Jyoti B Kaushal, Pratima Raut, Sakthivel Muniyan, Jawed A Siddiqui, Zahraa W Alsafwani, Parthasarathy Seshacharyulu, Sujit S Nair, Ashutosh K Tewari, Surinder K Batra
{"title":"Racial disparity in prostate cancer: an outlook in genetic and molecular landscape.","authors":"Jyoti B Kaushal, Pratima Raut, Sakthivel Muniyan, Jawed A Siddiqui, Zahraa W Alsafwani, Parthasarathy Seshacharyulu, Sujit S Nair, Ashutosh K Tewari, Surinder K Batra","doi":"10.1007/s10555-024-10193-8","DOIUrl":"10.1007/s10555-024-10193-8","url":null,"abstract":"<p><p>Prostate cancer (PCa) incidence, morbidity, and mortality rates are significantly impacted by racial disparities. Despite innovative therapeutic approaches and advancements in prevention, men of African American (AA) ancestry are at a higher risk of developing PCa and have a more aggressive and metastatic form of the disease at the time of initial PCa diagnosis than other races. Research on PCa has underlined the biological and molecular basis of racial disparity and emphasized the genetic aspect as the fundamental component of racial inequality. Furthermore, the lower enrollment rate, limited access to national-level cancer facilities, and deferred treatment of AA men and other minorities are hurdles in improving the outcomes of PCa patients. This review provides the most up-to-date information on various biological and molecular contributing factors, such as the single nucleotide polymorphisms (SNPs), mutational spectrum, altered chromosomal loci, differential gene expression, transcriptome analysis, epigenetic factors, tumor microenvironment (TME), and immune modulation of PCa racial disparities. This review also highlights future research avenues to explore the underlying biological factors contributing to PCa disparities, particularly in men of African ancestry.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"1233-1255"},"PeriodicalIF":7.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11560487/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141431487","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}
{"title":"Classification of anticancer drugs: an update with FDA- and EMA-approved drugs.","authors":"Lorena Ostios-Garcia, Daniel Martínez Pérez, Beatriz Castelo, Noelia Hernández Herradón, Pilar Zamora, Jaime Feliu, Enrique Espinosa","doi":"10.1007/s10555-024-10188-5","DOIUrl":"10.1007/s10555-024-10188-5","url":null,"abstract":"<p><p>Anticancer systemic therapy comprises a complex and growing group of drugs. Some of the new agents with novel mechanisms of action that have appeared are difficult to fit in the groups of classical chemotherapy, hormones, tyrosine-kinase inhibitors, and monoclonal antibodies. We propose a classification based on two levels of information: the site of action and the mechanism of action. Regarding the former, drugs can exert their action in the tumor cell, the tumor vasculature, the immune system, or the endocrine system. The mechanism of action refers to the molecular target.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"1561-1571"},"PeriodicalIF":7.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11554936/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141533686","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}
{"title":"Failure to progress: breast and prostate cancer cell lines in developing targeted therapies.","authors":"Chelsi James, Akeem Whitehead, Jasmine T Plummer, Rory Thompson, Simone Badal","doi":"10.1007/s10555-024-10202-w","DOIUrl":"10.1007/s10555-024-10202-w","url":null,"abstract":"<p><p>Developing anticancer drugs from preclinical to clinical takes approximately a decade in a cutting-edge biomedical lab and still 97% of most fail at clinical trials. Cell line usage is critical in expediting the advancement of anticancer therapies. Yet developing appropriate cell lines has been challenging and overcoming these obstacles whilst implementing a systematic approach of utilizing 3D models that recapitulate the tumour microenvironment is prudent. Using a robust and continuous supply of cell lines representing all ethnic groups from all locales is necessary to capture the evolving tumour landscape in culture. Next, the conversion of these models to systems on a chip that can by way of high throughput cytotoxic assays identify drug leads for clinical trials should fast-track drug development while markedly improving success rates. In this review, we describe the challenges that have hindered the progression of cell line models over seven decades and methods to overcome this. We outline the gaps in breast and prostate cancer cell line pathology and racial representation alongside their involvement in relevant drug development.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"1529-1548"},"PeriodicalIF":7.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141765550","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}
Fanglu Chen, Yucheng Xue, Wenkan Zhang, Hao Zhou, Zhiyi Zhou, Tao Chen, Eloy YinWang, Hengyuan Li, Zhaoming Ye, Junjie Gao, Shengdong Wang
{"title":"The role of mitochondria in tumor metastasis and advances in mitochondria-targeted cancer therapy.","authors":"Fanglu Chen, Yucheng Xue, Wenkan Zhang, Hao Zhou, Zhiyi Zhou, Tao Chen, Eloy YinWang, Hengyuan Li, Zhaoming Ye, Junjie Gao, Shengdong Wang","doi":"10.1007/s10555-024-10211-9","DOIUrl":"10.1007/s10555-024-10211-9","url":null,"abstract":"<p><p>Mitochondria are central actors in diverse physiological phenomena ranging from energy metabolism to stress signaling and immune modulation. Accumulating scientific evidence points to the critical involvement of specific mitochondrial-associated events, including mitochondrial quality control, intercellular mitochondrial transfer, and mitochondrial genetics, in potentiating the metastatic cascade of neoplastic cells. Furthermore, numerous recent studies have consistently emphasized the highly significant role mitochondria play in coordinating the regulation of tumor-infiltrating immune cells and immunotherapeutic interventions. This review provides a comprehensive and rigorous scholarly investigation of this subject matter, exploring the intricate mechanisms by which mitochondria contribute to tumor metastasis and examining the progress of mitochondria-targeted cancer therapies.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"1419-1443"},"PeriodicalIF":7.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11554835/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142280529","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}
Jasmine M Bacon, Johanna L Jones, Guei-Sheung Liu, Joanne L Dickinson, Kelsie Raspin
{"title":"Mitochondrial ribosomal proteins in metastasis and their potential use as prognostic and therapeutic targets.","authors":"Jasmine M Bacon, Johanna L Jones, Guei-Sheung Liu, Joanne L Dickinson, Kelsie Raspin","doi":"10.1007/s10555-024-10216-4","DOIUrl":"10.1007/s10555-024-10216-4","url":null,"abstract":"<p><p>The mitochondrion is an essential cell organelle known as the powerhouse of the cell. Mitochondrial ribosomal proteins (MRPs) are nuclear encoded, synthesised in the cytoplasm but perform their main functions in the mitochondria, which includes translation, transcription, cell death and maintenance. However, MRPs have also been implicated in cancer, particularly advanced disease and metastasis across a broad range of cancer types, where they play a central role in cell survival and progression. For some, their altered expression has been investigated as potential prognostic markers, and/or therapeutic targets, which is the focus of this review. Several therapies targeting MRPs are currently approved by the Food and Drug Administration and the European Medicines Agency for use in other diseases, revealing the opportunity for repurposing their use in advanced and metastatic cancer. Herein, we review the evidence supporting key MRPs as molecular drivers of advanced disease in multiple cancer types. We also highlight promising avenues for future use of MRPs as precision targets in the treatment of late-stage cancers for which there are currently very limited effective treatment options.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"1119-1135"},"PeriodicalIF":4.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11554709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361181","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}
Bryan Oronsky, Nacer Abrouk, Li Mao, Yunle Shen, Xiaohui Wang, Luyang Zhao, Scott Caroen, Tony Reid
{"title":"Lost at SCLC: a review of potential platinum sensitizers.","authors":"Bryan Oronsky, Nacer Abrouk, Li Mao, Yunle Shen, Xiaohui Wang, Luyang Zhao, Scott Caroen, Tony Reid","doi":"10.1007/s10555-024-10207-5","DOIUrl":"10.1007/s10555-024-10207-5","url":null,"abstract":"<p><p>The expression \"lost at sea\" means to be confused or perplexed. By extension, lost at SCLC references the current confusion about how to circumvent the chemoresistance, particularly platinum resistance, which so plagues the treatment of extensive-stage small cell lung cancer (ES-SCLC) that in 2012 the US National Cancer Institute (NCI) designated it a \"recalcitrant cancer.\" Over a decade later, despite the approval of immune checkpoint inhibitors and the conditional approval of lurbinectedin, the prognosis for ES-SCLC, and especially platinum-resistant ES-SCLC, has scarcely improved. The focus of this review, which briefly summarizes current treatment options for ES-SCLC, is on five clinical-stage therapies with the potential to successfully reverse the platinum resistance that is perhaps the biggest obstacle to better clinical outcomes.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"1573-1578"},"PeriodicalIF":4.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11554703/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142035333","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}
Shahad Sabaawi Ibrahim, Raghad Sabaawi Ibrahim, Batoul Arabi, Aranka Brockmueller, Mehdi Shakibaei, Dietrich Büsselberg
{"title":"The effect of GLP-1R agonists on the medical triad of obesity, diabetes, and cancer.","authors":"Shahad Sabaawi Ibrahim, Raghad Sabaawi Ibrahim, Batoul Arabi, Aranka Brockmueller, Mehdi Shakibaei, Dietrich Büsselberg","doi":"10.1007/s10555-024-10192-9","DOIUrl":"10.1007/s10555-024-10192-9","url":null,"abstract":"<p><p>Glucagon-like peptide-1 receptor (GLP-1R) agonists have garnered significant attention for their therapeutic potential in addressing the interconnected health challenges of diabetes, obesity, and cancer. The role of GLP-1R in type 2 diabetes mellitus (T2DM) is highlighted, emphasizing its pivotal contribution to glucose homeostasis, promoting β-cell proliferation, and facilitating insulin release. GLP-1R agonists have effectively managed obesity by reducing hunger, moderating food intake, and regulating body weight. Beyond diabetes and obesity, GLP-1R agonists exhibit a multifaceted impact on cancer progression across various malignancies. The mechanisms underlying these effects involve the modulation of signaling pathways associated with cell growth, survival, and metabolism. However, the current literature reveals a lack of in vivo studies on specific GLP-1R agonists such as semaglutide, necessitating further research to elucidate its precise mechanisms and effects, particularly in cancer. While other GLP-1R agonists have shown promising outcomes in mitigating cancer progression, the association between some GLP-1R agonists and an increased risk of cancer remains a topic requiring more profound investigation. This calls for more extensive research to unravel the intricate relationships between the GLP-1R agonist and different cancers, providing valuable insights for clinicians and researchers alike.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"1297-1314"},"PeriodicalIF":7.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11554930/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141154591","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}
{"title":"Role of MARCH E3 ubiquitin ligases in cancer development.","authors":"Abhayananda Behera, Deepanshi Sachan, Ganesh Kumar Barik, Aramati Bindu Madhava Reddy","doi":"10.1007/s10555-024-10201-x","DOIUrl":"10.1007/s10555-024-10201-x","url":null,"abstract":"<p><p>Membrane-associated RING-CH (MARCH) E3 ubiquitin ligases, a family of RING-type E3 ubiquitin ligases, have garnered increased attention for their indispensable roles in immune regulation, inflammation, mitochondrial dynamics, and lipid metabolism. The MARCH E3 ligase family consists of eleven distinct members, and the dysregulation of many of these members has been documented in several human malignancies. Over the past two decades, extensive research has revealed that MARCH E3 ligases play pivotal roles in cancer progression by ubiquitinating key oncogenes and tumor suppressors and orchestrating various signaling pathways. Some MARCH E3s act as oncogenes, while others act as tumor suppressors, and the majority of MARCH E3s play both oncogenic and tumor suppressive roles in a context-dependent manner. Notably, there is special emphasis on the sole mitochondrial MARCH E3 ligase MARCH5, which regulates mitochondrial homeostasis within cancer cells. In this review, we delve into the diverse functions of MARCH E3 ligases across different cancer types, shedding light on the underlying molecular mechanisms mediating their effects, their regulatory effects on cancer and their potential as therapeutic targets.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"1257-1277"},"PeriodicalIF":7.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141733571","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}
Caleb B Lill, Stephen Fitter, Andrew C W Zannettino, Kate Vandyke, Jacqueline E Noll
{"title":"Molecular and cellular mechanisms of chemoresistance in paediatric pre-B cell acute lymphoblastic leukaemia.","authors":"Caleb B Lill, Stephen Fitter, Andrew C W Zannettino, Kate Vandyke, Jacqueline E Noll","doi":"10.1007/s10555-024-10203-9","DOIUrl":"10.1007/s10555-024-10203-9","url":null,"abstract":"<p><p>Paediatric patients with relapsed B cell acute lymphoblastic leukaemia (B-ALL) have poor prognosis, as relapse-causing clones are often refractory to common chemotherapeutics. While the molecular mechanisms leading to chemoresistance are varied, significant evidence suggests interactions between B-ALL blasts and cells within the bone marrow microenvironment modulate chemotherapy sensitivity. Importantly, bone marrow mesenchymal stem cells (BM-MSCs) and BM adipocytes are known to support B-ALL cells through multiple distinct molecular mechanisms. This review discusses the contribution of integrin-mediated B-ALL/BM-MSC signalling and asparagine supplementation in B-ALL chemoresistance. In addition, the role of adipocytes in sequestering anthracyclines and generating a BM niche favourable for B-ALL survival is explored. Furthermore, this review discusses the role of BM-MSCs and adipocytes in promoting a quiescent and chemoresistant B-ALL phenotype. Novel treatments which target these mechanisms are discussed herein, and are needed to improve dismal outcomes in patients with relapsed/refractory disease.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"1385-1399"},"PeriodicalIF":7.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11554931/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141888501","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}
{"title":"CAR T-cells for pediatric solid tumors: where to go from here?","authors":"Tina Trautmann, Natalia Yakobian, Rosa Nguyen","doi":"10.1007/s10555-024-10214-6","DOIUrl":"10.1007/s10555-024-10214-6","url":null,"abstract":"<p><p>Despite the great success that chimeric antigen receptor (CAR) T-cells have had in patients with B-cell malignancies and multiple myeloma, they continue to have limited efficacy against most solid tumors. Especially in the pediatric population, pre- and post-treatment biopsies are rarely performed due to ethical reasons, and thus, our understanding is still very limited regarding the mechanisms in the tumor microenvironment by which tumor cells exclude effectors and attract immune-suppressive cells. Nevertheless, based on the principles that are known, current T-cell engineering has leveraged some of these processes and created more potent CAR T-cells. The recent discovery of new oncofetal antigens and progress made in CAR design have expanded the potential pool of candidate antigens for therapeutic development. The most promising approaches to enhance CAR T-cells are novel CAR gating strategies, creative ways of cytokine delivery to the TME without enhancing systemic toxicity, and hijacking the chemokine axis of tumors for migratory purposes. With these new modifications, the next step in the era of CAR T-cell development will be the clinical validation of these promising preclinical findings.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"1445-1461"},"PeriodicalIF":4.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11554711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342197","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}