":null,"abstract":"<p>Financial interactions between pharmaceutical companies and physicians introduce conflicts of interest among physicians, and can unduly influence physicians' clinical decision-making, such as increased use of non-recommended cancer treatments and higher healthcare expenditures. Breast cancer is the most common cancer for which there is a growing number of novel treatments. Nevertheless, the financial relationships between pharmaceutical companies and physicians treating patients with breast cancer remain unknown. Using payment data disclosed by major pharmaceutical companies in Japan between 2016 and 2020, this study examined size and trends in non-research payments from the pharmaceutical companies to breast cancer specialists who were board-certified by the Japanese Breast Cancer Society. A total of $17.2 million were made to 1349 or 77.8% of all board-certified breast cancer specialists over the five years. Of all specialists, 41.9% to 55.5% received the payments each year. The median payments per specialist were $1,149–$1,371 annually. Only 5op 1% and 10% of all specialists received 24.7% and 70.3% of all payments to the specialists. The payments per specialist significantly increased by 9.9% (95% confidence interval: 6.713.1, <i>p</i> &lt; 0.001) from 2016 to 2019, but decreased by 29.6% (95% CI: −34.4 to −24.5, <i>p</i> &lt; 0.001) in 2020 when the COVID-19 pandemic occurred. Given that even a small payment to physicians is associated with their clinical practice, it is imperative that these breast cancer specialists are more aware of the potential influence of payments on their decision-making.</p>","PeriodicalId":72605,"journal":{"name":"Clinical and translational discovery","volume":"4 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ctd2.331","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141966546","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":"Stroke in sickle cell patients, epidemiology, pathophysiology, systemic and surgical treatment options and prevention strategies","authors":"Siddharth Shah,&nbsp;Amelia H. Alberts,&nbsp;Tran B. Ngo,&nbsp;Brandon Lucke-Wold","doi":"10.1002/ctd2.303","DOIUrl":"https://doi.org/10.1002/ctd2.303","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>A hereditary haemoglobinopathy known as sickle cell disease (SCD) affects over 100 000 people in the United States severely. Cerebrovascular disease is a prominent consequence of SCD. By the age of 30, 53% of patients have silent cerebral infarcts (SCIs) (a stroke that occurs without any obvious symptoms because it damages a small part of the brain that isn't responsible for any essential functions), and by the age of 40, 3.8% have overt strokes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Main body</h3>\u0000 \u0000 <p>The multidimensional burden of cerebrovascular illness in SCD is reviewed in detail in this article, which includes both clinical strokes and the frequently asymptomatic SCIs. The intricate pathophysiology of SCD and stroke is explored. With SCD, there are currently very few methods for preventing primary and secondary stroke; the most common ones are hydroxyurea and blood transfusion. Nevertheless, not enough research has been done on the possible contributions of anticoagulation and aspirin to strokes linked to SCD. Promising evidence is also highlighted in the study, suggesting that new drugs intended to treat SCD may be able to alleviate leg ulcers and renal impairment in addition to reducing unusually high transcranial Doppler flow velocity – a crucial component of cerebrovascular events. Given that these novel medications specifically target haemolysis and vaso-occlusion, the two main causes of strokes in this population, more research is desperately needed to determine whether they are effective in avoiding strokes in people with SCD. The literature review also emphasizes how common healthcare inequities are and how they hinder advancements in SCD research and management in the United States.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>To successfully address these inequities, the evaluation recommends more funding for both SCD management and research, as well as for patient and clinician education. This multimodal viewpoint highlights the intricate terrain of cerebrovascular problems associated with SCD and the urgent need for all-encompassing and fair strategies to improve patient outcomes and advance research.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72605,"journal":{"name":"Clinical and translational discovery","volume":"4 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ctd2.303","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141968411","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":"The application of aptamers in the field of aging and age-related diseases","authors":"LiuJun Xu,&nbsp;Beier Jiang,&nbsp;WenJing Qiu,&nbsp;Chunxia Jiang,&nbsp;Feng Zhang,&nbsp;Weihong Tan","doi":"10.1002/ctd2.346","DOIUrl":"https://doi.org/10.1002/ctd2.346","url":null,"abstract":"<p>The world is transitioning into an aging society, a phenomenon that escalates the risk of age-related diseases, posing a significant threat to human health. Addressing how to delay aging or achieve healthy aging has become an urgent and pivotal issue. Presently, diverse anti-aging drugs are under development and entering clinical validation stages. However, the absence of specific aging biomarkers has hindered the identification of corresponding targets for diagnosing and treating aging and age-related diseases. Aptamer, a novel molecular recognition tool, has found broad application in diagnosing and treating various diseases. Additionally, cell-based selection holds the potential to identify unidentified molecules that could serve as biomarkers for diseases. Recent years have seen a surge in attention towards aging and age-related diseases, with the application of aptamer in this domain rapidly advancing. Consequently, this review will provide a concise overview of the aging, with a focus on the utilisation of aptamer in aging and age-related diseases.</p>","PeriodicalId":72605,"journal":{"name":"Clinical and translational discovery","volume":"4 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ctd2.346","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141968412","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":"Precision treatment paradigm: Genomic features and therapeutic implications in mesenchymal-epithelial transition-amplified gastric cancer","authors":"Yiyi Yu,&nbsp;Zhening Zhang,&nbsp;Mengxuan Zhu,&nbsp;Yu Shan,&nbsp;Yan Wang,&nbsp;Li Wei,&nbsp;Xuan Huang,&nbsp;Debin Sun,&nbsp;Zhao Peng,&nbsp;Tianshu Liu","doi":"10.1002/ctd2.350","DOIUrl":"https://doi.org/10.1002/ctd2.350","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Despite advances in treatments for gastric cancer (GC), new targets are needed to enhance treatment, especially when mesenchymal-epithelial transition (<i>MET</i>) amplification is involved. Therefore, we investigated the genomic features of <i>MET</i>-amplified GC and efficacy of anti-<i>MET</i> therapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Genomic features were investigated in 2284 patients (cohort 1) and 438 patients in the Cancer Genome Atlas (TCGA cohort). RNA data were obtained from TCGA for expression analysis. Clinical responses of 71 patients (cohort 2) were investigated. Survival rates were compared by Kaplan–Meier and log-rank tests.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In cohort 1, 95 (4.2%) exhibited <i>MET</i> amplifications. In TCGA cohort, 15 (3.4%) exhibited <i>MET</i> amplifications. The five top mutated genes were <i>TP53</i>, <i>CDH1</i>, <i>ARID1A</i>, <i>KMT2D</i> and <i>PIK3CA</i> in cohort 1 and <i>TTN</i>, <i>TP53</i>, <i>MUC16</i>, <i>LRP1B</i> and <i>SYNE1</i> in TCGA cohort. <i>TP53</i>, <i>PIK3CA</i>, <i>KRAS</i> and <i>GNAS</i> showed significant single nucleotide variants (SNVs) in cohort 1, and <i>TP53</i> SNVs were significant in TCGA cohort. Fifteen and 18 genes showed significant copy number variations (CNVs) between the <i>MET</i>- and non-<i>MET</i>-amplified groups in cohort 1 and TCGA cohort, respectively. The PI3K pathway was significantly activated in Chinese patients with <i>MET</i>-amplified GC (<i>p</i> = 0.002). TP53 expression is negatively associated with <i>MET</i> amplification. Real-world data obtained with cohort 2 revealed that anti-<i>MET</i> treatment significantly affected overall survival (OS) (<i>p</i> = 0.002), whereas CNVs did not affect progression-free or OS even when treatment lines were considered.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p><i>MET-</i>amplified GC has a distinctive mutation landscape. Our findings provide valuable information for clinicians who treat patients with <i>MET-</i>amplified GC.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72605,"journal":{"name":"Clinical and translational discovery","volume":"4 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ctd2.350","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141968416","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":"Exporting nuclear export inhibitors from hematologic to solid tumour malignancies","authors":"Alexandra Chirino,&nbsp;Alyssa Maye,&nbsp;Justin Taylor","doi":"10.1002/ctd2.356","DOIUrl":"https://doi.org/10.1002/ctd2.356","url":null,"abstract":"<p>Exportin 1 (XPO1), formerly known as chromosomal region maintenance 1, belongs to the karyopherin family of proteins that are responsible for the import and export of macromolecules through the nuclear pore complex. XPO1 is the sole exporter of hundreds of cargoes including several RNA species and key proteins such as tumor suppressors and cell cycle proteins. Despite its essential and housekeeping function in normal cells, in their review, Lai et al note that upregulation of XPO1 is associated with a wide variety of cancers, including but not limited to colorectal cancer, osteosarcoma, lung cancer, gastric cancer, ovarian cancer, glioma, pancreatic cancer and oesophagal cancer.<span>¹</span> In non-cancer cells, XPO1 shuttles RNA and proteins from the nucleus to the cytoplasm while also regulating mitosis during interphase. After performing its export function, XPO1 returns to the nucleus to repeat the process, making it a vital part of sustaining normal cellular physiological functions (Figure 1). However, increased expression of XPO1 leads to increased export and imbalance of nucleo-cytoplasmic transport.</p><p>Though the exact mechanisms regulating the overexpression of XPO1 in solid cancers are not yet completely understood, chromosome 2p amplification accounts for this in a subset of hematologic neoplasms. Another means of dysregulation of XPO1 that is found in hematologic malignancies is the missense mutation <i>XPO1</i> E517K, which has been linked to facilitating the growth of malignant B cells in chronic lymphocytic leukaemia and Hodgkin lymphoma.<span>²</span> Clinical trials of XPO1 inhibitors in hematologic malignancies have shown response rates ranging from 26% to 45% in those with advanced multiple myeloma, and a 28% response rate in those with relapsed or refractory diffuse large B cell lymphoma.<span>^3-5</span> Due to this success, selinexor, the first-in-class XPO1 inhibitor has been Food and Drug Administration-approved for these two indications.</p><p>This leads to the big question—can targeting XPO1 be successful in solid tumours? According to Lai et al, while promising, it comes with considerable challenges. The first XPO1 inhibitors were natural products that irreversibly bound XPO1 and caused severe toxic side effects, leading to the discontinuation of their development as anticancer therapies. In response, small molecule XPO1 inhibitors were designed to be slowly reversible and are more tolerable in patients. Preclinical data suggests that selinexor is active in tumours with previous drug resistance in vitro and in vivo and induces apoptosis in many cancerous cell lines including but not limited to prostate, bladder, and renal cell carcinoma. While reducing the tumour is the main goal for these preclinical studies, there are questions of dose dependency for cancers like sarcomas, which may not be feasible for humans in clinical trials.<span>⁶</span> However, that is not to di","PeriodicalId":72605,"journal":{"name":"Clinical and translational discovery","volume":"4 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ctd2.356","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141968288","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":"Bacterial surface derived extracellular vesicles: A ground-breaking approach in cancer therapy","authors":"Asmit Das,&nbsp;Swarup Sonar,&nbsp;Ketki Kalele,&nbsp;Vetriselvan Subramaniyan","doi":"10.1002/ctd2.351","DOIUrl":"10.1002/ctd2.351","url":null,"abstract":"<p>Conventional cancer therapies are often limited by inherent and acquired drug resistance, non-specific toxicity, and suboptimal drug delivery. Bacterial extracellular vesicles (BEVs), including outer membrane vesicles and membrane vesicles, present a novel therapeutic strategy for cancer treatment. BEVs were found in both Gram-negative and Gram-positive bacteria. This article provides a classified investigation of the therapeutic potential of BEVs in cancer treatment. We discuss the molecular mechanisms underlying their observed anti-tumor effects, including the induction of apoptosis in cancer cells, suppression of angiogenesis within the tumor microenvironment, and stimulation of both innate and adaptive anti-tumor immune responses. Moreover, BEVs being biocompatible opens avenue for targeted drug delivery systems, potentially improving the therapeutic index of conventional chemotherapeutics. Challenges to clinical translation, such as BEV heterogeneity and potential immunogenicity, are addressed. We also explore future directions for research and development, comprehensively highlighting how BEVs transform the landscape of precision oncology and cancer treatment, eventually improving patient outcomes.</p>","PeriodicalId":72605,"journal":{"name":"Clinical and translational discovery","volume":"4 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ctd2.351","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141797183","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":"The crosstalk between N6-methyladenosine readers and neuroblastoma","authors":"Liping Chen,&nbsp;Jing He,&nbsp;Zhenjian Zhuo","doi":"10.1002/ctd2.344","DOIUrl":"10.1002/ctd2.344","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Neuroblastoma (NB) is a heterogeneous pediatric solid tumour strongly influenced by epigenetic modifications.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This review explores the role of N6-methyladenosine (m6A) modifications and their readers in NB progression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Dysregulation of m6A readers, including YTHDF1/2, YTHDC1, IGF2BP1/2/3, HNRNPA2B1 and HNRNPC, has been associated with susceptibility and progression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Understanding the crosstalk between m6A readers and NB could offer new insights into diagnosis, prognosis, and treatment strategies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72605,"journal":{"name":"Clinical and translational discovery","volume":"4 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ctd2.344","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141810680","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":"Plant-derived exosomes: A Green Nanomedicine for Cancer","authors":"Swarup Sonar,&nbsp;Krishnan Anand","doi":"10.1002/ctd2.333","DOIUrl":"10.1002/ctd2.333","url":null,"abstract":"<p>Exosomes are signalling molecules related to cell-to-cell communication. Based on sources (plants, stem cells, and immune cells derived exosomes) it offers promising therapeutic activity against cancer. Plant-derived exosomes (PDEs) are natural extracellular vesicles (EVs) that are potent to provide organic precision nanomedicine to cancer therapeutics including targeted drug delivery. PDEs are gaining attention due to their safety and efficacy. There are plenty of different sources of PDEs in nature. This article explores various plants such as carrots, ginger, lemons, cabbages, blueberries, oranges, tomatoes, grapefruits, and tea leaves, which provide exosomes with distinct therapeutic properties, including anti-inflammatory, antioxidant, and anticancer activities. PDEs exhibit significant potential in drug delivery. Ongoing research and clinical trials predict that PDEs will become effective, and affordable solutions for cancer treatment.</p>","PeriodicalId":72605,"journal":{"name":"Clinical and translational discovery","volume":"4 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ctd2.333","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141818336","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}