Cancer metastasis reviews最新文献

{"title":"Lung tumour secretome and extracellular vesicles: mechanisms, biomarkers, and therapeutic opportunities.","authors":"Kota Shimizu, Yuanzheng Xia, Graeme Stuart Cottrell, Darius Widera","doi":"10.1007/s10555-026-10367-6","DOIUrl":"10.1007/s10555-026-10367-6","url":null,"abstract":"<p><p>Lung cancer progression is governed not only by tumour-intrinsic genetic alterations but also by dynamic communication between tumour cells and the surrounding microenvironment. An important component of this communication is the tumour secretome, comprising soluble factors and extracellular vesicles (EVs), which contribute to the regulation of tumour growth, invasion, immune evasion, and therapeutic resistance. Through these mechanisms, secretome components and EVs promote phenotypic plasticity, microenvironmental remodelling, and adaptive responses to hypoxia, immune surveillance, and therapeutic stress. Importantly, secretome-derived factors and EVs are released into accessible biofluids, including blood, bronchoalveolar lavage fluid, and pleural effusions, highlighting their potential as minimally invasive biomarkers. In this review, we examine the lung tumour secretome, including both soluble secreted factors and EVs, with an emphasis on their contributions to tumour progression, metastasis, immune modulation, and resistance to targeted therapies, immunotherapy, and radiation. We discuss methodological advances and persistent technical challenges in EV isolation, characterisation, and molecular profiling that influence reproducibility and interpretation. We further evaluate emerging clinical applications, including liquid biopsy, treatment monitoring, and therapeutic targeting, and consider their integration within precision oncology frameworks. Finally, we highlight key barriers to clinical translation and outline priorities for future research, including methodological standardisation, prospective clinical validation, and the development of strategies to target tumour-derived secretory signalling selectively.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468747/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148726616","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":"Recent advances in etiology and treatment of von Hippel-Lindau Disease (VHLD).","authors":"Shabnam Pirestani, Emmanuelle Nicolas, Robert L Broadrup, Margie L Clapper, Erica Golemis","doi":"10.1007/s10555-026-10370-x","DOIUrl":"10.1007/s10555-026-10370-x","url":null,"abstract":"<p><p>Von Hippel-Lindau disease (VHLD) is a rare autosomal dominant disease, occuring in ~ 1 in 35,000 individuals. Overall, individuals with inherited mutations in the VHL tumor suppressor gene are predisposed to a variety of cancer, including high frequencies of clear cell renal cell carcinoma (ccRCC), pancreatic neuroendocrine tumors, and hemangioblastomas, as well as benign cystic conditions and other cancers. The degree of risk for each of these pathological conditions depends on the location and severity of the inherited germline mutation, and the specific VHL protein interactions and functions disrupted. A core VHL protein function is as the targeting subunit of an E3 ligase complex, with protein degradation activity based on interactions with elongins (ELOB, ELOC), Cullin 2 (CUL2), and RBX1. For ccRCC and some other cancers, loss of VHL-dependent degradation of key substrates-the transcription factors hypoxia-inducible factor alpha (HIF-1α and HIF-2α)-and upregulation of HIF-dependent transcripts are critical to promote tumor formation. For this reason, drugs such as the HIF signaling inhibitor belzutifan have emerged as promising clinical agents for treatment of VHLD patients prone to ccRCC. However, other biological consequences of VHL loss are independent of HIFα degradation, and in some cases independent of the VHL ubiquitin ligase activity. Non-canonical activities of VHL include regulation of microtubule stability, mitotic progression, and ciliation, as well as formation of the extracellular matrix (ECM); the degree to which disruption of these activities contributes to VHLD is currently not well understood. This review provides a concise update of the current literature on VHLD pathogenesis, the relationship of VHL structure and protein interactions to the spectrum of phenotypes associated with VHLD, and current and proposed treatment, prevention, and interception of cancer formation for VHLD patients.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13473127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148726646","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":"Platelets as regulators of anti-tumor immunity: mechanisms and clinical implications.","authors":"Martin Schlesinger","doi":"10.1007/s10555-026-10362-x","DOIUrl":"10.1007/s10555-026-10362-x","url":null,"abstract":"<p><p>Platelets are increasingly recognized as important contributors to tumor progression and metastatic dissemination. Platelets facilitate cancer cell survival, their safe transit through the hostile bloodstream, arrest at distant organ sites, and ultimate outgrowth into metastatic lesions. Although multiple platelet-dependent mechanisms have been implicated in cancer progression-including epithelial-mesenchymal transition and the provision of tumor-supportive growth factors-recent studies increasingly highlight immune modulation as a central mechanism underlying platelet-mediated metastasis. Accordingly, this review summarizes current evidence on the molecular and cellular mechanisms by which platelets regulate cytotoxic T lymphocyte and natural killer (NK) cell-mediated anti-tumor immune responses. Special attention is given to platelet-associated immune checkpoint pathways, including the expression and intercellular transfer of Programmed Death-Ligand 1 (PD-L1), as well as to the release of immunomodulatory mediators such as transforming growth factor-β1 (TGF-β1), thromboxane A₂ (TXA₂), and adenosine generated by platelet ectoenzymes. Finally, the potential implications of platelet-immune interactions for cancer therapy are discussed, with a particular focus on their relevance for immunotherapeutic strategies and metastatic disease control.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13437663/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148674940","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":"Immunological and antitumor responses to HPV-targeted therapeutic vaccines in preclinical models of head and neck cancer: a systematic review.","authors":"Sara Fraser, Darya Tamashekan, Marco Mascarella, Livia Florianova, Grégoire B Morand, Alex M Mlynarek, Michael P Hier, Sabrina D S Wurzba","doi":"10.1007/s10555-026-10365-8","DOIUrl":"10.1007/s10555-026-10365-8","url":null,"abstract":"<p><p>Human papillomavirus (HPV)-associated head and neck squamous cell carcinoma (HNSCC) is increasingly prevalent and accounts for 22-70% of HNSCCs depending on the region. Although prophylactic HPV vaccines were approved in the early 2000s to prevent HPV infection and oncogenesis, they are ineffective against established HPV infections and related cancers. The standard of care for these HPV-associated oropharyngeal cancers combines radiotherapy, surgery, and chemotherapy. However, these treatments can result in significant lifelong side effects for patients with no new treatments entering regular clinical practice in the past decade. Therapeutic cancer vaccines represent an opportunity for novel treatment approaches in HPV-associated cancer, particularly because these cancers display viral tumor-specific antigens (TSAs) such as E6 and E7, making them easily targetable by this type of immunotherapy. Currently, there are no FDA-approved therapeutic vaccines for HPV-associated cancers, but preclinical and clinical studies are ongoing in this area. In this systematic review, we describe current HPV vaccination strategies, their biological mechanisms, and their immunological and therapeutic effects in preclinical cancer models. We discuss each component of therapeutic vaccines: antigens, delivery platforms, adjuvants, and combination agents. We also assess the results of recent preclinical studies evaluating HPV therapeutic vaccines to provide an outlook on the future of this treatment modality.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148671749","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":"The link between microplastics and colorectal cancer.","authors":"Anisha Lynch-Godrei, Christopher Leung","doi":"10.1007/s10555-026-10361-y","DOIUrl":"10.1007/s10555-026-10361-y","url":null,"abstract":"<p><p>Microplastics and nanoplastics (MNPLs) are known to enter the human body and accumulate within different tissues. As MNPLs have been shown to exert toxic effects in vivo, we aimed to evaluate the link between MNPLs and colorectal cancer tumorigenesis. A literature review was conducted, using Ovid MEDLINE and PubMed databases. MeSH terms \"colorectal carcinoma\" and \"microplastic\" were the foundations for the search strategy. Forty-one studies were initially identified, of which fourteen were ultimately selected for analysis. MNPLs are found within human colorectal tumors and are present at higher levels in the feces of colorectal cancer patients. The tissue sample studies however are limited by small sample sizes (n = 10 or 25), and are representative of mainly Chinese populations (five of the six human studies conducted in China). The mouse studies observed increased tumor loads and dysbiosis in mice exposed to MNPLs, and the in vitro studies observed increased reactive oxygen species (ROS) when cells were exposed to MNPLs in culture. Although the direct link between MNPLs and de novo development of colorectal cancer remains to be elucidated, these findings suggest that MNPLs can induce the molecular changes involved in tumorigenesis, and tumorigenesis itself when combined with a compromised gastrointestinal barrier. Given that barrier disruption occurs with inflammatory bowel disease, smoking, alcohol, stress, and infections, these populations may be most vulnerable to the effects of MNPLs.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13427794/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148633562","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":"Tumorigenesis of well-differentiated and dedifferentiated liposarcoma: 12q amplicon architecture, oncogenic cargo, and evolutionary progression.","authors":"Aobo Zhuang, Xiao Zhou, Chengfei Xu, YangJu Chen, Xueling Wang, Runchun Li, Jiajing Hu, Yinxue Cheng, Yunyan Wan, Ting Wu, Wengang Li","doi":"10.1007/s10555-026-10363-w","DOIUrl":"https://doi.org/10.1007/s10555-026-10363-w","url":null,"abstract":"<p><p>Well-differentiated liposarcoma (WDLPS) and dedifferentiated liposarcoma (DDLPS) are characterized by recurrent MDM2-centered amplification of chromosome 12q13-15, yet this diagnostic label reduces a complex structural lesion to a binary result. An architecture-resolved 12q amplicon platform requires an MDM2-centered dosage anchor plus direct evidence of nontrivial topology or carrier state; cargo, regulatory, and functional data define progressively higher-resolution features. When only MDM2 amplification is documented, the lesion is best described as diagnostic 12q amplification rather than a fully resolved platform. This review presents an evidence-graded architecture-to-function framework that separates direct WDLPS/DDLPS observations from mechanisms inferred from broader amplification biology. Disease-specific evidence supports heterogeneous 12q carriers, including ring, giant marker, rod-shaped, discontinuous, and neochromosome-like structures, as well as enhancer coamplification or altered 3D contacts. In contrast, chromothripsis, telomere crisis/BFB remodeling, ecDNA-like dynamics, and enhancer hubs are treated as extrapolated or testable mechanisms unless directly validated in liposarcoma. Conclusions are weighted by methodological resolution: cytogenetics/FISH define diagnostic amplification and visible carrier classes; MLPA or array-based assays define dosage and discontinuity; WGS with long-read or optical mapping is needed for junction-level architecture; and single-cell/spatial assays mainly resolve cellular-state or ecosystem context unless paired with structural readouts. MDM2-p53 and CDK4-RB remain central outputs, whereas selected cargo, lineage state, metabolism, and tumor-microenvironment programs are interpreted as evidence-ranked cooperating or downstream modules. Clinically, architecture-aware interpretation is proposed as a prospective framework for sampling, model design, biomarker development, and trial stratification, not as an established basis for routine management.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148623657","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":"MYCN-driven metabolic remodelling of the tumour microenvironment in neuroblastoma: implications for stromal biology and CAF heterogeneity.","authors":"Mekonnen Sisay Shiferaw, Klaartje Somers, Zaklina Kovacevic","doi":"10.1007/s10555-026-10355-w","DOIUrl":"10.1007/s10555-026-10355-w","url":null,"abstract":"<p><p>Neuroblastoma (NB) is the most common extracranial solid tumour of childhood and remains a leading cause of paediatric cancer mortality, particularly in high-risk disease driven by MYCN amplification. Although MYCN is a central oncogenic driver, its role as a transcription factor has limited direct therapeutic targeting, shifting attention toward downstream metabolic and microenvironmental dependencies. Increasing evidence indicates that MYCN-driven metabolic rewiring extends beyond tumour-intrinsic processes to reshape the tumour microenvironment (TME), influencing immune composition and stromal dynamics. Recent advances in single-cell and spatial profiling technologies have revealed substantial heterogeneity within the NB TME, highlighting complex interactions between tumour cells, immune populations, and stromal components. Among these, cancer-associated fibroblasts (CAFs) have emerged as key regulators of extracellular matrix architecture, immune modulation, and metabolic crosstalk. However, CAF identity, functional diversity, and lineage relationships in NB remain incompletely defined, with significant overlap between tumour-intrinsic mesenchymal programs and stromal fibroblast signatures. In this review, we synthesise current understanding of MYCN-driven metabolic reprogramming and its impact on CAF heterogeneity and immune regulation. We integrate insights from adult cancers with emerging data in NB to critically evaluate CAF functional states, including inflammatory and myofibroblastic programs, and their roles in shaping tumour progression, immune exclusion, and therapeutic response. By framing NB as a MYCN-remodelled tumour ecosystem, this review identifies key knowledge gaps in stromal biology and highlights the need to resolve CAF heterogeneity and tumour-stroma interactions. These insights have broader implications for MYC-driven malignancies and support the development of integrated therapeutic strategies targeting both tumour cells and their supportive microenvironment.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13400697/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148581972","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":"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}