{"title":"Vaping and tumor metastasis: current insights and progress.","authors":"Yibo Xi, Lei Yang, Barbara Burtness, He Wang","doi":"10.1007/s10555-024-10221-7","DOIUrl":"10.1007/s10555-024-10221-7","url":null,"abstract":"<p><p>Tumor metastasis is the primary cause of cancer-related mortality and remains a major hurdle in cancer treatment. Traditional cigarette smoking has been extensively studied for its role in promoting metastasis. However, the impact of e-cigarette (e-cig) on cancer metastasis is not well understood despite their increasing popularity as a supposedly safer alternative. This mini review synthesizes current literature on the effects of e-cig on cancer metastasis, focusing on the processes of dissemination, dormancy, and colonization. It also incorporates recent findings from our laboratory regarding the role of e-cig in tumor progression. E-cig exposure enhances metastatic potential through various mechanisms: it induces epithelial-mesenchymal transition (EMT), increasing cell migratory and invasive capabilities; promotes lymphangiogenesis, aiding tumor cell spread; and alters the pre-metastatic niche to support dormant tumor cells, enhancing their reactivation and colonization. Furthermore, e-cig induce significant epigenetic changes, such as DNA methylation and histone modifications, which regulate genes involved in metastasis. Our data suggest that e-cig upregulate histone demethylases like KDM6B in macrophages, impacting the TME and promoting metastasis. These findings underscore the need for further research to understand the long-term health implications of e-cig use and inform public health policies to reduce e-cig use.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":"44 1","pages":"4"},"PeriodicalIF":7.7,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11792352/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709184","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}
Ain Syafiza Mohd Amin, Sarah Eastwood, Courtney Pilcher, Jia Q Truong, Richard Foitzik, Joanne Boag, Kylie L Gorringe, Jessica K Holien
{"title":"KIF18A inhibition: the next big player in the search for cancer therapeutics.","authors":"Ain Syafiza Mohd Amin, Sarah Eastwood, Courtney Pilcher, Jia Q Truong, Richard Foitzik, Joanne Boag, Kylie L Gorringe, Jessica K Holien","doi":"10.1007/s10555-024-10225-3","DOIUrl":"10.1007/s10555-024-10225-3","url":null,"abstract":"<p><p>Kinesin-like protein 18A (KIF18A) is a member of the kinesin family of molecular motor proteins, which utilise energy from the hydrolysis of adenosine triphosphate (ATP) to regulate critical cellular processes such as chromosome movement and microtubule dynamics. KIF18A plays a vital role in controlling microtubule length, which is crucial for maintaining proper cell function and division. Notably, increased expression levels of KIF18A have been observed in various types of cancer, indicating its potential involvement in tumour progression. Although preclinical studies have demonstrated that KIF18A is not essential for normal somatic cell division, it appears to be crucial for the survival and division of cancer cells, particularly those exhibiting chromosomal instability. This dependency makes KIF18A a promising target for developing new therapeutic strategies aimed at treating chromosomally unstable cancers. This review delves into the structural and functional aspects of KIF18A, and its role in cancer development, and evaluates current and emerging approaches to targeting KIF18A with innovative cancer treatments.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":"44 1","pages":"3"},"PeriodicalIF":7.7,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695298","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}
{"title":"A possible role of plasmin-dependent activation of TGF-β in cancer-associated thrombosis: Implications for therapy.","authors":"Marta Smeda, Ebrahim H Maleki, Agnieszka Jasztal","doi":"10.1007/s10555-024-10222-6","DOIUrl":"10.1007/s10555-024-10222-6","url":null,"abstract":"<p><p>While the prevalence of cancer-associated thrombosis (CAT) is high in cancer patients, its molecular mechanisms have not been fully elucidated. Moreover, the risks of recurrent CAT events and mortality remain high in cancer patients despite the introduction of anticoagulant/antiplatelet therapy. Here, we discuss the possibility that increased plasmin activity driven by anticoagulant/antiplatelet treatment might be the major mechanism responsible for the activation of an excess of cancer-derived transforming growth factor-beta (TGF-β) originating from cancer cells and the tumour microenvironment. Hence, high coagulation and fibrinolysis rates in cancer patients may be linked to high rates of TGF-β activation, especially the excess of TGF-β derived from cancer cells. In turn, high TGF-β activation could contribute directly to maintaining high thrombotic risk and CAT recurrence in cancer patients since TGF-β signalling increases gene expression and secretion of the fibrinolysis inhibitor plasminogen activator inhibitor 1 (PAI1). Thus, TGF-β could directly contribute to the high number of deaths among patients with cancer experiencing CAT, despite anticoagulant/antiplatelet treatment. In a longer-term perspective, increased TGF-β activation, by supporting a pro-coagulant cancer microenvironment, might also accelerate cancer progression. This review aims to discuss the published evidence that might support the scenario described above, and to put forward the hypothesis that cancer patients experiencing CAT events would largely benefit from anti-TGF-β therapy.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":"44 1","pages":"2"},"PeriodicalIF":7.7,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11584501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686226","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}
Madison M Purkerson, Sarah R Amend, Kenneth J Pienta
{"title":"Bystanders or active players: the role of extra centrosomes as signaling hubs.","authors":"Madison M Purkerson, Sarah R Amend, Kenneth J Pienta","doi":"10.1007/s10555-024-10224-4","DOIUrl":"10.1007/s10555-024-10224-4","url":null,"abstract":"<p><p>Centrosomes serve as microtubule-organizing organelles that function in spindle pole organization, cell cycle progression, and cilia formation. A non-canonical role of centrosomes that has gained traction in recent years is the ability to act as signal transduction centers. Centrosome amplification, which includes numerical and structural aberrations of centrosomes, is a candidate hallmark of cancer. The function of centrosomes as signaling centers in cancer cells with centrosome amplification is poorly understood. Establishing a model of how cancer cells utilize centrosomes as signaling platforms will help elucidate the role of extra centrosomes in cancer cell survival and tumorigenesis. Centrosomes act in a diverse array of cellular processes, including cell migration, cell cycle progression, and proteasomal degradation. Given that cancer cells with amplified centrosomes exhibit an increased number and larger area of these signaling platforms, extra centrosomes may be acting to promote tumor development by enhancing signaling kinetics in pathways that are essential for the formation and growth of cancer. In this review, we identify the processes centrosomes are involved in as signal transduction platforms and highlight ways in which cancer cells with centrosome amplification may be taking advantage of these mechanisms.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":"44 1","pages":"1"},"PeriodicalIF":7.7,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11582193/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680957","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}
Magdalena Rados, Anna Landegger, Lukas Schmutzler, Kimberlie Rabidou, Sabine Taschner-Mandl, Irfete S. Fetahu
{"title":"Natural killer cells in neuroblastoma: immunological insights and therapeutic perspectives","authors":"Magdalena Rados, Anna Landegger, Lukas Schmutzler, Kimberlie Rabidou, Sabine Taschner-Mandl, Irfete S. Fetahu","doi":"10.1007/s10555-024-10212-8","DOIUrl":"https://doi.org/10.1007/s10555-024-10212-8","url":null,"abstract":"<p>Natural killer (NK) cells have multifaceted roles within the complex tumor milieu. They are pivotal components of innate immunity and shape the dynamic landscape of tumor-immune cell interactions, and thus can be leveraged for use in therapeutic interventions. NK-based immunotherapies have had remarkable success in hematological malignancies, but these therapies are met with many challenges in solid tumors, including neuroblastoma (NB), a childhood tumor arising from the sympathetic nervous system. With a focus on NB, this review outlines the mechanisms employed by NK cells to recognize and eliminate malignant cells, delving into the dynamic relationship between ligand-receptor interactions, cytokines, and other molecules that facilitate the cross talk between NK and NB cells. We discuss the immunomodulatory functions of NK cells and the mechanisms that contribute to loss of this immunosurveillance in NB, with a focus on how this dynamic has been utilized in recent immunotherapy advancements for NB.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":"05 1","pages":""},"PeriodicalIF":9.2,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142249830","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}
Rebecca Ronsley, Kelsey C. Bertrand, Edward Z. Song, Andrea Timpanaro, Michelle Choe, Dana Tlais, Nicholas A. Vitanza, Julie R. Park
{"title":"CAR T cell therapy for pediatric central nervous system tumors: a review of the literature and current North American trials","authors":"Rebecca Ronsley, Kelsey C. Bertrand, Edward Z. Song, Andrea Timpanaro, Michelle Choe, Dana Tlais, Nicholas A. Vitanza, Julie R. Park","doi":"10.1007/s10555-024-10208-4","DOIUrl":"https://doi.org/10.1007/s10555-024-10208-4","url":null,"abstract":"<p>Central nervous system (CNS) tumors are the leading cause of cancer-related death in children. Typical therapy for CNS tumors in children involves a combination of surgery, radiation, and chemotherapy. While upfront therapy is effective for many high-grade tumors, therapy at the time of relapse remains limited. Furthermore, for diffuse intrinsic pontine glioma (DIPG) and diffuse midline glioma (DMG), there are currently no curative therapies. Chimeric antigen receptor T (CAR T) cell therapy is a promising novel treatment avenue for these tumors. Here, we review the preclinical evidence for CAR T cell use in pediatric brain tumors, the preliminary clinical experience of CNS CAR T cell trials, toxicity associated with systemic and locoregional CAR T cell therapy for CNS tumors, challenges in disease response evaluation with CAR T cell therapy, and the knowledge gained from correlative biologic studies from these trials in the pediatric and young adult population.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":"254 1","pages":""},"PeriodicalIF":9.2,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142208498","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}
Yan Xu, Zhipeng Gao, Xiaoyu Sun, Jun Li, Toshinori Ozaki, Du Shi, Meng Yu, Yuyan Zhu
{"title":"The role of circular RNA during the urological cancer metastasis: exploring regulatory mechanisms and potential therapeutic targets.","authors":"Yan Xu, Zhipeng Gao, Xiaoyu Sun, Jun Li, Toshinori Ozaki, Du Shi, Meng Yu, Yuyan Zhu","doi":"10.1007/s10555-024-10182-x","DOIUrl":"10.1007/s10555-024-10182-x","url":null,"abstract":"<p><p>Metastasis is a major contributor to treatment failure and death in urological cancers, representing an important biomedical challenge at present. Metastases form as a result of cancer cells leaving the primary site, entering the vasculature and lymphatic vessels, and colonizing clones elsewhere in the body. However, the specific regulatory mechanisms of action underlying the metastatic process of urological cancers remain incompletely elucidated. With the deepening of research, circular RNAs (circRNAs) have been found to not only play a significant role in tumor progression and prognosis but also show aberrant expression in various tumor metastases, consequently impacting tumor metastasis through multiple pathways. Therefore, circRNAs are emerging as potential tumor markers and treatment targets. This review summarizes the research progress on elucidating how circRNAs regulate the urological cancer invasion-metastasis cascade response and related processes, as well as their role in immune microenvironment remodeling and circRNA vaccines. This body of work highlights circRNA regulation as an emerging therapeutic target for urological cancers, which should motivate further specific research in this regard.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"1055-1074"},"PeriodicalIF":7.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140334760","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}
Zhi Yi Su, Pui Yan Siak, Yu Yu Lwin, Shiau-Chuen Cheah
{"title":"Epidemiology of nasopharyngeal carcinoma: current insights and future outlook.","authors":"Zhi Yi Su, Pui Yan Siak, Yu Yu Lwin, Shiau-Chuen Cheah","doi":"10.1007/s10555-024-10176-9","DOIUrl":"10.1007/s10555-024-10176-9","url":null,"abstract":"<p><p>Nasopharyngeal carcinoma (NPC) is characterised by its remarkable geographical and ethnic distribution. The interplay between genetic susceptibility, environmental exposures, and Epstein-Barr virus (EBV) infections is indicated in the development of NPC. Exposure to tobacco smoking, dietary factors, and inhalants has been associated with the risk of NPC. Genetic association studies have revealed NPC-associated susceptibility loci, including genes involved in immune responses, xenobiotic metabolism, genome maintenance, and cell cycle regulation. EBV exposure timing and strain variation might play a role in its carcinogenicity, although further investigations are required. Other factors including medical history and oral hygiene have been implicated in NPC. Prevention strategies, including primary prevention and secondary prevention through early detection, are vital in reducing mortality and morbidity of NPC. The current review discusses the global and regional distribution of NPC incidences, the risk factors associated with NPC, and the public health implications of these insights. Future investigations should consider international, large-scale prospective studies to elucidate the mechanisms underlying NPC pathogenesis and develop individualized interventions for NPC.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"919-939"},"PeriodicalIF":7.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140012211","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}
Bicky Thapa, Shumei Kato, Daisuke Nishizaki, Hirotaka Miyashita, Suzanna Lee, Mary K Nesline, Rebecca A Previs, Jeffery M Conroy, Paul DePietro, Sarabjot Pabla, Razelle Kurzrock
{"title":"OX40/OX40 ligand and its role in precision immune oncology.","authors":"Bicky Thapa, Shumei Kato, Daisuke Nishizaki, Hirotaka Miyashita, Suzanna Lee, Mary K Nesline, Rebecca A Previs, Jeffery M Conroy, Paul DePietro, Sarabjot Pabla, Razelle Kurzrock","doi":"10.1007/s10555-024-10184-9","DOIUrl":"10.1007/s10555-024-10184-9","url":null,"abstract":"<p><p>Immune checkpoint inhibitors have changed the treatment landscape for various malignancies; however, their benefit is limited to a subset of patients. The immune machinery includes both mediators of suppression/immune evasion, such as PD-1, PD-L1, CTLA-4, and LAG-3, all of which can be inhibited by specific antibodies, and immune-stimulatory molecules, such as T-cell co-stimulatory receptors that belong to the tumor necrosis factor receptor superfamily (TNFRSF), including OX40 receptor (CD134; TNFRSF4), 4-1BB (CD137; TNFRSF9), and glucocorticoid-induced TNFR-related (GITR) protein (CD357; TNFRSF18). In particular, OX40 and its binding ligand OX40L (CD134L; TNFSF4; CD252) are critical for immunoregulation. When OX40 on activated T cells binds OX40L on antigen-presenting cells, T-cell activation and immune stimulation are initiated via enhanced T-cell survival, proliferation and cytotoxicity, memory T-cell formation, and abrogation of regulatory T cell (Treg) immunosuppressive functions. OX40 agonists are in clinical trials both as monotherapy and in combination with other immunotherapy agents, in particular specific checkpoint inhibitors, for cancer treatment. To date, however, only a minority of patients respond. Transcriptomic profiling reveals that OX40 and OX40L expression vary between and within tumor types, and that only ~ 17% of cancer patients have high OX40 and low OX40L, one of the expression patterns that might be theoretically amenable to OX40 agonist enhancement. Taken together, the data suggest that the OX40/OX40L machinery is a critical part of the immune stimulatory system and that understanding endogenous expression patterns of these molecules and co-existing checkpoints merits further investigation in the context of a precision immunotherapy strategy for cancer therapy.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"1001-1013"},"PeriodicalIF":7.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140287001","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}
Shabnam Malik, Mohammed Sikander, Mohd Wahid, Anupam Dhasmana, Maryam Sarwat, Sheema Khan, Everardo Cobos, Murali M Yallapu, Meena Jaggi, Subhash C Chauhan
{"title":"Deciphering cellular and molecular mechanism of MUC13 mucin involved in cancer cell plasticity and drug resistance.","authors":"Shabnam Malik, Mohammed Sikander, Mohd Wahid, Anupam Dhasmana, Maryam Sarwat, Sheema Khan, Everardo Cobos, Murali M Yallapu, Meena Jaggi, Subhash C Chauhan","doi":"10.1007/s10555-024-10177-8","DOIUrl":"10.1007/s10555-024-10177-8","url":null,"abstract":"<p><p>There has been a surge of interest in recent years in understanding the intricate mechanisms underlying cancer progression and treatment resistance. One molecule that has recently emerged in these mechanisms is MUC13 mucin, a transmembrane glycoprotein. Researchers have begun to unravel the molecular complexity of MUC13 and its impact on cancer biology. Studies have shown that MUC13 overexpression can disrupt normal cellular polarity, leading to the acquisition of malignant traits. Furthermore, MUC13 has been associated with increased cancer plasticity, allowing cells to undergo epithelial-mesenchymal transition (EMT) and metastasize. Notably, MUC13 has also been implicated in the development of chemoresistance, rendering cancer cells less responsive to traditional treatment options. Understanding the precise role of MUC13 in cellular plasticity, and chemoresistance could pave the way for the development of targeted therapies to combat cancer progression and enhance treatment efficacy.</p>","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"981-999"},"PeriodicalIF":7.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140142784","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}