<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chen JE</submitter><funding>Mayo Clinic Brain Tumor Patient-Derived Xenograft National Resource</funding><funding>NIBIB NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>National Institute of Diabetes and Digestive and Kidney Diseases</funding><funding>National Cancer Institute</funding><funding>NCI NIH HHS</funding><funding>NINDS NIH HHS</funding><funding>National Institute of Biomedical Imaging and Bioengineering</funding><pagination>346</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7677841</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>17(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Glioblastoma is the most common and deadly form of primary brain cancer, accounting for more than 13,000 new diagnoses annually in the USA alone. Microglia are the innate immune cells within the central nervous system, acting as a front-line defense against injuries and inflammation via a process that involves transformation from a quiescent to an activated phenotype. Crosstalk between GBM cells and microglia represents an important axis to consider in the development of tissue engineering platforms to examine pathophysiological processes underlying GBM progression and therapy.&lt;h4>Methods&lt;/h4>This work used a brain-mimetic hydrogel system to study patient-derived glioblastoma specimens and their interactions with microglia. Here, glioblastoma cells were either cultured a</pubmed_abstract><journal>Journal of neuroinflammation</journal><pubmed_title>Crosstalk between microglia and patient-derived glioblastoma cells inhibit invasion in a three-dimensional gelatin hydrogel model.</pubmed_title><pmcid>PMC7677841</pmcid><funding_grant_id>P50 CA108961</funding_grant_id><funding_grant_id>R01 DK099528</funding_grant_id><funding_grant_id>R24 NS092940</funding_grant_id><funding_grant_id>R01 CA197488</funding_grant_id><funding_grant_id>T32 CA009370</funding_grant_id><funding_grant_id>T32 EB019944</funding_grant_id><funding_grant_id>R01CA197488</funding_grant_id><funding_grant_id>R01DK099528</funding_grant_id><funding_grant_id>T32EB019944</funding_grant_id><pubmed_authors>Gaskins HR</pubmed_authors><pubmed_authors>Lumibao J</pubmed_authors><pubmed_authors>Steelman AJ</pubmed_authors><pubmed_authors>Harley BAC</pubmed_authors><pubmed_authors>Chen JE</pubmed_authors><pubmed_authors>Leary S</pubmed_authors><pubmed_authors>Sarkaria JN</pubmed_authors></additional><is_claimable>false</is_claimable><name>Crosstalk between microglia and patient-derived glioblastoma cells inhibit invasion in a three-dimensional gelatin hydrogel model.</name><description>&lt;h4>Background&lt;/h4>Glioblastoma is the most common and deadly form of primary brain cancer, accounting for more than 13,000 new diagnoses annually in the USA alone. Microglia are the innate immune cells within the central nervous system, acting as a front-line defense against injuries and inflammation via a process that involves transformation from a quiescent to an activated phenotype. Crosstalk between GBM cells and microglia represents an important axis to consider in the development of tissue engineering platforms to examine pathophysiological processes underlying GBM progression and therapy.&lt;h4>Methods&lt;/h4>This work used a brain-mimetic hydrogel system to study patient-derived glioblastoma specimens and their interactions with microglia. Here, glioblastoma cells were either cultured a</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Nov</publication><modification>2025-04-18T14:43:10.51Z</modification><creation>2024-11-12T23:46:40.653Z</creation></dates><accession>S-EPMC7677841</accession><cross_references><pubmed>33208156</pubmed><doi>10.1186/s12974-020-02026-6</doi></cross_references></HashMap>