<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Granoski MB</submitter><funding>NIDDK NIH HHS</funding><pagination>1427113</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11518795</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15</volume><pubmed_abstract>&lt;h4>Introduction&lt;/h4>The FOXC2 transcription factor has been tied to a wide range of disease states, serving as a promising prognostic biomarker associated with aggressive basal-like human breast cancers (increased cancer invasion and metastasis). Dysregulation of FOXC2 expression has also been found to promote defects in lymphatic remodeling and hyperplastic lymphedema-distichiasis (LD). Since chronic lymphedema is a forerunner of several malignancies and cancers have been known to arise from poorly healing chronic wounds (e.g., Marjolin ulcers), we examined the effect of Foxc2 dysfunction on skin wound healing.&lt;h4>Methods&lt;/h4>We used our splinted excisional wounding model that mimics human-like wound healing on wildtype and Foxc2&lt;sup>+/-&lt;/sup> mice (n = 4), which demonstrate incomplete l</pubmed_abstract><journal>Frontiers in physiology</journal><pubmed_title>Cancer and lymphatic marker FOXC2 drives wound healing and fibrotic tissue formation.</pubmed_title><pmcid>PMC11518795</pmcid><funding_grant_id>R01 DK074095</funding_grant_id><pubmed_authors>Kussie HC</pubmed_authors><pubmed_authors>Chen K</pubmed_authors><pubmed_authors>Gurtner GC</pubmed_authors><pubmed_authors>Yasmeh JP</pubmed_authors><pubmed_authors>Mora Pinos MG</pubmed_authors><pubmed_authors>Granoski MB</pubmed_authors><pubmed_authors>Hostler AC</pubmed_authors><pubmed_authors>McKenna E</pubmed_authors><pubmed_authors>Hahn WW</pubmed_authors><pubmed_authors>Fischer KS</pubmed_authors><pubmed_authors>Erickson RP</pubmed_authors><pubmed_authors>Sivaraj D</pubmed_authors><pubmed_authors>Quintero F</pubmed_authors><pubmed_authors>Alsharif AM</pubmed_authors><pubmed_authors>Witte MH</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cancer and lymphatic marker FOXC2 drives wound healing and fibrotic tissue formation.</name><description>&lt;h4>Introduction&lt;/h4>The FOXC2 transcription factor has been tied to a wide range of disease states, serving as a promising prognostic biomarker associated with aggressive basal-like human breast cancers (increased cancer invasion and metastasis). Dysregulation of FOXC2 expression has also been found to promote defects in lymphatic remodeling and hyperplastic lymphedema-distichiasis (LD). Since chronic lymphedema is a forerunner of several malignancies and cancers have been known to arise from poorly healing chronic wounds (e.g., Marjolin ulcers), we examined the effect of Foxc2 dysfunction on skin wound healing.&lt;h4>Methods&lt;/h4>We used our splinted excisional wounding model that mimics human-like wound healing on wildtype and Foxc2&lt;sup>+/-&lt;/sup> mice (n = 4), which demonstrate incomplete l</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024</publication><modification>2026-07-15T17:47:51.744Z</modification><creation>2025-04-04T01:58:38.473Z</creation></dates><accession>S-EPMC11518795</accession><cross_references><pubmed>39473610</pubmed><doi>10.3389/fphys.2024.1427113</doi></cross_references></HashMap>