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This study analyzes CMP expression using bulk, single-cell, and spatial anatomical resolutions, linking CMP enrichment with worse survival, oncogenic alterations, mesenchymal state, pro-tumor immune infiltration, and immune checkpoint expression. A 17-gene Matrisome17 signature outperforms MGMT promoter methylation and canonical subtypes and may predict PD1 blockade benefit, enabling patient stratification for treatment selection and optimization.",{"@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/a-prognostic-matrix-gene-expression-signature-defines-functional-glioblastoma-phenotypes-and-niches/443255/",{"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/a-prognostic-matrix-gene-expression-signature-defines-functional-glioblastoma-phenotypes-and-niches/443255.png","ImageObject",300,407,{"name":92,"@type":93},"Hazel","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-11-01","2026-09-29",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",12,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"What niche interactions are emphasized in glioblastoma, and why do they matter?","Question",{"text":113,"@type":114},"The study highlights interactions among tumor, immune, and vascular niches as major drivers of GBM malignancy and treatment response. It focuses on how extracellular core matrix proteins (CMPs) mediate these interactions.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"How does CMP enrichment relate to patient outcomes in GBM?",{"text":118,"@type":114},"CMP enrichment is associated with worse patient survival. It also correlates with specific oncogenic alterations, a mesenchymal state, pro-tumor immune infiltration, and immune checkpoint expression.",{"name":120,"@type":111,"acceptedAnswer":121},"What is Matrisome17 (M17), and how is it different from existing biomarkers?",{"text":122,"@type":114},"Matrisome17 (M17) is a 17-gene CMP signature identified as a stronger prognostic factor than MGMT promoter methylation status and canonical GBM subtypes. The signature may also predict responses to PD1 blockade.","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},443255,1790816561,{"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":36,"preview_page_count":4},137441390410,"https://ap-avatar.wpscdn.com/avatar/2000252f4ab5702993?_k=1776741390130283984","communications biology Article  \n\n| A Nature Portfolio journal | |\n| --- | --- |\n| [https://doi.org/10.1038/s42003-025-09245-8](https://doi.org/10.1038/s42003-025-09245-8) |  |\n| A prognostic matrix gene expression signature defi nes functional glioblastoma phenotypes and niches\u003Cbr> Check for updates |  |\n| Monika Vishnoi 1,2, Zeynep Dereli3, Zheng Yin4, Elisabeth K. Kong3,5, Meric Kinali6, Kisan Thapa6, Ozgun Babur6, Kyuson Yun 7,8, Nourhan Abdelfattah 7,8, Xubin Li3, Behnaz Bozorgui 3, Mary C. Farach-Carson9,10, Robert C. Rostomily 1,2,11  & Anil Korkut 3  |  |\n\nInteractions among tumor, immune, and vascular niches play major roles in glioblastoma (GBM) malignancy and treatment responses. The composition and heterogeneity of extracellular core matrix proteins (CMPs) that mediate such interactions are not well understood. Here, we present an analysis of the clinical relevance of CMP expression in GBM at bulk, single-cell, and spatial anatomical resolution. We show that CMP enrichment is associated with worse patient survival, specific driveroncogenic alterations, mesenchymal state, pro-tumor immune infiltration, and immune checkpoint expression. Matrisome expression is enriched in vascular and leading edge/infiltrative niches that are known to harbor glioma stem cells. Finally, we identify a17-gene CMP signature, termed Matrisome17 (M17), which is a stronger prognostic factor compared to MGMT promoter methylation status as well as canonical subtypes, and importantly, may predict responsesto PD1blockade. Patient stratification based on matrisome profiles can contribute to the selection and optimization of treatment strategies.  \nGlioblastoma (GBM) is an aggressive disease wherein meaningful improvements in survival have yet to be realized in a significant number of patients1. A high degree of intratumor heterogeneity, invasive growth and myriad mechanisms of treatment resistance limit the effectiveness of standard of care chemoradiation, targeted precision approaches and immunotherapy2,3. Central to the success of precision therapy is the integration of molecular and/or cellular data that accurately captures therapeutic targets and prognostic markers. TheMGMTpromoter methylation status, actionable driver mutations and immune checkpoint status have emerged as candidate biomarkers to inform chemotherapy, targeted therapy, and immunotherapy, respectively4. Despite their conceptual appeal, precision therapy and immunotherapy have yet to significantly improve durable outcomes1,5–11. The lack of progress with these approaches, and  \nlimited efficacy ofstandard genotoxic therapies, reflects, in part, insufficient understanding of factors that impact GBM malignancy and treatment responses.  \nThe genomic landscape in GBM is well described with established correlations between clinical properties and transcriptomic GBM subtypes termed Mesenchymal, Classical, and Proneural12–14. However, the functional and clinical relevance as well as diversity of the GBM extracellular matrix (ECM) at the anatomic, tissue, and cellular levels are not as well established15–17. The ECM is organized as a large network of proteins, collectively termed the matrisome18, 19, comprised of core matrix proteins (CMPs, including glycoproteins, collagens, and proteoglycans) and matrix associated proteins (MAPs)18,20. CMPs provide a structural/functional scaffold while MAPs interact with and regulate the CMPs to promote cell adhesion and signaling and regulation of ECM composition and structure19,20. Thematrisome proteins play critical roles in regulating normal and pathologic processes, including cancer malignancy21,22. Mechanistically, matrisome-tumor interactions mediated by CMPs contribute to cancer phenotypes through ligand-receptor interactions and structural mechanobiological effects that directly regulate tumor and stromal cell signaling or  \n1Department of Neurosurgery, Houston Methodist Research Institute, Houston, TX, USA. 2Department of Neurosurgery, Weill Cornell ","cbCaidD5V5aQdzWw","https://ap.wps.com/l/cbCaidD5V5aQdzWw","pdf",4741847,16,"English","# CMP expression and clinical relevance in GBM\n## Association with survival, mutations, and immune context\n# Matrisome17 (M17) prognostic signature\n## Comparison with MGMT methylation and canonical subtypes\n## Prediction of PD1 blockade response\n# Precision oncology implications\n## Patient stratification and therapy optimization","[{\"question\":\"What niche interactions are emphasized in glioblastoma, and why do they matter?\",\"answer\":\"The study highlights interactions among tumor, immune, and vascular niches as major drivers of GBM malignancy and treatment response. It focuses on how extracellular core matrix proteins (CMPs) mediate these interactions.\"},{\"question\":\"How does CMP enrichment relate to patient outcomes in GBM?\",\"answer\":\"CMP enrichment is associated with worse patient survival. It also correlates with specific oncogenic alterations, a mesenchymal state, pro-tumor immune infiltration, and immune checkpoint expression.\"},{\"question\":\"What is Matrisome17 (M17), and how is it different from existing biomarkers?\",\"answer\":\"Matrisome17 (M17) is a 17-gene CMP signature identified as a stronger prognostic factor than MGMT promoter methylation status and canonical GBM subtypes. The signature may also predict responses to PD1 blockade.\"}]","A prognostic matrix gene expression signature defines functional glioblastoma phenotypes and niches | PDF",1790703442]