[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"detail-sidebar-cat-0-en-105":3,"doc-seo-381110-105":59,"doc-detail-381110-en":131},{"code":4,"msg":5,"data":6},0,"success",[7,13,18,23,28,33,38,43,48,51,55],{"id":8,"doc_module":4,"doc_module_name":9,"category_name":10,"show_sort_weight":11,"slug":12},1,"Document","Story & Novel",90,"story-novel",{"id":14,"doc_module":4,"doc_module_name":9,"category_name":15,"show_sort_weight":16,"slug":17},2,"Literature",80,"literature",{"id":19,"doc_module":4,"doc_module_name":9,"category_name":20,"show_sort_weight":21,"slug":22},4,"Exam",70,"exam",{"id":24,"doc_module":4,"doc_module_name":9,"category_name":25,"show_sort_weight":26,"slug":27},5,"Comic",60,"comic",{"id":29,"doc_module":4,"doc_module_name":9,"category_name":30,"show_sort_weight":31,"slug":32},6,"Technology",50,"technology",{"id":34,"doc_module":4,"doc_module_name":9,"category_name":35,"show_sort_weight":36,"slug":37},7,"Healthcare",40,"healthcare",{"id":39,"doc_module":4,"doc_module_name":9,"category_name":40,"show_sort_weight":41,"slug":42},8,"Research & Report",30,"research-report",{"id":44,"doc_module":4,"doc_module_name":9,"category_name":45,"show_sort_weight":46,"slug":47},9,"Religion & Spirituality",20,"religion-spirituality",{"id":46,"doc_module":4,"doc_module_name":9,"category_name":49,"show_sort_weight":46,"slug":50},"World Cup","world-cup",{"id":52,"doc_module":4,"doc_module_name":9,"category_name":53,"show_sort_weight":52,"slug":54},10,"Lifestyle","lifestyle",{"id":56,"doc_module":4,"doc_module_name":9,"category_name":57,"show_sort_weight":24,"slug":58},19,"General","general",{"code":4,"msg":60,"data":61},"ok",{"site_id":62,"language":63,"slug":64,"title":65,"keywords":66,"description":67,"schema_data":68,"social_meta":124,"head_meta":126,"extra_data":128,"updated_unix":130},105,"en","tumor-microenvironment-signaling-and-therapeutics-in-cancer-progression","Tumor microenvironment signaling and therapeutics in cancer progression","","Tumor microenvironment (TME) signaling is a central driver of cancer progression, shaping interactions among cancer cells and surrounding stromal and immune components. The review surveys key TME elements and major molecular mediators, including ECM remodeling, chemokines and cytokines, and immune-regulatory pathways involving macrophages, fibroblasts, dendritic cells, and T/NK cells. It also outlines therapeutic implications, highlighting targets and strategies that modulate these signaling networks to improve anti-tumor responses.",{"@graph":69,"@context":123},[70,84,106],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/tumor-microenvironment-signaling-and-therapeutics-in-cancer-progression/381110/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/tumor-microenvironment-signaling-and-therapeutics-in-cancer-progression/381110.png","ImageObject",300,407,{"name":92,"@type":93},"Asher","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-11-04","2026-09-24",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",11,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"What does the tumor microenvironment signaling influence in cancer progression?","Question",{"text":113,"@type":114},"It governs communication between cancer cells and the surrounding stromal and immune compartments, thereby affecting tumor growth and progression. The review emphasizes pathway-level control of these interactions.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"Which cell types and components are highlighted as part of the tumor microenvironment?",{"text":118,"@type":114},"The text lists tumor-associated macrophages and cancer-associated fibroblasts, along with antigen-presenting and immune effector populations such as dendritic cells, T cells, and NK cells. Extracellular matrix (ECM) and extracellular vesicles are also referenced as important components.",{"name":120,"@type":111,"acceptedAnswer":121},"How does the review connect signaling mechanisms to therapeutics?",{"text":122,"@type":114},"It surveys molecular mediators and immune-regulatory signals to identify actionable targets and intervention strategies. The emphasis is on therapeutics that can modulate the same TME signaling networks that drive progression.","https://schema.org",{"og:url":83,"og:type":125,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":127,"canonical":83},"index,follow",{"doc_id":129,"site_id":62},381110,1790465200,{"code":4,"msg":5,"data":132},{"doc_id":129,"user_id":133,"nickname":92,"user_avatar":134,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":105,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":140,"language":141,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":142,"faqs":143,"seo_title":144,"seo_description":67,"update_tm":145,"read_time":146},687197207639,"https://ap-avatar.wpscdn.com/davatar_a8503ba1806abce46bf441b54a3ca4cd","DOI: 10.1002/cac2.12416  \nREVIEW  \nTumor microenvironment signaling and therapeutics in cancer progression  \nAnshika Goenka1  Fatima Khan2   BhupenderVerma3  Priyanka Sinha4 Crismita C. Dmello2  Manasi P. Jogalekar5  Prakash Gangadaran6, 7  Byeong-Cheol Ahn6, 7   \n1The Ken & Ruth Davee Department of Neurology, The Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, 60611, IL, USA  \n2 Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, 60611, IL, USA  \n3 Department of Ophthalmology, Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, 02114, MA, USA  \n4 Department of Neurology, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, 02129, MA, USA  \n5 Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, 94143, CA, USA  \n6 BK21 FOUR KNU Convergence Educational Program of Biomedical Sciences for Creative Future Talents, Department of Biomedical Science, School of Medicine, Kyungpook National University, Daegu, 41944, South Korea  \nAbbreviations: TME, tumor microenvironment; ECM, extracellular matrix; MMP, matrix metalloproteinase; TAM, tumor-associated macrophage; CAF, cancer-associated fibroblast; APC, antigen-presenting cell; DC, dendritic cell; Teff, effector T cell; NK, natural Killer cell; XCL, X-C Motif Chemokine Ligand; CCL, CC motif chemokine ligand; FLT3LG, FMS Related Receptor Tyrosine Kinase 3 Ligand; FGF, fibroblast growth factor; CXCL, CXC motif chemokine ligand; VEGF, vascular endothelial growth factor; SDF-1, stromal cell-derived factor 1; TGF-ß, transforming growth factor ß; IL, interleukin; IDO, indoleamine 2,3-dioxygenase; TDO2, tryptophan 2,3-dioxygenase; SLIT2, slit guidance ligand 2; CD, cluster of differentiation; PDGF, platelet-derived growth factor; PDGFR, platelet-derived growth factor receptor; HGF, hepatocyte growth factor; MET, mesenchymal-epithelial transition factor; EC, Endothelial cell; CAR-T Cell, Chimeric antigen receptor-T cell; PSMA, prostate-specific membrane antigen; TNF α, tumor necrosis factor α; NICD, notch-intracellular domain; ASO, antisense oligonucleotides; BiP, binding-immunoglobulin protein; HIF, hypoxia-inducible factor; PD-1, Programmed cell death protein 1; PD-L1, Programmed cell death protein ligand 1; CCR, C-C chemokine receptor type; 3D, Three (3D)-dimensional; PDX, patient-derived tumor xenograft; WNT, Wingless/Integrated; PKC, protein kinase C; ER, Endoplasmic Reticulum; cGAS, cyclic GMP–AMP synthase; STING, stimulator of interferon genes; CTLA4, Cytotoxic T-Lymphocyte Associated Protein 4; TIM-3, T-cell immunoglobulin mucin-3; LAG3, Lymphocyte Activating 3; PAK4, p21-Activated kinase 4; EGFRvIII, Epidermal growth factor receptor variant III; FGF, Fibroblast growth factor; PEGPH20, pegvorhyaluronidase alfa; DON, 6-diazo-5-oxo-l-norleucine; GM-CSF, Granulocyte-macrophage colony-stimulating factor; Th, T helper; Teff, T effector; HOX, Homeobox; DAG, diacylglycerol; STAT, Signal Transducer And Activator Of Transcription; NF-κB, Nuclear factor-κB; DLL1, delta like canonical Notch ligand 1; JAG2, jagged canonical Notch ligand 2; NICD, intracellular domain of the Notch receptor; ADC, antibody-drug conjugates; IRE1α, inositol-requiring enzyme 1α; SLC16A, solute carrier family 16 member; LDHA, lactate dehydrogenase A; CHC, cyano-4-hydroxycinnamate; ROS, Reactive Oxygen Species; IDH, Isocitrate dehydrogenase; D2HG,  \nD-2-Hydroxyglutarate; GBM, Glioblastoma; AML, Acute myeloid leukemia; TCGA, The Cancer Genome Atlas; TMEM, transmembrane protein 173; TBK-1, TANK-binding kinase 1; IRF-3, Interferon regulatory factor 3; PCDH, protocadherin; Cx, connexin 43; IKK, nuclear factor-κB (IκB) kinase; IFN-I, Type I interferons; MDSC, Myeloid-derived suppressor cell; BTLA, B and T lymphocyte attenuator; scRNA-seq, single-cell RNA sequ","cbCaikCd7Zb7i29x","https://ap.wps.com/l/cbCaikCd7Zb7i29x","pdf",2259778,37,"English","# Review Overview\n## Tumor Microenvironment (TME) Signaling\n## Molecular Mediators and Immune Crosstalk\n## Therapeutic Opportunities","[{\"question\":\"What does the tumor microenvironment signaling influence in cancer progression?\",\"answer\":\"It governs communication between cancer cells and the surrounding stromal and immune compartments, thereby affecting tumor growth and progression. The review emphasizes pathway-level control of these interactions.\"},{\"question\":\"Which cell types and components are highlighted as part of the tumor microenvironment?\",\"answer\":\"The text lists tumor-associated macrophages and cancer-associated fibroblasts, along with antigen-presenting and immune effector populations such as dendritic cells, T cells, and NK cells. Extracellular matrix (ECM) and extracellular vesicles are also referenced as important components.\"},{\"question\":\"How does the review connect signaling mechanisms to therapeutics?\",\"answer\":\"It surveys molecular mediators and immune-regulatory signals to identify actionable targets and intervention strategies. The emphasis is on therapeutics that can modulate the same TME signaling networks that drive progression.\"}]","Tumor microenvironment signaling and therapeutics in cancer progression | PDF",1790243633,93]