Biochimica et biophysica acta. Reviews on cancer最新文献

英文中文

Precision oncology: Using cancer genomics for targeted therapy advancements 精准肿瘤学：利用癌症基因组学推进靶向治疗。

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2025-02-01 DOI: 10.1016/j.bbcan.2024.189250

Cigir Biray Avci , Bakiye Goker Bagca , Behrouz Shademan , Leila Sabour Takanlou , Maryam Sabour Takanlou , Alireza Nourazarian

Cancer genomics plays a crucial role in oncology by enhancing our understanding of how genes drive cancer and facilitating the development of improved treatments. This field meticulously examines various cancers' genetic makeup through various methodologies, leading to groundbreaking discoveries. Innovative tools such as rapid gene sequencing, single-cell studies, spatial gene mapping, epigenetic analysis, liquid biopsies, and computational modeling have significantly progressed the field. These techniques uncover genetic alterations, tumor heterogeneity, and the evolutionary dynamics of cancers. Genetic abnormalities and molecular markers that initiate and propagate distinct cancer types are classified according to tumor type. The integration of precision medicine with cancer genomics emphasizes the significance of utilizing genetic data in treatment decision-making, enabling personalized care and enhancing patient outcomes. Critical topics in cancer genomics encompass tumor diversity, alterations in non-coding DNA, epigenetic modifications, cancer-specific proteins, metabolic changes, and the impact of inherited genes on cancer risk.

癌症基因组学在肿瘤学中发挥着至关重要的作用，增强了我们对基因驱动癌症的理解，促进了改进治疗方法的发展。该领域通过各种方法细致地检查各种癌症的基因组成，从而产生突破性的发现。快速基因测序、单细胞研究、空间基因定位、表观遗传分析、液体活检和计算模型等创新工具在该领域取得了重大进展。这些技术揭示了基因改变、肿瘤异质性和癌症的进化动力学。启动和传播不同癌症类型的遗传异常和分子标记根据肿瘤类型进行分类。精准医学与癌症基因组学的结合强调了在治疗决策中利用基因数据、实现个性化护理和提高患者预后的重要性。癌症基因组学的关键课题包括肿瘤多样性、非编码DNA的改变、表观遗传修饰、癌症特异性蛋白、代谢变化以及遗传基因对癌症风险的影响。

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引用次数: 0

A comprehensive view of N-glycosylation as clinical biomarker in prostate cancer n -糖基化作为前列腺癌临床生物标志物的综合观点。

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2025-02-01 DOI: 10.1016/j.bbcan.2024.189239

Lissa Eggermont , Nicolaas Lumen , Charles Van Praet , Joris Delanghe , Sylvie Rottey , Tijl Vermassen

Alterations in the prostate cancer (PCa) N-glycome have gained attention as a potential biomarker. This comprehensive review explores the diversity of N-glycosylation patterns observed in PCa-related cell lines, tissue, serum and urine, focusing on prostate-specific antigen (PSA) and the total pool of glycoproteins. Within the context of PCa, altered N-glycosylation patterns are a mechanism of immune escape and a disruption in normal glycoprotein distribution and trafficking. Glycoproteins with PCa-induced N-glycosylation patterns tend to accumulate in prostate tissue and the bloodstream, thereby diminishing N-glycan proportions in urine. Based on literary observations, aberrations in N-glycan branching are probably a characteristic of metabolic reprogramming and (chronic) inflammation. Changes in (core) fucosylation, specific N-glycosylation structures (such as N,N′-diacetyllactosamine) and high-mannose glycans otherwise are more likely indicators of cancer development and progression. Further investigation into these PCa-specific alterations holds promise in the discovery of new diagnostic, prognostic and response prediction biomarkers in PCa.

作为一种潜在的生物标记物，前列腺癌（PCa）N-糖基化结果的改变已引起人们的关注。本综述探讨了在 PCa 相关细胞系、组织、血清和尿液中观察到的 N-糖基化模式的多样性，重点是前列腺特异性抗原（PSA）和糖蛋白总库。在 PCa 的背景下，N-糖基化模式的改变是一种免疫逃逸机制，也是正常糖蛋白分布和运输的中断。具有 PCa 诱导的 N-糖基化模式的糖蛋白往往会在前列腺组织和血液中积聚，从而降低尿液中 N-糖的比例。根据文献观察，N-糖分支的畸变可能是新陈代谢重编程和（慢性）炎症的一个特征。而（核心）岩藻糖基化、特定 N-糖基化结构（如 N,N'-二乙酰半乳糖胺）和高甘露糖的变化则更有可能是癌症发展和恶化的指标。对这些 PCa 特异性改变的进一步研究有望发现新的 PCa 诊断、预后和反应预测生物标志物。

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引用次数: 0

The comparison of pathogenic role and mechanism of Kallistatin and PEDF in tumors

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2025-01-27 DOI: 10.1016/j.bbcan.2025.189273

Jiayi Lyu , Simin Wang , Jingnan Chen , Xia Yang , Guoquan Gao , Ti Zhou

Tumors are diseases caused by abnormal cell division and growth, which can be life-threatening if not treated properly. Serpin inhibitors play a crucial role in regulating pathophysiological process and are promising drug targets. Kallistatin (SERPINA4) and Pigment Epithelium-Derived Factor (PEDF, SERPINF1) are two serpins that lack protease inhibitory activity but are abundant in blood. They exhibit anti-angiogenic effects and are involved in tumorigenesis. The pathogenic role and mechanism of Kallistatin and pigment epithelium-derived factor (PEDF) have been extensively studied for their potential use in cancer therapy. Kallistatin and PEDF play significant roles in controlling tumor growth and progression. While they share some common mechanisms of action, such as promoting apoptosis and inhibiting angiogenesis, they also have distinct differences in effectiveness and range of anti-tumor activities. This review compares and contrasts the expression patterns, structural features, expression regulation, disease roles, signaling pathways, and potential clinical value of Kallistatin and PEDF, aiming to provide a comprehensive understanding of their biomedical and clinical potential.

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引用次数: 0

An update on regulation and function of G protein-coupled receptors in cancer: A promising strategy for cancer therapy 癌症中 G 蛋白偶联受体的调控和功能的最新进展：一种前景广阔的癌症治疗策略

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2025-01-27 DOI: 10.1016/j.bbcan.2025.189266

Lin Li , Zihao An , Chao Lin , Qiang Xu , Chao Tang

G protein-coupled receptors (GPCRs) are a large family of cell surface receptors that play a crucial role in signal transduction and cellular communication. GPCR proteins are involved in a wide range of physiological processes, including cell growth, migration, and survival. Dysregulation of GPCR protein expression has been implicated in the pathogenesis of various diseases, including cancer, and GPCR proteins have been shown to modulate these processes in various types of cancer, highlighting their importance as potential therapeutic targets. In this review, we summarize the expression regulation of GPCRs in cancer cells, update the various ways by which the abnormal expression of GPCR protein affects the behavior of tumor cells, and discuss the current research directions and potentially facing problems of strategies on GPCR-targeting therapy.

引用次数: 0

Modulation of N-glycosylation in the PD-1: PD-L1 axis as a strategy to enhance cancer immunotherapies

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2025-01-26 DOI: 10.1016/j.bbcan.2025.189274

Monika Granica , Gustaw Laskowski , Paweł Link-Lenczowski , Agnieszka Graczyk-Jarzynka

The modulation of the N-glycosylation status in immune checkpoints, particularly the PD-1/PD-L1 axis, has emerged as a promising approach to enhance cancer immunotherapies. While immune checkpoint inhibitors (ICIs) targeting PD-1 and PD-L1 have achieved significant clinical success, recent studies highlight the critical role of N-glycosylation in regulating their expression, stability, and function. Alterations in N-glycosylation might affect the efficacy of ICIs by modulating the interactions between immune checkpoints and antibodies used in therapy. This review focuses on the glycosylation of PD-1 and its ligands PD-L1 and PD-L2, examining how N-glycans influence immune responses and contribute to immune evasion by tumors. It explores innovative strategies to modulate glycosylation in tumor and immune cells, including the use of N-glycosylation inhibitors and novel genetic manipulation techniques. Understanding the interplay between N-glycosylation and immune checkpoint functions is essential for optimizing immunotherapy outcomes and overcoming therapeutic resistance in cancer patients.

{"title":"Modulation of N-glycosylation in the PD-1: PD-L1 axis as a strategy to enhance cancer immunotherapies","authors":"Monika Granica , Gustaw Laskowski , Paweł Link-Lenczowski , Agnieszka Graczyk-Jarzynka","doi":"10.1016/j.bbcan.2025.189274","DOIUrl":"10.1016/j.bbcan.2025.189274","url":null,"abstract":"<div><div>The modulation of the <em>N</em>-glycosylation status in immune checkpoints, particularly the PD-1/PD-L1 axis, has emerged as a promising approach to enhance cancer immunotherapies. While immune checkpoint inhibitors (ICIs) targeting PD-1 and PD-L1 have achieved significant clinical success, recent studies highlight the critical role of <em>N-</em>glycosylation in regulating their expression, stability, and function. Alterations in <em>N</em>-glycosylation might affect the efficacy of ICIs by modulating the interactions between immune checkpoints and antibodies used in therapy. This review focuses on the glycosylation of PD-1 and its ligands PD-L1 and PD-L2, examining how <em>N-</em>glycans influence immune responses and contribute to immune evasion by tumors. It explores innovative strategies to modulate glycosylation in tumor and immune cells, including the use of <em>N-</em>glycosylation inhibitors and novel genetic manipulation techniques. Understanding the interplay between <em>N-</em>glycosylation and immune checkpoint functions is essential for optimizing immunotherapy outcomes and overcoming therapeutic resistance in cancer patients.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 2","pages":"Article 189274"},"PeriodicalIF":9.7,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143061566","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}

引用次数: 0

Membrane drug transporters in cancer: From chemoresistance mechanism to therapeutic strategies

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2025-01-23 DOI: 10.1016/j.bbcan.2025.189272

Chao Pan , Leo Tsz On Lee

Chemoresistance is a multifactorial phenomenon and the primary cause to the ineffectiveness of oncotherapy and cancer recurrence. Membrane drug transporters are crucial for drug delivery and disposition in cancer cells. Changes in the expression and functionality of these transporters lead to decreased intracellular accumulation and reduced toxicity of antineoplastic drugs. As the mechanism has been better understood and genetic engineering technology progressed quickly in recent years, some novel targeting strategies have come to light. This article summarizes the regulatory mechanisms of membrane drug transporters and provides an extensive review of current approaches to address transporters-mediated chemoresistance. These strategies include the use of chemical inhibitors to block efflux transporters, the development of copper chelators to enhance platinum drug uptake, the delivery of genetic drugs to alter transporter expression, the regulation of transcription and post-translational modifications. Additionally, we provide information of the clinical trial performance of the related targeting strategies, along with the ongoing challenges. Even though some clinical trials failed due to unexpected side effects and limited therapeutic efficacy, the advent of targeting membrane drug transporters still presents a hopeful path for overcoming chemoresistance.

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引用次数: 0

Epigenetic modulation by oncolytic viruses: Implications for cancer therapeutic efficacy

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2025-01-22 DOI: 10.1016/j.bbcan.2025.189270

Muhammad Haris Sultan, Qi Zhan, Hao Jin, Xiaoyuan Jia, Yigang Wang

Among various therapeutic agents, Oncolytic Viruses (OVs) are the most promising anticancer therapeutics because of their tumor-specific targeting and capability to mediate an antitumor immune response. In this review, we will discuss how epigenetic reprogramming of both the host and tumor can facilitate increased sensitivity of tumors to OV therapy. OVs infect tumor cells and modulate epigenetic landscapes, including DNA methylation, histone modifications, and chromatin remodeling, as well as non-coding RNA expression that consequently induces immune responses. These epigenetic changes, including hypermethylation of tumor-associated antigen genes and chromatin accessibility alterations, enhance the immunogenicity of tumors to facilitate recognition by the immune system. Here, we provide a general review addressing this question by discussing the potential benefits of combining OVs with epigenetic drugs to combat resistance and promote treatment efficacy. This information illustrates the importance of personalized OV therapy regarding epigenome in individual profiles and transitions. Still, it extends difficulty in inducing with acquisitions of viral-induced changes globally and making translatable steps by creating cancer-specific predictive treatment models.

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引用次数: 0

An overview of BAP1 biological functions and current therapeutics

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2025-01-21 DOI: 10.1016/j.bbcan.2025.189267

Abdelrahman M. Elsayed , Muaiad Kittaneh , Colleen M. Cebulla , Mohamed H. Abdel-Rahman

BRCA1-associated protein 1 (BAP1) is a tumor suppressor gene that was first identified in 1998. Germline loss-of-function variants in BAP1 are associated with a tumor predisposition syndrome with at least four cancers: uveal melanoma (UM), malignant mesothelioma (MMe), renal cell carcinoma (RCC), and cutaneous melanoma (CM). Furthermore, somatic BAP1 mutations are important drivers for several cancers most notably UM, MMe, RCC, intrahepatic cholangiocarcinoma (ICC) and hepatocellular carcinoma (HCC). Emerging evidence substantiates the fundamental role of BAP1 in suppressing cancer initiation and progression by tuning DNA damage repair, apoptosis, ferroptosis, immune response, Warburg phenomenon, and metastasis. Multiple treatment strategies such as poly (ADP-ribose) polymerase (PARP) inhibitors, EZH2 inhibitors, alkylating agents, and immunotherapy have been used as potential therapies for BAP1-mutated tumors. Although these agents showed promising results in BAP1-mutated tumors in preclinical studies, the results of most clinical trials are still dismal. The objectives of this review are to summarize the current state of knowledge regarding the biological functions of BAP1, the implications of these functions in tumorigenesis, and the current progress in BAP1-targeted therapy.

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引用次数: 0

Neuromedin U in the tumor microenvironment - Possible actions in tumor progression

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2025-01-20 DOI: 10.1016/j.bbcan.2025.189269

Patrycja Przygodzka , Izabela Szulc-Kielbik , Michal Kielbik , Marcin Pacholczyk , Magdalena Klink

Tumor microenvironment (TME) has become a major focus of cancer research as a promising therapeutic target. TME comprises cancer cells surrounded by nonmalignant cells, vessels, lymphoid organs, immune cells, nerves, intercellular components, molecules and metabolites located within or near the tumor lesion.

Neuromedin U (NMU), a secretory peptide identified in the TME, has gained much attention as an important player in cancer and nonmalignant cell crosstalk. NMU receptors were detected in cancer cells as well as in nonmalignant TME components, such as immune, stromal and endothelial cells.

We propose here to discuss the concept that NMU secreted by cancer cells activates cellular components of TME and thus contributes to the formation of microenvironment that favors tumor growth and cancer progression. We summarized the available data on cancer tissues and cell types that have been identified as a source of NMU and/or receptor-expressing NMU targets. We made a critical selection of NMU-receptor positive cell types that are known components of the TME of most malignant tumors. Finally, we discussed whether NMUs and NMU receptors represent a potential therapeutic target for cancer treatment, and summarized information on the tools available to modulate their activity.

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引用次数: 0

Metformin as an immunomodulatory agent in enhancing head and neck squamous cell carcinoma therapies 二甲双胍作为免疫调节剂在头颈部鳞状细胞癌治疗中的作用。

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2025-01-17 DOI: 10.1016/j.bbcan.2025.189262

Wenting Li , Nanshu Liu , Mingwei Chen , Dongjuan Liu , Sai Liu

Head and neck squamous cell carcinoma (HNSCC) remains a significant clinical challenge due to its aggressive behavior and poor prognosis, making the development of novel therapeutics with enhanced efficacy and minimal side effects critical. Metformin, a widely used antidiabetic agent, has recently emerged as a potential adjunctive therapy for HNSCC, exhibiting both direct anti-tumor and immunomodulatory effects. This review comprehensively explores the multifaceted role of metformin in shaping the tumor immune microenvironment within HNSCC. We emphasize its pivotal role in modulating immune cell populations and its potential for synergistic action with immunotherapeutic strategies. Furthermore, we address the current challenges associated with optimizing dosing regimens, identifying predictive biomarkers, and integrating metformin with immunotherapy. By dissecting these aspects, this review aims to pave the way for the development of personalized HNSCC treatment strategies that fully exploit the therapeutic potential of metformin.

头颈部鳞状细胞癌（HNSCC）由于其侵袭性行为和预后差，仍然是一个重大的临床挑战，因此开发具有增强疗效和最小副作用的新型治疗方法至关重要。二甲双胍是一种广泛使用的降糖药，最近被认为是一种潜在的辅助治疗HNSCC的药物，具有直接的抗肿瘤和免疫调节作用。这篇综述全面探讨了二甲双胍在塑造HNSCC肿瘤免疫微环境中的多方面作用。我们强调其在调节免疫细胞群中的关键作用及其与免疫治疗策略协同作用的潜力。此外，我们还解决了当前与优化给药方案、识别预测性生物标志物以及将二甲双胍与免疫疗法结合相关的挑战。通过剖析这些方面，本综述旨在为充分利用二甲双胍治疗潜力的个性化HNSCC治疗策略的发展铺平道路。

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