<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>7(1)</volume><submitter>Jabbour C</submitter><pubmed_abstract>&lt;h4>Abstract&lt;/h4>BackgroundDiaphanous-related formin 3 (DIAPH3) is a member of the formin family, a group of proteins that regulate actin and microtubule dynamics. During mitosis, DIAPH3 localizes specifically to the centrosome. Its loss destabilizes microtubules and disrupts mitotic spindle polarity, leading to multipolar mitoses and abnormal chromosome segregation, which ultimately causes aneuploidy in daughter cells.&lt;h4>Methods&lt;/h4>We investigated &lt;i>DIAPH3&lt;/i> expression in glioma samples-including low-grade and high-grade gliomas-using publicly available datasets (The Cancer Genome Atlas and a single-cell RNA-seq study). We also explored the impact of &lt;i>DIAPH3&lt;/i> expression on aneuploidy in cultured glioblastoma cells.&lt;h4>Results&lt;/h4>&lt;i>DIAPH3&lt;/i> expression was specifically increas</pubmed_abstract><journal>Neuro-oncology advances</journal><pagination>vdaf233</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12746597</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>DIAPH3 is upregulated in high-grade gliomas and linked to chromosomal instability.</pubmed_title><pmcid>PMC12746597</pmcid><pubmed_authors>Jabbour C</pubmed_authors><pubmed_authors>Beka M</pubmed_authors><pubmed_authors>Gailly P</pubmed_authors><pubmed_authors>Tajeddine N</pubmed_authors></additional><is_claimable>false</is_claimable><name>DIAPH3 is upregulated in high-grade gliomas and linked to chromosomal instability.</name><description>&lt;h4>Abstract&lt;/h4>BackgroundDiaphanous-related formin 3 (DIAPH3) is a member of the formin family, a group of proteins that regulate actin and microtubule dynamics. During mitosis, DIAPH3 localizes specifically to the centrosome. Its loss destabilizes microtubules and disrupts mitotic spindle polarity, leading to multipolar mitoses and abnormal chromosome segregation, which ultimately causes aneuploidy in daughter cells.&lt;h4>Methods&lt;/h4>We investigated &lt;i>DIAPH3&lt;/i> expression in glioma samples-including low-grade and high-grade gliomas-using publicly available datasets (The Cancer Genome Atlas and a single-cell RNA-seq study). We also explored the impact of &lt;i>DIAPH3&lt;/i> expression on aneuploidy in cultured glioblastoma cells.&lt;h4>Results&lt;/h4>&lt;i>DIAPH3&lt;/i> expression was specifically increas</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Jan-Dec</publication><modification>2026-06-09T03:10:33.189Z</modification><creation>2026-06-09T03:07:35.283Z</creation></dates><accession>S-EPMC12746597</accession><cross_references><pubmed>41473744</pubmed><doi>10.1093/noajnl/vdaf233</doi></cross_references></HashMap>