Cancer metastasis reviews最新文献

{"title":"Reframing early gastric carcinogenesis through lineage, niche, and evolution.","authors":"Xuyu Chen, Siying Wang, Juan Li","doi":"10.1007/s10555-026-10376-5","DOIUrl":"https://doi.org/10.1007/s10555-026-10376-5","url":null,"abstract":"<p><p>Early gastric cancer is still commonly conceptualized as the endpoint of a linear sequence from chronic gastritis to intestinal metaplasia, dysplasia, and invasion. Yet recent single-cell, spatial, genomic, and functional studies indicate that this model incompletely captures the biology of early gastric carcinogenesis. Malignant potential is established progressively within a precancerous gastric field already shaped by somatic evolution, chronic inflammatory injury, and epithelial lineage distortion. Within this field, progression is concentrated in a restricted set of precursor states, particularly incomplete, hybrid, and stem-like metaplastic populations that display plasticity, persistence, and increasing compatibility with a supportive microenvironment. Fibroblast niche remodeling, immune protection loss, endothelial rewiring, genomic instability, epigenetic drift, and selective retention of advantageous molecular alterations further promote malignant commitment. In parallel, diffuse gastric cancer appears to follow a distinct route that may arise independently of conventional intestinal metaplasia through E-cadherin-deficient epithelial transformation and downstream chromatin reprogramming. Here, we synthesize recent evidence to propose an updated framework for early gastric carcinogenesis based on field evolution, lineage instability, ecosystem support, and pathway divergence. Rather than replacing the classical Correa cascade, this framework seeks to refine it by shifting the unit of risk assessment from histologic stage alone to biologically defined precursor states shaped by lineage instability, clonal persistence, niche permissiveness, and pathway-specific molecular constraints. This perspective shifts the emphasis of prevention from detecting smaller cancers to identifying and intercepting biologically committed precursor states before invasion occurs.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148946357","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":"Langerhans cell histiocytosis: molecular mechanisms underlying pathogenesis and emerging targeted therapeutics.","authors":"Quan Li, Jiancheng Hu","doi":"10.1007/s10555-026-10378-3","DOIUrl":"10.1007/s10555-026-10378-3","url":null,"abstract":"<p><p>Langerhans cell histiocytosis (LCH) is a nonhereditary myeloid neoplasm driven by somatic alterations in the mitogen-activated protein kinase (MAPK) signaling pathway, most commonly involving BRAF and MAP2K1 (MEK1). Oncogenic BRAF alterations activate MAPK signaling through diverse structural mechanisms. The prominent BRAF(V600E) mutation traps BRAF in a constitutively active status by forming the K507-E600 salt bridge independent of upstream RAS signaling. In contrast, non-V600E BRAF mutants exhibit variable kinase activity, among which kinase-dead variants rely on BRAF/CRAF heterodimerization and transactivate CRAF. In parallel, oncogenic MEK1 mutations disrupt autoinhibition or enhance MEK1 homodimerization, sustaining MAPK activation. Furthermore, RAF/MEK heterodimerization modulates pathway output and persistence. These mechanistic insights provide a strong biological rationale for therapeutic targeting of the MAPK pathway in LCH, thereby driving the clinical use of BRAF inhibitors (BRAFi) including vemurafenib and dabrafenib, as well as MEK inhibitors (MEKi) such as trametinib and cobimetinib. However, the efficacy is frequently limited by acquired resistance associated with MAPK pathway reactivation through RAF and MEK dimerization-dependent mechanisms. Collectively, these altered molecular interactions contribute to the pathway dysregulation and signaling persistence, thereby providing a mechanistic basis for adaptive resistance and for developing next-generation RAFi and MEKi. This review therefore summarizes the current understanding of the molecular mechanisms underlying MAPK pathway activation and therapeutic resistance in LCH, with particular emphasis on conformational switch-based regulations of RAF and MEK proteins, and discusses emerging strategies involving next-generation RAFi and RAFi plus MEKi combinations aimed to achieve more durable MAPK pathway suppression and improving long-term outcomes of LCH treatment.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13562304/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148932436","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":"Mechanical memory as a metastatic compass: a comparative framework for understanding organotropism through biophysical priming.","authors":"Muhammed Emin Bedir, Abdulhadi Cihangir Uguz, Mustafa Unal","doi":"10.1007/s10555-026-10375-6","DOIUrl":"https://doi.org/10.1007/s10555-026-10375-6","url":null,"abstract":"<p><p>The seed and soil hypothesis has long explained organotropic metastasis through biochemical compatibility between tumor cells and distant tissues. However, accumulating evidence points to the role of mechanobiology in this process. This review proposes a framework in which cellular mechanical memory, the persistent adaptation to physical cues, functions as a mechanical compass that influences metastatic destination. We analyze how cancer cells, conditioned by the physical properties of the primary tumor (such as stiffness and viscosity), are epigenetically programmed to colonize distant organs with compatible mechanical signatures. We examine stiffness matching in bone metastasis, where cells conditioned by fibrotic tumors preferentially home to rigid skeletal niches, mediated by pathways including YAP/TAZ and RUNX2. We then address the paradox of soft tissue metastasis (brain, liver), proposing that a dual mechanical memory enables adaptation to compliant, viscoelastic environments. The role of dynamic forces, including fluid shear stress and cyclic strain, is examined in the context of lung colonization. By synthesizing these findings, we establish a comparative framework in which multidimensional mechanical memory, spanning static stiffness, viscoelasticity, and dynamic forces, contributes to organotropism as a complementary determinant alongside biochemical signaling. This framework generates testable predictions: that pharmacological disruption of specific mechanosensors or epigenetic erasure of stiffness memory should alter organ-specific metastatic patterns in preclinical models. Such a mechanobiological and biomechanical perspective may open therapeutic opportunities aimed at disrupting these physical memories to reduce metastatic dissemination.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148883389","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":"Molecular biomarkers in metastatic clear cell renal cell carcinoma treated with first-line immune combinations: a systematic review of phase III randomized clinical trials by Meet-URO group.","authors":"Anna Amela Valsecchi, Michele Maffezzoli, Maria Concetta Cursano, Fabrizio Di Costanzo, Andrea Malgeri, Mattia Alberto Di Civita, Brigida Maiorano, Carlo Messina, Giuseppe Procopio, Davide Bimbatti, Sebastiano Buti, Sara Elena Rebuzzi, Massimo Di Maio","doi":"10.1007/s10555-026-10371-w","DOIUrl":"10.1007/s10555-026-10371-w","url":null,"abstract":"<p><p>Immune checkpoint inhibitor (ICI)-based combinations represent the standard first-line treatment for metastatic clear cell renal cell carcinoma (mRCC), although robust biomarkers for treatment selection remain undefined. We conducted a systematic review to identify biomarkers assessed in randomized clinical trials (RCTs) on first-line ICI-based regimens. Following PRISMA guidelines, we searched PubMed, Web of Science and Scopus (January 2018-October 2025) for phase III RCTs investigating first-line ICI-based therapies in mRCC with molecular or circulating biomarker analyses. Given heterogeneity across studies, a qualitative synthesis was performed. Sixteen reports were included. Biomarkers were assessed using immunohistochemistry, transcriptomics, genomic sequencing and blood analyses. PD-L1 expression did not reliably discriminate benefit across ICI-based combinations, although it revealed a negative prognostic influence with sunitinib and a potential predictive role for nivolumab-ipilimumab. Tumours with angiogenic signatures were consistently associated with improved outcomes, suggesting prognostic relevance, while derived limited additional benefit from ICIs. Immune-related signatures were associated with ICI response, whereas proliferation and MYC-related signatures identified disease with poor prognosis across treatments. Individual mutations (e.g. PBRM1, VHL, BAP1, PTEN) showed heterogeneous and mainly prognostic associations, whereas composite gene panels (e.g. rDM) may offer better predictive value. Circulating biomarkers, including inflammatory cytokines and KIM-1 dynamics, demonstrated promising prognostic and early predictive signals. No validated biomarker currently supports treatment selection among first-line ICI-based combinations in mRCC. Future research should prioritize adaptive, biomarker-guided trial designs integrating longitudinal multi-omic profiling and circulating biomarkers to generate clinical evidence and support personalized treatments.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13518418/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148835836","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":"Epithelial-mesenchymal transition in carcinoma: navigating phenotypic states to target resistance and metastasis.","authors":"Xuecong Wang, Cecilia Xi Zhang, Yi Zhao, Jianxing He, Jean Paul Thiery","doi":"10.1007/s10555-026-10368-5","DOIUrl":"10.1007/s10555-026-10368-5","url":null,"abstract":"<p><p>Epithelial-mesenchymal transition (EMT), historically described as a binary morphological change from an epithelium to a mesenchymal state, no longer adequately accounts for carcinoma cell phenotypes observed in patients. Single-cell sequencing, spatial-omics, and lineage tracing converge on a different picture as carcinoma cells rarely undergo a unidirectional transition ending as sarcoma-like cells. Instead, carcinoma cells distribute across a continuum of intermediate states in which partial EMT often as hybrid epithelial/mesenchymal phenotypes couple adhesion and survival to motility, stress tolerance, and adaptive reprogramming. While EMT signatures remain a recurrent hallmark of metastasis, treatment failure, and disease relapse in epithelial cancers, functional cell plasticity is fundamentally shaped by distinct histotypes, tumor stages, malignancy grades, and local microenvironmental ecosystems. Carcinoma cells may not need to acquire a fixed position in the EMT spectrum to invade and metastasize, and \"more mesenchymal\" does not necessarily translate to \"more dangerous.\" The clinical translation of EMT-directed interventions faces steep methodological hurdles, primarily driven by unverified causal dynamics and unresolved therapeutic safety profiles. Overcoming these hurdles will require dynamic, multi-pronged strategies tailored to specific carcinoma cell states and spatial niches. Effective regimens must simultaneously deploy oncogene inhibition, state-plasticity restriction, and microenvironmental, metabolic, or extracellular matrix-directed remodeling.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13499848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148805271","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":"Osteomimetic microcalcification shapes the breast tumor microenvironment and metastatic potential.","authors":"Atsushi Fushimi","doi":"10.1007/s10555-026-10372-9","DOIUrl":"https://doi.org/10.1007/s10555-026-10372-9","url":null,"abstract":"<p><p>Microcalcifications are among the most reliable mammographic signs of breast cancer, particularly of non-palpable and in situ disease, yet for decades they were regarded as inert by-products of cellular degeneration-a view that delayed inquiry into their biology. A growing body of in vitro, ex vivo, and tissue-based evidence now reframes breast microcalcification as a process that can be actively regulated and cell-driven, recapitulating physiological and pathological mineralization elsewhere in the body. In this review, we synthesize the mechanistic basis of this paradigm shift and argue that mineral formation is not a passive marker but a participant in tumor biology. Two mineral species-calcium oxalate and calcium hydroxyapatite-carry different biological meaning and are separable on routine histopathology by birefringence and histochemistry. Hydroxyapatite can promote proliferation, matrix remodeling, and invasion, yet it is also the mineral of most benign calcifications, so its significance lies in composition and cellular origin, not presence alone. We discuss the osteomimetic program through which mammary tumor cells acquire bone-like mineralizing capacity, including the roles of alkaline phosphatase activity, ion transport, and PI3K-Akt signaling, and we distinguish osteomimicry-a phenotype of the tumor cell-from the bone metastatic niche that such cells may exploit. We then consider how mineral composition and microstructure encode the surrounding microenvironment and connect to clinical observations: association with HER2-positive disease, behavior under neoadjuvant chemotherapy, prognostic associations, and an emerging link with bone metastasis. We close with an integrated framework and a research agenda positioning mineral biology at the interface of the tumor microenvironment and metastatic progression.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148805296","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":"Three decades of anaplastic lymphoma kinase: from physiological roles to cancer and immune evasion.","authors":"Hesham M Amin, Shiva Aminnia, Mona M Saber, Mahesh Kumar Kannan, Justin Hung","doi":"10.1007/s10555-026-10364-9","DOIUrl":"10.1007/s10555-026-10364-9","url":null,"abstract":"<p><p>Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase with structural criteria shared among members of the insulin receptor subfamily. ALK plays crucial physiological roles such as in neural tissue development as well as in thinness and body weight regulation. In addition, ALK is a key driver of systemic inflammation that may lead to lethal sepsis. The oncogenic potential of ALK was first described in 1994 when 2 independent research groups discovered that ALK is aberrantly expressed in a rare aggressive subtype of T-cell lymphoma descriptively known as anaplastic large-cell lymphoma. Later, it was found that the aberrant expression of ALK extends to include other neoplasms such as non-small cell lung cancer, neuroblastoma, inflammatory myofibroblastic tumors, and others. In these neoplasms, ALK plays a central oncogenic role by upregulating the activity of a comprehensive network of upstream and downstream survival systems, which causes tumor cell survival and proliferation. The development of selective ALK inhibitors has led to paradigm shift in how ALK-expressing tumors, particularly non-small cell lung cancer, are treated. More recently, ALK has been implicated in disturbing the integrity of the immune system and sustaining immune evasion. In this review, we highlight 3 decades of ALK research, briefly discuss its physiological and pathological roles with a focus on cancer and immunity, and provide an update on the clinical utilization and mechanisms of resistance to ALK inhibitors.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13490271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148805289","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":"Biofabrication and artificial intelligence strategies for investigating solid- and fluid-pressure mechanobiology in pancreatic ductal adenocarcinoma.","authors":"Yahui Ding, Peiyuan Zhao, Yan Jin, Yan Li, Zifei Wang, Ye Lu, Yichen Zhang, Hongzhuan Chen, Weidong Zhang, Xin Luan, Min Tang","doi":"10.1007/s10555-026-10366-7","DOIUrl":"https://doi.org/10.1007/s10555-026-10366-7","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is shaped by a mechanically abnormal tumor microenvironment (TME) in which dysregulated mechanotransduction promotes malignant progression and therapeutic resistance. Two coupled but distinct pressure states dominate this landscape: solid stress and interstitial fluid pressure (IFP). Solid stress arises from constrained tumor growth, stromal contractility, and extracellular matrix remodeling. By contrast, IFP reflects hydrostatic pressure within the interstitial fluid compartment and is elevated by vascular leakage, impaired drainage, and low tissue hydraulic conductivity. Together, these abnormalities compress vessels, disrupt transport, and activate mechanotransduction programs that reinforce malignant adaptation. Here we integrate solid stress and IFP within a unified pressure-state framework for PDAC. We examine how these forces shape tumor progression, drug transport, and therapeutic response. We then evaluate spheroid, organoid, hydrogel, bioprinted, and microfluidic models according to what they truly control, directly measure, or merely infer. This distinction separates pressure-relevant systems from pressure-reconstructing models. We also discuss stromal normalization and the emerging role of artificial intelligence and machine learning (AI/ML) in model engineering and patient stratification. Current computational approaches can optimize mechanically defined models and infer pressure-related tumor states from multimodal data. However, they still rely largely on surrogates rather than direct measurements of solid stress or IFP. Our framework defines the biomechanical validation required to develop clinically predictive models of PDAC mechanobiology.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148805237","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":"Decoding osteosarcoma mechanobiology: PIEZO channels in tumor progression, immune remodeling, and pain.","authors":"Baicheng Yang, Zhangfu Li, Jethro Wang Zih-Shuo, Timothy M Pawlik, Shengji Yu","doi":"10.1007/s10555-026-10373-8","DOIUrl":"https://doi.org/10.1007/s10555-026-10373-8","url":null,"abstract":"<p><p>Osteosarcoma arises in a mechanically active skeletal environment, but how physical cues shape tumor behavior, immunity, and pain remains poorly defined. This review examines PIEZO1 and PIEZO2 as compartment-specific mechanotransducers and distinguishes direct osteosarcoma evidence from disease-relevant preclinical findings and broader evidence from bone, immune, neural, and pain systems. PIEZO1 is best established in osteoblast-lineage cells and osteocytes, where it regulates bone remodeling and mechanical adaptation; its causal role in human osteosarcoma remains unresolved. In osteosarcoma models, PIEZO1-associated responses to stiffness and strain are linked to invasion, adhesion remodeling, YAP/TAZ signaling, and phenotypic plasticity. PIEZO2 is less well supported as a tumor-cell regulator and is more convincingly positioned in sensory neurons that mediate mechanically evoked bone cancer pain. PIEZO1 may also influence myeloid, dendritic-cell, and T-cell behavior, although this immune axis remains unvalidated in osteosarcoma. These compartment-specific roles expose a mechanotherapeutic paradox: pathways required for skeletal adaptation and repair may also be used by malignant or stromal compartments. Resolving this problem will require spatially resolved human studies, orthotopic immunocompetent models, and cell-type-selective perturbation.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148805310","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":"N-Acetyltransferase 10 (NAT10) at the crossroads of metabolism, immunology, and cancer biology.","authors":"Peng Xu, Qin Yan","doi":"10.1007/s10555-026-10369-4","DOIUrl":"https://doi.org/10.1007/s10555-026-10369-4","url":null,"abstract":"<p><p>The multi-functional protein N-acetyltransferase 10 (NAT10), highly conserved from bacteria to human, is a versatile enzyme with an N-acetyltransferase domain, an RNA helicase domain, and a tRNA-binding domain, known for its ability to acetylate proteins and multiple RNA species. Specifically, NAT10 was reported to catalyze the N4-acetylcytidine (ac4C) modification on tRNA, rRNA, mRNA, and even viral RNA and to regulate translation efficiency, RNA stability, and eventually gene expression. NAT10 draws increasing attention for its emerging roles in rewiring metabolism, including amino acid, lipid, and glucose metabolism, and modulating immune responses to drive cancer progression, metastasis, and therapeutic resistance. In this review, we provide a conceptual framework of how the dysfunction of the highly conserved NAT10 leads to tumorigenesis, metastasis, and therapeutic resistance. We also summarize the major findings that reveal how NAT10 regulates cancer metabolism and immune responses. Lastly, we review the opportunities and challenges of targeting NAT10 to treat cancer and overcome drug resistance.</p>","PeriodicalId":520582,"journal":{"name":"Cancer metastasis reviews","volume":"45 3","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148766035","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}