<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>7(6)</volume><submitter>Uehara Y</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>We analyzed the FGF/FGFR and co-alteration cancer landscape, hypothesizing that combination therapy might be useful in the presence of co-drivers.&lt;h4>Materials and methods&lt;/h4>We describe FGF/FGFR-altered pathways, prognosis, and co-alterations [cBioPortal (N = 7574)] and therapeutic outcomes [University of California San Diego Molecular Tumor Board (MTB) (N = 16)].&lt;h4>Results&lt;/h4>Patients whose cancers harbored FGF/FGFR alterations (N = 1074) versus those without them (N = 6500) had shorter overall survival (OS) (median: 23.1 versus 26.4 months, P = 0.038) (cBioPortal). Only 6.1% (65/1074 patients) had no pathogenic co-alterations accompanying FGF/FGFR axis abnormalities. The most frequently co-altered pathways/genes involved: TP53 (70%); cell cycle (58%); PI3K (55%); a</pubmed_abstract><journal>ESMO open</journal><pagination>100647</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9808461</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Targeting the FGF/FGFR axis and its co-alteration allies.</pubmed_title><pmcid>PMC9808461</pmcid><pubmed_authors>Okamura R</pubmed_authors><pubmed_authors>Lee S</pubmed_authors><pubmed_authors>Sicklick JK</pubmed_authors><pubmed_authors>Kurzrock R</pubmed_authors><pubmed_authors>Ikeda S</pubmed_authors><pubmed_authors>Lim HJ</pubmed_authors><pubmed_authors>Kim KH</pubmed_authors><pubmed_authors>Uehara Y</pubmed_authors><pubmed_authors>Kato S</pubmed_authors><pubmed_authors>Persha HE</pubmed_authors><pubmed_authors>Adashek JJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Targeting the FGF/FGFR axis and its co-alteration allies.</name><description>&lt;h4>Background&lt;/h4>We analyzed the FGF/FGFR and co-alteration cancer landscape, hypothesizing that combination therapy might be useful in the presence of co-drivers.&lt;h4>Materials and methods&lt;/h4>We describe FGF/FGFR-altered pathways, prognosis, and co-alterations [cBioPortal (N = 7574)] and therapeutic outcomes [University of California San Diego Molecular Tumor Board (MTB) (N = 16)].&lt;h4>Results&lt;/h4>Patients whose cancers harbored FGF/FGFR alterations (N = 1074) versus those without them (N = 6500) had shorter overall survival (OS) (median: 23.1 versus 26.4 months, P = 0.038) (cBioPortal). Only 6.1% (65/1074 patients) had no pathogenic co-alterations accompanying FGF/FGFR axis abnormalities. The most frequently co-altered pathways/genes involved: TP53 (70%); cell cycle (58%); PI3K (55%); a</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2026-03-16T08:10:30.452Z</modification><creation>2025-04-19T04:47:45.493Z</creation></dates><accession>S-EPMC9808461</accession><cross_references><pubmed>36455506</pubmed><doi>10.1016/j.esmoop.2022.100647</doi></cross_references></HashMap>