<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>40(9)</volume><submitter>Paur J</submitter><pubmed_abstract>&lt;h4>Background &amp; aims&lt;/h4>Recently, overexpression of the fibroblast growth factor receptor 3 (FGFR3) splice variants FGFR3-IIIb and FGFR3-IIIc was found in ~50% of hepatocellular carcinoma (HCC). Here, we aim to identify FGFR3-IIIb/IIIc ligands, which drive the progression of HCC.&lt;h4>Methods&lt;/h4>FACS, MTT assay and/or growth curves served to identify the FGFR3-IIIb/IIIc ligand being most effective to induce growth of hepatoma/hepatocarcinoma cell lines, established from human HCC. The most potent FGF was characterized regarding the expression levels in epithelial and stromal cells of liver and HCC and impact on neoangiogenesis, clonogenicity and invasive growth of hepatoma/hepatocarcinoma cells.&lt;h4>Results&lt;/h4>Among all FGFR3-IIIb/IIIc ligands tested, FGF9 was the most potent growth facto</pubmed_abstract><journal>Liver international : official journal of the International Association for the Study of the Liver</journal><pagination>2279-2290</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7496895</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Interaction of FGF9 with FGFR3-IIIb/IIIc, a putative driver of growth and aggressive behaviour of hepatocellular carcinoma.</pubmed_title><pmcid>PMC7496895</pmcid><pubmed_authors>Holzmann K</pubmed_authors><pubmed_authors>Paur J</pubmed_authors><pubmed_authors>Valler M</pubmed_authors><pubmed_authors>Schimming J</pubmed_authors><pubmed_authors>Marian B</pubmed_authors><pubmed_authors>Taxauer K</pubmed_authors><pubmed_authors>Grasl-Kraupp B</pubmed_authors><pubmed_authors>Mohr T</pubmed_authors><pubmed_authors>Gvozdenovich A</pubmed_authors><pubmed_authors>Unterberger A</pubmed_authors><pubmed_authors>Grusch M</pubmed_authors><pubmed_authors>Berger W</pubmed_authors><pubmed_authors>Sienel R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Interaction of FGF9 with FGFR3-IIIb/IIIc, a putative driver of growth and aggressive behaviour of hepatocellular carcinoma.</name><description>&lt;h4>Background &amp; aims&lt;/h4>Recently, overexpression of the fibroblast growth factor receptor 3 (FGFR3) splice variants FGFR3-IIIb and FGFR3-IIIc was found in ~50% of hepatocellular carcinoma (HCC). Here, we aim to identify FGFR3-IIIb/IIIc ligands, which drive the progression of HCC.&lt;h4>Methods&lt;/h4>FACS, MTT assay and/or growth curves served to identify the FGFR3-IIIb/IIIc ligand being most effective to induce growth of hepatoma/hepatocarcinoma cell lines, established from human HCC. The most potent FGF was characterized regarding the expression levels in epithelial and stromal cells of liver and HCC and impact on neoangiogenesis, clonogenicity and invasive growth of hepatoma/hepatocarcinoma cells.&lt;h4>Results&lt;/h4>Among all FGFR3-IIIb/IIIc ligands tested, FGF9 was the most potent growth facto</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Sep</publication><modification>2025-04-22T21:52:22.392Z</modification><creation>2020-09-30T07:01:56Z</creation></dates><accession>S-EPMC7496895</accession><cross_references><pubmed>32378800</pubmed><doi>10.1111/liv.14505</doi></cross_references></HashMap>