<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>66(15)</volume><submitter>Tura A</submitter><pubmed_abstract>&lt;h4>Purpose&lt;/h4>In uveal melanoma (UM), coexistence of the fatal monosomy 3 with the benign gain of chromosome 6p occurs rarely. The spatial organization of chromosomes can be influenced by the nucleoli, which become larger under hyperglycemia. We therefore hypothesized that hyperglycemia may be responsible for chromosome-specific aberrations in UM and analyzed its effect on nucleolar organization, chromosome territories, and missegregation rates in vitro.&lt;h4>Methods&lt;/h4>UM cell lines 92.1 and OMM2.5, UM cells from the primary tumors of two patients, and Tenon fibroblasts from a control were incubated in normo- or hyperglycemic medium (with 5.5 or 25 mM glucose, respectively) for one day, followed by the mitotic arrest with Nocodazole for 18-24 hours and recovery in fresh medium. Co-detect</pubmed_abstract><journal>Investigative ophthalmology &amp; visual science</journal><pagination>10</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12697705</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Missegregation of Chromosome 3 and Generation of Monosomy 3 in the Proliferating Uveal Melanoma Cells Under Hyperglycemia.</pubmed_title><pmcid>PMC12697705</pmcid><pubmed_authors>Grisanti S</pubmed_authors><pubmed_authors>Sonntag SR</pubmed_authors><pubmed_authors>von Bubnoff NCC</pubmed_authors><pubmed_authors>Tura A</pubmed_authors><pubmed_authors>Spielmann M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Missegregation of Chromosome 3 and Generation of Monosomy 3 in the Proliferating Uveal Melanoma Cells Under Hyperglycemia.</name><description>&lt;h4>Purpose&lt;/h4>In uveal melanoma (UM), coexistence of the fatal monosomy 3 with the benign gain of chromosome 6p occurs rarely. The spatial organization of chromosomes can be influenced by the nucleoli, which become larger under hyperglycemia. We therefore hypothesized that hyperglycemia may be responsible for chromosome-specific aberrations in UM and analyzed its effect on nucleolar organization, chromosome territories, and missegregation rates in vitro.&lt;h4>Methods&lt;/h4>UM cell lines 92.1 and OMM2.5, UM cells from the primary tumors of two patients, and Tenon fibroblasts from a control were incubated in normo- or hyperglycemic medium (with 5.5 or 25 mM glucose, respectively) for one day, followed by the mitotic arrest with Nocodazole for 18-24 hours and recovery in fresh medium. Co-detect</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Dec</publication><modification>2026-06-06T01:24:10.132Z</modification><creation>2026-05-24T03:11:46.498Z</creation></dates><accession>S-EPMC12697705</accession><cross_references><pubmed>41328998</pubmed><doi>10.1167/iovs.66.15.10</doi></cross_references></HashMap>