Molecular Aspects of Medicine最新文献

英文中文

Targeting and engineering biomarkers for prostate cancer therapy

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-03-04 DOI: 10.1016/j.mam.2025.101359

Dhirodatta Senapati , Santosh Kumar Sahoo , Bhabani Shankar Nayak , Satyanarayan Senapati , Gopal C. Kundu , Subrat Kumar Bhattamisra

Prostate cancer (PCa) is the second most commonly occurring cancer among men worldwide. Although the clinical management of PCa has significantly improved, a number of limitations have been identified in both early diagnosis and therapeutic treatment. Because multiple studies show that prostate-specific antigen (PSA) screening frequently results in overdiagnosis and overtreatment, the use of PSA alone as a diagnostic marker for PCa screening has been controversial. For individuals with locally advanced or metastatic PCa, androgen deprivation therapy (ADT) is the standard initially successful treatment; nonetheless, the majority of patients will eventually develop lethal metastatic castration-resistant prostate cancer (CRPC). Alternative treatment options, including chemo-, immuno-,or radio-therapy, can only prolong the survival of CRPC patients for several months with the most developing resistance. Considering this background, there is an urgent need to discuss about selective prostate-specific biomarkers that can predict clinically relevant PCa diagnosis and to develop biomarker-driven treatments to counteract CRPC. This review addresses several PCa-specific biomarkers that will assist physicians in determining which patients are at risk of having high-grade PCa, focusing on the clinical relevance of these biomarker-based tests among PCa patients. Secondly, this review highlights the effective use of these markers as drug targets to develop precision medicine or targeted therapies to counteract CRPC. Altogether, translating this biomarker-based research into the clinic will pave the way for the effective execution of personalized therapies for the benefit of healthcare providers, the biopharmaceutical industry, and patients.

{"title":"Targeting and engineering biomarkers for prostate cancer therapy","authors":"Dhirodatta Senapati , Santosh Kumar Sahoo , Bhabani Shankar Nayak , Satyanarayan Senapati , Gopal C. Kundu , Subrat Kumar Bhattamisra","doi":"10.1016/j.mam.2025.101359","DOIUrl":"10.1016/j.mam.2025.101359","url":null,"abstract":"<div><div>Prostate cancer (PCa) is the second most commonly occurring cancer among men worldwide. Although the clinical management of PCa has significantly improved, a number of limitations have been identified in both early diagnosis and therapeutic treatment. Because multiple studies show that prostate-specific antigen (PSA) screening frequently results in overdiagnosis and overtreatment, the use of PSA alone as a diagnostic marker for PCa screening has been controversial. For individuals with locally advanced or metastatic PCa, androgen deprivation therapy (ADT) is the standard initially successful treatment; nonetheless, the majority of patients will eventually develop lethal metastatic castration-resistant prostate cancer (CRPC). Alternative treatment options, including chemo-, immuno-,or radio-therapy, can only prolong the survival of CRPC patients for several months with the most developing resistance. Considering this background, there is an urgent need to discuss about selective prostate-specific biomarkers that can predict clinically relevant PCa diagnosis and to develop biomarker-driven treatments to counteract CRPC. This review addresses several PCa-specific biomarkers that will assist physicians in determining which patients are at risk of having high-grade PCa, focusing on the clinical relevance of these biomarker-based tests among PCa patients. Secondly, this review highlights the effective use of these markers as drug targets to develop precision medicine or targeted therapies to counteract CRPC. Altogether, translating this biomarker-based research into the clinic will pave the way for the effective execution of personalized therapies for the benefit of healthcare providers, the biopharmaceutical industry, and patients.</div></div>","PeriodicalId":49798,"journal":{"name":"Molecular Aspects of Medicine","volume":"103 ","pages":"Article 101359"},"PeriodicalIF":8.7,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143548694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Decoding driver and phenotypic genes in cancer: Unveiling the essence behind the phenomenon

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-03-03 DOI: 10.1016/j.mam.2025.101358

Dequan Liu , Lei Liu , Xiaoman Zhang , Xinming Zhao , Xiaorui Li , Xiangyu Che , Guangzhen Wu

Gray hair, widely regarded as a hallmark of aging. While gray hair is associated with aging, reversing this trait through gene targeting does not alter the fundamental biological processes of aging. Similarly, certain oncogenes (such as CXCR4, MMP-related genes, etc.) can serve as markers of tumor behavior, such as malignancy or prognosis, but targeting these genes alone may not lead to tumor regression. We pioneered the name of this class of genes as "phenotypic genes". Historically, cancer genetics research has focused on tumor driver genes, while genes influencing cancer phenotypes have been relatively overlooked. This review explores the critical distinction between driver genes and phenotypic genes in cancer, using the MAPK and PI3K/AKT/mTOR pathways as key examples. We also discuss current research techniques for identifying driver and phenotypic genes, such as whole-genome sequencing (WGS), RNA sequencing (RNA-seq), RNA interference (RNAi), CRISPR-Cas9, and other genomic screening methods, alongside the concept of synthetic lethality in driver genes. The development of these technologies will help develop personalized treatment strategies and precision medicine based on the characteristics of relevant genes. By addressing the gap in discussions on phenotypic genes, this review significantly contributes to clarifying the roles of driver and phenotypic genes, aiming at advancing the field of targeted cancer therapy.

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引用次数: 0

Interactions between pathological and functional amyloid: A match made in Heaven or Hell?

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-03-01 DOI: 10.1016/j.mam.2025.101351

Daniel E. Otzen , Samuel Peña-Díaz , Jeremias Widmann , Anders Ogechi Hostrup Daugberg , Zhefei Zhang , Yanting Jiang , Chandrika Mittal , Morten K.D. Dueholm , Nikolaos Louros , Huabing Wang , Ibrahim Javed

The amyloid state of proteins occurs in many different contexts in Nature and in modern society, ranging from the pathological kind (neurodegenerative diseases and amyloidosis) via man-made forms (food processing and – to a much smaller extent - protein biologics) to functional versions (bacterial biofilm, peptide hormones and signal transmission). These classes all come together in the human body which endogenously produces amyloidogenic protein able to form pathological human amyloid (PaHA), hosts a microbiome which continuously makes functional bacterial amyloid (FuBA) and ingests food which can contain amyloid. This can have grave consequences, given that PaHA can spread throughout the body in a “hand-me-down” fashion from cell to cell through small amyloid fragments, which can kick-start growth of new amyloid wherever they encounter monomeric amyloid precursors. Amyloid proteins can also self- and cross-seed across dissimilar peptide sequences. While it is very unlikely that ingested amyloid plays a role in this crosstalk, FuBA-PaHA interactions are increasingly implicated in vivo amyloid propagation. We are now in a position to understand the structural and bioinformatic basis for this cross-talk, thanks to the very recently obtained atomic-level structures of the two major FuBAs CsgA (E. coli) and FapC (Pseudomonas). While there are many reports of homology-driven heterotypic interactions between different PaHA, the human proteome does not harbor significant homology to CsgA and FapC. Yet we and others have uncovered significant cross-stimulation (and in some cases inhibition) of FuBA and PaHA both in vitro and in vivo, which we here rationalize based on structure and sequence. These interactions have important consequences for the transmission and development of neurodegenerative diseases, not least because FuBA and PaHA can come into contact via the gut-brain interface, recurrent infections with microbes and potentially even through invasive biofilm in the brain. Whether FuBA and PaHA first interact in the gut or the brain, they can both stimulate and block each other's aggregation as well as trigger inflammatory responses. The microbiome may also affect amyloidogenesis in other ways, e.g. through their own chaperones which recognize and block growth of both PaHA and FuBA as we show both experimentally and computationally. Heterotypic interactions between and within PaHA and FuBA both in vitro and in vivo are a vital part of the amyloid phenomenon and constitute a vibrant and exciting frontier for future research.

{"title":"Interactions between pathological and functional amyloid: A match made in Heaven or Hell?","authors":"Daniel E. Otzen , Samuel Peña-Díaz , Jeremias Widmann , Anders Ogechi Hostrup Daugberg , Zhefei Zhang , Yanting Jiang , Chandrika Mittal , Morten K.D. Dueholm , Nikolaos Louros , Huabing Wang , Ibrahim Javed","doi":"10.1016/j.mam.2025.101351","DOIUrl":"10.1016/j.mam.2025.101351","url":null,"abstract":"<div><div>The amyloid state of proteins occurs in many different contexts in Nature and in modern society, ranging from the pathological kind (neurodegenerative diseases and amyloidosis) via man-made forms (food processing and – to a much smaller extent - protein biologics) to functional versions (bacterial biofilm, peptide hormones and signal transmission). These classes all come together in the human body which endogenously produces amyloidogenic protein able to form pathological human amyloid (PaHA), hosts a microbiome which continuously makes functional bacterial amyloid (FuBA) and ingests food which can contain amyloid. This can have grave consequences, given that PaHA can spread throughout the body in a “hand-me-down” fashion from cell to cell through small amyloid fragments, which can kick-start growth of new amyloid wherever they encounter monomeric amyloid precursors. Amyloid proteins can also self- and cross-seed across dissimilar peptide sequences. While it is very unlikely that ingested amyloid plays a role in this crosstalk, FuBA-PaHA interactions are increasingly implicated <em>in vivo</em> amyloid propagation. We are now in a position to understand the structural and bioinformatic basis for this cross-talk, thanks to the very recently obtained atomic-level structures of the two major FuBAs CsgA (<em>E. coli</em>) and FapC (<em>Pseudomonas</em>). While there are many reports of homology-driven heterotypic interactions between different PaHA, the human proteome does not harbor significant homology to CsgA and FapC. Yet we and others have uncovered significant cross-stimulation (and in some cases inhibition) of FuBA and PaHA both <em>in vitro</em> and <em>in vivo,</em> which we here rationalize based on structure and sequence. These interactions have important consequences for the transmission and development of neurodegenerative diseases, not least because FuBA and PaHA can come into contact via the gut-brain interface, recurrent infections with microbes and potentially even through invasive biofilm in the brain. Whether FuBA and PaHA first interact in the gut or the brain, they can both stimulate and block each other's aggregation as well as trigger inflammatory responses. The microbiome may also affect amyloidogenesis in other ways, <em>e.g.</em> through their own chaperones which recognize and block growth of both PaHA and FuBA as we show both experimentally and computationally. Heterotypic interactions between and within PaHA and FuBA both <em>in vitro</em> and <em>in vivo</em> are a vital part of the amyloid phenomenon and constitute a vibrant and exciting frontier for future research.</div></div>","PeriodicalId":49798,"journal":{"name":"Molecular Aspects of Medicine","volume":"103 ","pages":"Article 101351"},"PeriodicalIF":8.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143526764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Metabolic reprogramming shapes post-translational modification in macrophages

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-02-19 DOI: 10.1016/j.mam.2025.101338

Ziyi Han , Yinhao Shen , Yuqi Yan , Peng Bin , Meimei Zhang , Zhending Gan

Polarized macrophages undergo metabolic reprogramming, as well as extensive epigenetic and post-translational modifications (PTMs) switch. Metabolic remodeling and dynamic changes of PTMs lead to timely macrophage response to infection or antigenic stimulation, as well as its transition from a pro-inflammatory to a reparative phenotype. The transformation of metabolites in the microenvironment also determines the PTMs of macrophages. Here we reviewed the current understanding of the altered metabolites of glucose, lipids and amino acids in macrophages shape signaling and metabolism pathway during macrophage polarization via PTMs, and how these metabolites in some macrophage-associated diseases affect disease progression by shaping macrophage PTMs.

引用次数: 0

The recent blooming of therapeutic aptamers

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-02-10 DOI: 10.1016/j.mam.2025.101350

Valeriana Cesarini , Silvia Lucia Appleton , Vittorio de Franciscis , Daniele Catalucci

In the dynamic landscape of biomedical research, therapeutic RNA aptamers have recently come to the forefront, showing significant potential in diagnostics and therapeutics. This review aims to raise awareness of aptamer technology within the scientific community by exploring the progress made in the therapeutic field, from the lessons learned in research to the future opportunities and impact that these innovative molecules are increasingly having on society to meet current health needs, i.e. targeted and personalized therapies.

引用次数: 0

Disentangling the nutrition-microbiota liaison in inflammatory bowel disease

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-02-07 DOI: 10.1016/j.mam.2025.101349

Marilina Florio , Lucilla Crudele , Fabio Sallustio , Antonio Moschetta , Marica Cariello , Raffaella M. Gadaleta

Inflammatory Bowel Disease (IBD) is a set of chronic intestinal inflammatory disorders affecting the gastrointestinal (GI) tract. Beside compromised intestinal barrier function and immune hyperactivation, a common IBD feature is dysbiosis, characterized by a reduction of some strains of Firmicutes, Bacteroidetes, Actinobacteria and an increase in Proteobacteria and pathobionts. Emerging evidence points to diet and nutrition-dependent gut microbiota (GM) modulation, as etiopathogenetic factors and adjuvant therapies in IBD. Currently, no nutritional regimen shows universal efficacy, and advice are controversial, especially those involving restrictive diets potentially resulting in malnutrition. This review provides an overview of the role of macronutrients, dietary protocols and GM modulation in IBD patients. A Western-like diet contributes to an aberrant mucosal immune response to commensal bacteria and impairment of the intestinal barrier integrity, thereby triggering intestinal inflammation. Conversely, a Mediterranean nutritional pattern appears to be one of the most beneficial dietetic regimens able to restore the host intestinal physiology, by promoting eubiosis and preserving the intestinal barrier and immune function, which in turn create a virtuous cycle improving patient adherence to the pattern. Further clinical studies are warranted, to corroborate current IBD nutritional guidelines, and develop more accurate models to move forward precision nutrition and ameliorate patients’ quality of life.

{"title":"Disentangling the nutrition-microbiota liaison in inflammatory bowel disease","authors":"Marilina Florio , Lucilla Crudele , Fabio Sallustio , Antonio Moschetta , Marica Cariello , Raffaella M. Gadaleta","doi":"10.1016/j.mam.2025.101349","DOIUrl":"10.1016/j.mam.2025.101349","url":null,"abstract":"<div><div>Inflammatory Bowel Disease (IBD) is a set of chronic intestinal inflammatory disorders affecting the gastrointestinal (GI) tract. Beside compromised intestinal barrier function and immune hyperactivation, a common IBD feature is dysbiosis, characterized by a reduction of some strains of <em>Firmicutes</em>, <em>Bacteroidetes</em>, <em>Actinobacteria</em> and an increase in <em>Proteobacteria</em> and pathobionts. Emerging evidence points to diet and nutrition-dependent gut microbiota (GM) modulation, as etiopathogenetic factors and adjuvant therapies in IBD. Currently, no nutritional regimen shows universal efficacy, and advice are controversial, especially those involving restrictive diets potentially resulting in malnutrition. This review provides an overview of the role of macronutrients, dietary protocols and GM modulation in IBD patients. A Western-like diet contributes to an aberrant mucosal immune response to commensal bacteria and impairment of the intestinal barrier integrity, thereby triggering intestinal inflammation. Conversely, a Mediterranean nutritional pattern appears to be one of the most beneficial dietetic regimens able to restore the host intestinal physiology, by promoting eubiosis and preserving the intestinal barrier and immune function, which in turn create a virtuous cycle improving patient adherence to the pattern. Further clinical studies are warranted, to corroborate current IBD nutritional guidelines, and develop more accurate models to move forward precision nutrition and ameliorate patients’ quality of life.</div></div>","PeriodicalId":49798,"journal":{"name":"Molecular Aspects of Medicine","volume":"102 ","pages":"Article 101349"},"PeriodicalIF":8.7,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143349940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

When to suspect and how properly early detect and treat patients with endemic mycoses

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-02-05 DOI: 10.1016/j.mam.2025.101348

Arnaldo L. Colombo , Paula M. Peçanha-Pietrobom , Daniel Wagner de C.L. Santos , Diego H. Caceres

Endemic mycoses are caused by dimorphic fungi and eventually molds, as the case of implantation mycoses. In general, these diseases are acquired through trauma or inhalation of fungal elements in the environment, and less frequently by zoonotic acquisition or transmitted during organ transplantation. The target population for endemic mycoses is usually represented by normal hosts with low-income and intensive outdoor activities. Awareness of these diseases remains limited, even in regions with high prevalence, resulting in delayed diagnosis, and affecting the quality of life and outcomes of patients who suffer from these entities. In this review, we summarized relevant information about epidemiological, clinical, diagnostic, and treatment aspects of the most common endemic mycoses, including blastomycosis, coccidioidomycosis, histoplasmosis, paracoccidioidomycoses, talaromycosis, and implantation mycoses. The main goal of this review is to provide key concepts in terms of when to suspect, how early diagnose, and properly treat patients with these mycoses.

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引用次数: 0

The molecular code of kidney cancer: A path of discovery for gene mutation and precision therapy 肾癌的分子密码：基因突变和精准治疗的发现之路。

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-02-01 DOI: 10.1016/j.mam.2024.101335

Deqian Xie , Guandu Li , Zunwen Zheng , Xiaoman Zhang , Shijin Wang , Bowen Jiang , Xiaorui Li , Xiaoxi Wang , Guangzhen Wu

Renal cell carcinoma (RCC) is a malignant tumor with highly heterogeneous and complex molecular mechanisms. Through systematic analysis of TCGA, COSMIC and other databases, 24 mutated genes closely related to RCC were screened, including VHL, PBRM1, BAP1 and SETD2, which play key roles in signaling pathway transduction, chromatin remodeling and DNA repair. The PI3K/AKT/mTOR signaling pathway is particularly important in the pathogenesis of RCC. Mutations in genes such as PIK3CA, MTOR and PTEN are closely associated with metabolic abnormalities and tumor cell proliferation. Clinically, mTOR inhibitors and VEGF-targeted drugs have shown significant efficacy in personalized therapy. Abnormal regulation of metabolic reprogramming, especially glycolysis and glutamine metabolic pathways, provides tumor cells with continuous energy supply and survival advantages, and GLS1 inhibitors have shown promising results in preclinical studies. This paper also explores the potential of immune checkpoint inhibitors in combination with other targeted drugs, as well as the promising application of nanotechnology in drug delivery and targeted therapy. In addition, unique molecular mechanisms are revealed and individualized therapeutic strategies are explored for specific subtypes such as TFE3, TFEB rearrangement type and SDHB mutant type. The review summarizes the common gene mutations in RCC and their molecular mechanisms, emphasizes their important roles in tumor diagnosis, treatment and prognosis, and looks forward to the application prospects of multi-pathway targeted therapy, metabolic targeted therapy, immunotherapy and nanotechnology in RCC treatment, providing theoretical support and clinical guidance for individualized treatment and new drug development.

肾细胞癌（RCC）是一种具有高度异质性和复杂分子机制的恶性肿瘤。通过对TCGA、COSMIC等数据库的系统分析，筛选出24个与RCC密切相关的突变基因，包括VHL、PBRM1、BAP1和SETD2，这些基因在信号通路转导、染色质重塑和DNA修复中发挥关键作用。PI3K/AKT/mTOR信号通路在RCC的发病机制中尤为重要。PIK3CA、MTOR和PTEN等基因突变与代谢异常和肿瘤细胞增殖密切相关。临床上，mTOR抑制剂和vegf靶向药物在个体化治疗中已显示出显著的疗效。异常调节代谢重编程，特别是糖酵解和谷氨酰胺代谢途径，为肿瘤细胞提供了持续的能量供应和生存优势，GLS1抑制剂在临床前研究中显示出良好的效果。本文还探讨了免疫检查点抑制剂与其他靶向药物联合的潜力，以及纳米技术在药物传递和靶向治疗中的应用前景。此外，还揭示了TFE3、TFEB重排型和SDHB突变型等特定亚型的独特分子机制，并探索了个体化治疗策略。综述了RCC常见基因突变及其分子机制，强调其在肿瘤诊断、治疗和预后中的重要作用，展望了多途径靶向治疗、代谢靶向治疗、免疫治疗和纳米技术在RCC治疗中的应用前景，为个体化治疗和新药开发提供理论支持和临床指导。

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引用次数: 0

The folding and misfolding of multidomain proteins 多结构域蛋白的折叠和错误折叠。

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-02-01 DOI: 10.1016/j.mam.2025.101337

Stefano Gianni, Maurizio Brunori

Protein folding represents a vital process for any living organism. While significant insights have been gained from studying single-domain proteins, our current knowledge on the folding mechanisms of multidomain proteins remains relatively limited, primarily due to their inherent complexity. The principal aim of this review lies in summarizing the emerging view pertaining multi-domain folding, emphasizing their modular nature, which minimizes misfolding and facilitates evolutionary innovation. We discuss the energetic interplay between domains, highlighting particularly the cases where domain interactions lead to transient misfolded intermediates. These interactions can result in diverse effects, including cooperative folding and domain-specific perturbations, which are particularly relevant to the pathogenesis of neurodegenerative diseases like polyglutamine disorders. The review underscores the critical need to understand multidomain folding, to better comprehend and potentially mitigate the molecular underpinnings of protein misfolding diseases.

蛋白质折叠对任何生物体来说都是一个重要的过程。虽然从研究单域蛋白中获得了重要的见解，但我们目前对多域蛋白折叠机制的了解仍然相对有限，主要是由于它们固有的复杂性。本综述的主要目的在于总结有关多畴折叠的新兴观点，强调它们的模块化性质，从而最大限度地减少错误折叠并促进进化创新。我们讨论了区域之间的能量相互作用，特别强调了区域相互作用导致瞬态错误折叠中间体的情况。这些相互作用可导致多种影响，包括合作折叠和区域特异性扰动，这与神经退行性疾病（如多谷氨酰胺疾病）的发病机制特别相关。这篇综述强调了了解多结构域折叠的迫切需要，以便更好地理解和潜在地减轻蛋白质错误折叠疾病的分子基础。

引用次数: 0

Cancer vaccines: Target antigens, vaccine platforms and preclinical models 癌症疫苗：靶抗原、疫苗平台和临床前模型。

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-02-01 DOI: 10.1016/j.mam.2024.101324

Francesca Ruzzi , Federica Riccardo , Laura Conti , Lidia Tarone , Maria Sofia Semprini , Elisabetta Bolli , Giuseppina Barutello , Elena Quaglino , Pier-Luigi Lollini , Federica Cavallo

This review provides a comprehensive overview of the evolving landscape of cancer vaccines, highlighting their potential to revolutionize tumor prevention. Building on the success of vaccines against virus-related cancers, such as HPV- and HBV-associated cervical and liver cancers, the current challenge is to extend these achievements to the prevention of non-viral tumors and the treatment of preneoplastic or early neoplastic lesions. This review analyzes the critical aspects of preventive anti-cancer vaccination, focusing on the choice of target antigens, the development of effective vaccine platforms and technologies, and the use of various model systems for preclinical testing, from laboratory rodents to companion animals.

这篇综述全面概述了癌症疫苗的发展前景，强调了它们在肿瘤预防方面的革命性潜力。在针对病毒相关癌症（如与人乳头瘤病毒和乙肝病毒相关的宫颈癌和肝癌）的疫苗取得成功的基础上，目前的挑战是将这些成就扩展到预防非病毒性肿瘤和治疗肿瘤前或早期肿瘤病变。本文分析了预防性抗癌疫苗接种的关键方面，重点是目标抗原的选择，有效疫苗平台和技术的发展，以及从实验室啮齿动物到伴侣动物的各种临床前试验模型系统的使用。

引用次数: 0

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