{"title":"Organoids in lung cancer brain metastasis: Foundational research, clinical translation, and prospective outlooks","authors":"Mei Zheng , Jialin Qu , Dongxi Xiang , Ligang Xing","doi":"10.1016/j.bbcan.2024.189235","DOIUrl":"10.1016/j.bbcan.2024.189235","url":null,"abstract":"<div><div>Brain metastasis stands as a leading contributor to mortality in lung cancer patients, yet the intricate mechanism underlying this phenomenon remains elusive. This underscores the need for robust preclinical models and effective treatment strategies. Emerging as viable in vitro models that closely replicate actual tumors, three-dimensional culture systems, particularly organoids derived from non-malignant cells or cancer organoids, have emerged as promising avenues. This review delves into the forefronts of fundamental research and clinical applications focused on lung cancer brain metastasis-derived organoids, highlighting current challenges and delineating prospects. These studies offer tremendous potential for clinical application despite being in nascent status.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 1","pages":"Article 189235"},"PeriodicalIF":9.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142796466","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":"Precision oncology: Using cancer genomics for targeted therapy advancements","authors":"Cigir Biray Avci , Bakiye Goker Bagca , Behrouz Shademan , Leila Sabour Takanlou , Maryam Sabour Takanlou , Alireza Nourazarian","doi":"10.1016/j.bbcan.2024.189250","DOIUrl":"10.1016/j.bbcan.2024.189250","url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 1","pages":"Article 189250"},"PeriodicalIF":9.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142866308","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}
Lissa Eggermont , Nicolaas Lumen , Charles Van Praet , Joris Delanghe , Sylvie Rottey , Tijl Vermassen
{"title":"A comprehensive view of N-glycosylation as clinical biomarker in prostate cancer","authors":"Lissa Eggermont , Nicolaas Lumen , Charles Van Praet , Joris Delanghe , Sylvie Rottey , Tijl Vermassen","doi":"10.1016/j.bbcan.2024.189239","DOIUrl":"10.1016/j.bbcan.2024.189239","url":null,"abstract":"<div><div>Alterations in the prostate cancer (PCa) <em>N</em>-glycome have gained attention as a potential biomarker. This comprehensive review explores the diversity of <em>N</em>-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 <em>N</em>-glycosylation patterns are a mechanism of immune escape and a disruption in normal glycoprotein distribution and trafficking. Glycoproteins with PCa-induced <em>N</em>-glycosylation patterns tend to accumulate in prostate tissue and the bloodstream, thereby diminishing <em>N</em>-glycan proportions in urine. Based on literary observations, aberrations in <em>N</em>-glycan branching are probably a characteristic of metabolic reprogramming and (chronic) inflammation. Changes in (core) fucosylation, specific <em>N</em>-glycosylation structures (such as <em>N,N′</em>-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.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 1","pages":"Article 189239"},"PeriodicalIF":9.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142822982","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}
Jiayi Lyu , Simin Wang , Jingnan Chen , Xia Yang , Guoquan Gao , Ti Zhou
{"title":"The comparison of pathogenic role and mechanism of Kallistatin and PEDF in tumors","authors":"Jiayi Lyu , Simin Wang , Jingnan Chen , Xia Yang , Guoquan Gao , Ti Zhou","doi":"10.1016/j.bbcan.2025.189273","DOIUrl":"10.1016/j.bbcan.2025.189273","url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 2","pages":"Article 189273"},"PeriodicalIF":9.7,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143069570","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}
Lin Li , Zihao An , Chao Lin , Qiang Xu , Chao Tang
{"title":"An update on regulation and function of G protein-coupled receptors in cancer: A promising strategy for cancer therapy","authors":"Lin Li , Zihao An , Chao Lin , Qiang Xu , Chao Tang","doi":"10.1016/j.bbcan.2025.189266","DOIUrl":"10.1016/j.bbcan.2025.189266","url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 2","pages":"Article 189266"},"PeriodicalIF":9.7,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143049209","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}
Monika Granica , Gustaw Laskowski , Paweł Link-Lenczowski , Agnieszka Graczyk-Jarzynka
{"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}
{"title":"Regulation of NLRP3/TRIM family signaling in gut inflammation and colorectal cancer","authors":"Bibhashee Mohapatra , Kousalya Lavudi , Rekha Rani Kokkanti , Srinivas Patnaik","doi":"10.1016/j.bbcan.2025.189271","DOIUrl":"10.1016/j.bbcan.2025.189271","url":null,"abstract":"<div><div>CRC (Colorectal cancer) ranks among the most prevalent tumors in humans and remains a leading cause of cancer-related mortality worldwide. Numerous studies have highlighted the connection between inflammasome over-activation and the initiation and progression of CRC. The activation of the NLRP3 (NOD-like receptor family, pyrin domain containing 3) inflammasome is dependent on the nuclear NF-kβ (Nuclear Factor kappa-light-chain-enhancer of activated B cells) pathway, leading to the maturation and release of inflammatory cytokines such as IL-1ß (Interleukin 1 beta) and IL-18 (Interleukin 18). While inflammation is crucial for defense mechanisms and tissue repair, excessive information can pose significant risks. Mounting evidence suggests that overactivation of the inflammasome contributes to the pathogenesis of inflammatory diseases. Consequently, there is a concerted effort to tightly regulate inflammasome activity and mitigate excessive inflammatory responses, particularly in conditions such as IBD (Inflammatory Bowel Disease), which includes Ulcerative Colitis and Crohn's Disease. The tripartite motif (TRIM) protein family, characterized by a conserved structure and rapid evolutionary diversification, includes members with critical roles in ubiquitination and other regulatory functions. Their importance in modulating inflammatory responses is widely acknowledged. This article aims to investigate the interplay between TRIM proteins and the NLRP3 Inflammasome in CRC and gut inflammation, offering insights for future research endeavors and potential therapeutic strategies.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 2","pages":"Article 189271"},"PeriodicalIF":9.7,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143049319","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":"Membrane drug transporters in cancer: From chemoresistance mechanism to therapeutic strategies","authors":"Chao Pan , Leo Tsz On Lee","doi":"10.1016/j.bbcan.2025.189272","DOIUrl":"10.1016/j.bbcan.2025.189272","url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 2","pages":"Article 189272"},"PeriodicalIF":9.7,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043501","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}
Muhammad Haris Sultan, Qi Zhan, Hao Jin, Xiaoyuan Jia, Yigang Wang
{"title":"Epigenetic modulation by oncolytic viruses: Implications for cancer therapeutic efficacy","authors":"Muhammad Haris Sultan, Qi Zhan, Hao Jin, Xiaoyuan Jia, Yigang Wang","doi":"10.1016/j.bbcan.2025.189270","DOIUrl":"10.1016/j.bbcan.2025.189270","url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 2","pages":"Article 189270"},"PeriodicalIF":9.7,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043497","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}
Abdelrahman M. Elsayed , Muaiad Kittaneh , Colleen M. Cebulla , Mohamed H. Abdel-Rahman
{"title":"An overview of BAP1 biological functions and current therapeutics","authors":"Abdelrahman M. Elsayed , Muaiad Kittaneh , Colleen M. Cebulla , Mohamed H. Abdel-Rahman","doi":"10.1016/j.bbcan.2025.189267","DOIUrl":"10.1016/j.bbcan.2025.189267","url":null,"abstract":"<div><div><em>BRCA1-associated protein 1</em> (<em>BAP1</em>) is a tumor suppressor gene that was first identified in 1998. Germline loss-of-function variants in <em>BAP1</em> 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 <em>BAP1</em> 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 <em>BAP1</em>-mutated tumors. Although these agents showed promising results in <em>BAP1</em>-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.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 2","pages":"Article 189267"},"PeriodicalIF":9.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143026146","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}