Cancer metastasis reviews最新文献

{"title":"Towards implementation of precision medicine biomarkers in early detection and prognostication of prostate cancer.","authors":"Angela Yee, Jim Smith, Rajiv Kumar, Akash Sali, Euan J Rodger, Aniruddha Chatterjee","doi":"10.1007/s10555-026-10357-8","DOIUrl":"10.1007/s10555-026-10357-8","url":null,"abstract":"<p><p>Prostate cancer is the second-highest cause of cancer-related incidence and the fifth-highest cause of cancer mortality in males. Prostate cancer is a heterogeneous disease with a wide spectrum of clinical behaviour, ranging from indolent to highly aggressive. Molecular approaches, such as genomic testing, can augment existing clinical risk stratifications and tailor management to the individual. Genomic tests that sample biopsy or surgical tissue can provide a molecular risk assessment and identify actionable therapy targets. Liquid biopsy, while still emerging, may provide a non-invasive alternative to tissue tests and enable longitudinal monitoring of tumour status. We first discuss the molecular landscape of prostate cancer, before providing a detailed overview of the molecular approaches available for early detection and prognostication. Furthermore, methodological considerations and barriers towards clinical implementation for these tests are discussed, highlighting areas of future research.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13395839/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148564252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From bench to bedside: advancing our understanding of radioresistance in rectal cancer.","authors":"Diogo Estêvão, Miguel da Cruz-Ribeiro, Diogo Coelho, Joana Lencart, Olga Sousa, Bruno Sarmento, Olivier de Wever, Maria J Oliveira, Tânia Cruz","doi":"10.1007/s10555-026-10359-6","DOIUrl":"10.1007/s10555-026-10359-6","url":null,"abstract":"<p><p>The global incidence of rectal cancer (RC) is increasing at an alarming rate, with over 50% of cases still diagnosed at advanced stages, despite improvements in early detection. While neoadjuvant (chemo)radiotherapy regimens remain a cornerstone of treatment, up to 20-40% of tumours exhibit or develop resistance to ionising radiation, limiting therapeutic options and leading to disease evolution. This review offers a comprehensive insight into the complex biological and molecular mechanisms underlying RC radioresistance within the fundamental 6Rs of radiobiology: Repair, Reoxygenation, Redistribution, Radiosensitivity, Repopulation, and Reactivation. More specifically, DNA damage repair pathways, cell cycle regulation, hypoxia, transcriptional plasticity regulators such as cancer stem cells, and non-coding RNAs are comprehensively reviewed. Additionally, the critical roles of tumour-infiltrating lymphocytes, cancer-associated macrophages, and inflammatory cancer-associated fibroblasts in radioresistance are also dissected, which collectively shape an immunosuppressive and pro-metastatic niche following radiotherapy. Furthermore, a less explored mechanism, namely the metabolic rewiring of cancer cells after radiotherapy, is proposed as a new 7th R of Radiobiology, namely \"Reprogramming\", that enables tumour survival and promotes aggressive phenotypes. This new perspective adds a new layer of complexity to the molecular understanding of RC resistance and provides a mechanistic insight currently missing in radiobiology research. Additionally, advanced experimental models, such as spheroids, patient-derived organoids, and animal models, are discussed as valuable platforms for pre-clinical research and therapeutic testing. This review also integrates mechanistic insights with biomarker-guided clinical decision-making to support RC management. By unravelling these multifactorial mechanisms, we highlight opportunities to develop predictive biomarkers and tailored therapeutic strategies to overcome resistance and improve patient outcomes.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13388369/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148552081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sarcoma metastasis: distinct biological principles beyond the carcinoma paradigm.","authors":"Nadja Chevalier, Paul C Nathan, Ivan Stamenkovic","doi":"10.1007/s10555-026-10360-z","DOIUrl":"10.1007/s10555-026-10360-z","url":null,"abstract":"<p><p>Sarcomas are rare in adults but constitute a substantial fraction of pediatric malignancies and are characterized by a high propensity for hematogenous dissemination and poor outcomes once metastatic. Yet, most mechanistic understanding of metastasis derives from carcinomas and is frequently extrapolated to sarcomas despite major biological differences. This review synthesizes current evidence on sarcoma metastasis and highlights key knowledge gaps across the metastatic cascade. It frames sarcomas as malignancies often arising from mesenchymal stromal cells, whose intrinsic motility, plasticity, and stem-like features may predispose transformed cells to dissemination without requiring a classic epithelial-to-mesenchymal transition program. The concept of metastasis-initiating cells is discussed in the context of sarcoma cancer stem cell biology, clonal evolution, and epigenetic reprogramming, emphasizing that the relative genomic simplicity of certain pediatric sarcomas driven by recurrent fusion oncogenes may provide powerful models to dissect metastasis dependencies. The review examines how the sarcoma tumor microenvironment, often immunosuppressive and macrophage-rich, may shape invasion, intravasation, survival in circulation, extravasation, and organotropism, particularly the strong predilection for pulmonary metastasis. It summarizes emerging data on circulating tumor cells and complementary liquid biopsy approaches, while underscoring technical limitations caused by sarcoma heterogeneity and lack of robust markers. Finally, the review appraises current treatment limitations for metastatic sarcoma and argues that improved mechanistic resolution, especially of plasticity, epigenetic states, microenvironmental interactions, and dormancy, will be essential to identify actionable vulnerabilities and improve outcomes for patients with disseminated disease.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13385083/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148521724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding cachexia and muscle dysfunction in the context of metastatic breast cancer.","authors":"Alastair A E Saunders, Robin L Anderson, Paul Gregorevic","doi":"10.1007/s10555-026-10358-7","DOIUrl":"10.1007/s10555-026-10358-7","url":null,"abstract":"<p><p>Cancer cachexia significantly impacts the quality of life of cancer patients, predicting therapy response and survival. Cachexia prevalence and severity increases over the course of disease progression, affecting up to 80% of patients with metastatic cancer. Despite this, cachexia is relatively understudied in the context of metastatic breast cancer, despite it affecting a significant proportion of patients with this common cancer. In this review we highlight the relative prevalence of cachexia in breast cancer, with 25% of all patients and up to half of those with metastatic disease impacted. Given the metastatic distribution pattern of breast cancer (e.g. high rates of bone metastases), we reviewed the unique systemic and local muscle cues leading to cachexia in this context and have reviewed areas for further investigation. Furthermore, anti-cancer therapies also contribute to cachexia progression. Recently, novel mouse models for study of cachexia in breast cancer have been developed. These models can further the field's understanding of cachexia in metastatic cancer patients and aid in the development of anti-cachectic agents. However, it is important that these models accurately recapitulate human disease. In this review we provide an appraisal of the relative utility of the currently available models. Overall, this review highlights that understanding cachexia in the context of breast cancer and metastasis may uncover novel mechanisms to target this condition, thereby improving the quality of life and survival prospects of metastatic cancer patients.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13379479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148475581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rewiring cancer cell fate toward vasculogenic mimicry: from classical to unconventional processes.","authors":"Edgar A Méndez-Pérez, Janice García-Quiroz, Euclides Avila, Rocío García-Becerra, Lorenza Díaz","doi":"10.1007/s10555-026-10356-9","DOIUrl":"10.1007/s10555-026-10356-9","url":null,"abstract":"<p><p>Pathological vasculogenic mimicry (VM) is the process by which aggressive tumor stem cells form perfusable, matrix-rich, vessel-like networks, facilitating tumor perfusion and metastasis. Several well-characterized VM drivers include hypoxia, acidity, growth factors, and inflammatory molecules. Likewise, canonical and non-canonical transitions, such as epithelial-to-mesenchymal, epithelial-to-endothelial, endothelial-to-mesenchymal, and epithelial-mesenchymal plasticity contribute to VM formation. In addition, atypical mechanisms such as cell-cell fusion, polyploidization, gene silencing, and processes associated with viral infections have also been linked to VM induction. Clinically, VM has been associated with poor prognosis, metastasis, and resistance to antiangiogenic, chemo- and radiotherapeutic compounds, which may independently trigger or exacerbate VM. Therapeutic strategies to fight this highly adaptive process include combination regimens that simultaneously inhibit angiogenesis and VM, thereby preventing the emergence of alternative survival mechanisms. Likewise, key nodes and signaling pathways involved in VM, such as Notch, Wnt, and PI3K/AKT, are under active preclinical evaluation, together with pro-differentiating factors that attenuate stem-associated traits. However, despite its therapeutic relevance, the mechanistic basis of VM remains insufficiently integrated, leaving a gap in biomedical literature. To address this, the aim of this review was to provide comprehensive coverage of current evidence encompassing both well-established processes associated with VM and those not yet fully characterized. Our work integrates the analysis of signaling pathways, key molecular players, lineage plasticity, and microenvironmental factors that orchestrate VM. In addition, therapeutic challenges and opportunities are also discussed.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148440734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metastasis as a breakdown of the multicellular social contract.","authors":"Laurine Lagache, Michel Salzet","doi":"10.1007/s10555-026-10352-z","DOIUrl":"10.1007/s10555-026-10352-z","url":null,"abstract":"<p><p>Multicellular organisms are not just collections of cells; they are evolutionary compromises in which cell-level fitness is subordinated to organism-level integrity. Cancer begins when that compromise is locally subverted, but metastasis is the decisive escalation: malignant cells must cross tissue boundaries, survive a hostile systemic phase, condition remote organs, enter or escape dormancy and construct a new permissive ecology. This Perspective uses the social-contract metaphor as a disciplined heuristic, not as a claim of intention or moral agency, to integrate metastasis biology with eco-evolutionary thinking. We argue that the metastatic cascade can be read as serial failure of multicellular governance: local architecture loses territorial control; vascular and immune systems fail to exclude or destroy emigrant cells; distant tissues become preconditioned by tumour-derived signals; dormant disseminated cells persist as residual insurgencies and colonisation emerges when organ-specific restraint is converted into support. The framework becomes most useful when it also explains the paradox that cells which defect from host-level cooperation may cooperate locally with each other and with recruited stroma. Public goods, collective dissemination, metabolic exchange and premetastatic niche construction create dependencies that may be exploitable therapeutically. We give the Black Queen Hypothesis a precise but bounded role: it is a testable model for dependency-generating loss or outsourcing of costly shared functions, not a universal law of cancer evolution. Finally, we outline translational implications for metastasis: rearming immune enforcement, blocking niche education, maintaining or eradicating dormant disease, disrupting shared dependencies and using adaptive schedules to manage evolutionary escape. The social-contract lens is valuable only when it remains evidence-led and mechanistically anchored; used this way, it makes metastatic dormancy and colonisation a sharper target for ecological cancer therapy.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148400353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HER2 assessment in urothelial carcinoma: standardization challenges and the path forward.","authors":"Peipei Xie, Yajie Wang, Lei Lu, Jiayuan Chen, Jinchang Wei, Yiran Huang, Citing Guo, Juan Li, Xieqiao Yan, Jun Guo, Xiaowen Wu, Xinan Sheng","doi":"10.1007/s10555-026-10353-y","DOIUrl":"10.1007/s10555-026-10353-y","url":null,"abstract":"<p><p>Human epidermal growth factor receptor 2 (HER2) is a crucial oncogenic factor, highly expressing in various cancers, with urothelial carcinoma (UC) showing one of the highest levels of HER2 overexpression. HER2 serves as an ideal therapeutic target in UC. Current HER2-targeted therapies primarily include tyrosine kinase inhibitors, monoclonal antibodies, and antibody-drug conjugates (ADCs). Among these, ADCs combined with immunotherapy have shown outstanding clinical potential, which have changed the treatment landscape in UC. However, the assessment of HER2 status in UC is still facing major challenges. There is no unified consensus on testing methods and the definition of HER2 positivity, accompanied by significant spatiotemporal expression heterogeneity. These challenges significantly making HER2 assessment difficult in UC, hindering the more precise clinical application of HER2-targeted therapies especially ADCs. In this review, we focus on analyzing the current challenges in standardizing HER2 detection and positivity definitions in UC, elaborating on the spatiotemporal heterogeneity of HER2 expression, and systematically summarizing new HER2 testing methods. It is aimed to provide theoretical insights and new perspectives for HER2 testing and assessment in UC. In order to adress the challenges in HER2 assessment in UC, future researches should concentrate on establishing a unified standard for UC-specific HER2 assessment algorithm, and exploring new HER2 testing methods tailored to clinical needs.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148371699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resolving translational challenges in cancer biology through yeast experimental evolution.","authors":"Li-Tzu Wang, Han-Ying Jhuang","doi":"10.1007/s10555-026-10351-0","DOIUrl":"10.1007/s10555-026-10351-0","url":null,"abstract":"<p><p>Cancer genomics, molecular pathology, targeted therapy, and immunotherapy have transformed how tumors are diagnosed and treated, yet several problems remain hard to resolve prospectively, including the interpretation of variants of uncertain significance, variable penetrance, recurrent drug resistance, and the early trajectories that predispose later therapeutic failure. Many of these are fundamentally evolutionary questions about which adaptive routes are accessible under selection and how reproducibly they arise. Here, we make the case that yeast experimental evolution can serve cancer biologists as a practical upstream discovery platform, because its control, scale, and temporal resolution expose recurrent adaptive routes, transient intermediates, compensatory mechanisms, and genotype-to-fitness relationships that mammalian systems resolve only slowly. We organize representative studies by evolutionary dynamic, set out design principles and an operational workflow, and mark where these models are strong, where they mislead, and where fission yeast adds complementary strengths. Together, these elements frame yeast evolution as a way to prioritize and sharpen downstream validation in cancer systems.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148348594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spheroids and organoids to study long noncoding RNAs in cancer: how they could replace animal models.","authors":"Ana Maria Capela, João Pessoa, Hugo Arede, Bruno Bernardes de Jesus","doi":"10.1007/s10555-026-10350-1","DOIUrl":"10.1007/s10555-026-10350-1","url":null,"abstract":"<p><p>Spheroids, organoids, and further three-dimensional cellular models represent an intermediate stage of supra-cellular complexity between monolayered cell cultures and animal models. In the present review, we identified conditions in which spheroids and organoids could replace animal models in biomedical research, using long noncoding RNA (lncRNA) research in cancer as a study object. In tumor spheroids and patient-derived organoids, chemosensitivity can be enhanced through therapeutic overexpression or silencing of specific lncRNAs (depending on the lncRNA and context), which then decreases spheroid/organoid size or formation efficiency. These outcomes consistently mimic observations in xenograft mouse models, in which the same lncRNA intervention decreases tumor volume. Therefore, as a proxy of tumor growth assessment, animal models could be largely replaced with spheroids or organoids, taking advantage of their inexpensiveness and patient-specific features, respectively. The use of animal models could be restricted to bystander or pleiotropic effects, such as the assessment of parameters including metastasis and survival rates.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13309473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148341888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Strategies and successes of smoking cessation methods in head and neck cancer patients: a systematic review.","authors":"Vincent Vander Poorten, Justine Van Rossum, Malene Roosens, Sandra Nuyts, Carol R Bradford, Juan Pablo Rodrigo, Remco De Bree, Karthik N Rao, Orlando Guntinas-Lichius, Nabil F Saba, Alfio Ferlito","doi":"10.1007/s10555-026-10348-9","DOIUrl":"10.1007/s10555-026-10348-9","url":null,"abstract":"<p><p>Tobacco use and especially smoking tobacco is a key risk factor in the development and the progression of head and neck squamous cell carcinoma (HNSCC). Continued smoking after diagnosis worsens treatment outcomes, survival rates, and quality of life significantly. This systematic review evaluates the effectiveness of smoking cessation interventions in HNSCC patients, aiming to provide an evidence-based foundation supporting smoking cessation efforts. A comprehensive search of five databases yielded 2492 studies, of which 11 met the inclusion criteria (total patient number = 1593). These covered a range of interventions, including behavioral counseling, pharmacotherapy (nicotine replacement therapy (NRT), bupropion, and varenicline), and digital or structural support tools. Reported cessation rates ranged from 23.9 to 74% depending on the intervention type, intensity, and timing. Interventions combining counseling with pharmacological support and structured follow-up were generally more effective, particularly when initiated shortly after diagnosis. The review also highlights the potential benefits of digital tools, integrated care approaches, and opt-out systems. Despite the substantial heterogeneity across studies, which prohibited a formal meta-analysis, the findings underscore the importance of a tailored, multimodal approach to smoking cessation in HNSCC patients. Implementation barriers such as limited resources and organizational constraints persist, and further research is needed to determine the optimal follow-up strategies and address comorbidity-inducing behavioral factors.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 2","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13346323/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148255535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}