<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-05-21T23:07:06Z</responseDate><request verb="GetRecord" identifier="oai:repisalud.isciii.es:20.500.12105/23443" metadataPrefix="marc">https://repisalud.isciii.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:repisalud.isciii.es:20.500.12105/23443</identifier><datestamp>2024-11-28T19:30:46Z</datestamp><setSpec>com_20.500.12105_15322</setSpec><setSpec>com_20.500.12105_2051</setSpec><setSpec>col_20.500.12105_16967</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Sesé, Borja</subfield>
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      <subfield code="a">Íñiguez-Muñoz, Sandra</subfield>
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      <subfield code="a">Ensenyat-Mendez, Miquel</subfield>
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      <subfield code="a">Orozco, Javier IJ</subfield>
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      <subfield code="a">Marzese, Diego M</subfield>
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      <subfield code="a">Glioma stem cells (GSCs) have self-renewal and tumor-initiating capacities involved in drug resistance and immune evasion mechanisms in glioblastoma (GBM). Core-GSCs (c-GSCs) were identified by selecting cells co-expressing high levels of embryonic stem cell (ESC) markers from a single-cell RNA-seq patient-derived GBM dataset (n = 28). Induced c-GSCs (ic-GSCs) were generated by reprogramming GBM-derived cells (GBM-DCs) using induced pluripotent stem cell (iPSC) technology. The characterization of ic-GSCs and GBM-DCs was conducted by immunostaining, transcriptomic, and DNA methylation (DNAm) analysis. We identified a GSC population (4.22% ﾱ 0.59) exhibiting concurrent high expression of ESC markers and downregulation of immune-associated pathways, named c-GSCs. In vitro ic-GSCs presented high expression of ESC markers and downregulation of antigen presentation HLA proteins. Transcriptomic analysis revealed a strong agreement of enriched biological pathways between tumor c-GSCs and in vitro ic-GSCs (? = 0.71). Integration of our epigenomic profiling with 833 functional ENCODE epigenetic maps identifies increased DNA methylation on HLA genes' regulatory regions associated with polycomb repressive marks in a stem-like phenotype. This study unravels glioblastoma immune-evasive mechanisms involving a c-GSC population. In addition, it provides a cellular model with paired gene expression, and DNA methylation maps to explore potential therapeutic complements for GBM immunotherapy.</subfield>
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      <subfield code="a">Sesé B, Íñiguez-Muñoz S, Ensenyat-Mendez M, Llinàs-Arias P, Ramis G, Orozco JIJ, et al. Glioblastoma Embryonic-like Stem Cells Exhibit Immune-Evasive Phenotype. Cancers. 2022 Apr 21;14(9):2070.</subfield>
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      <subfield code="a">Glioblastoma Embryonic-like Stem Cells Exhibit Immune-Evasive Phenotype</subfield>
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