<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lu P</submitter><funding>NICHD NIH HHS</funding><funding>NIEHS NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>77-87</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2582391</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>321(1)</volume><pubmed_abstract>FGF signaling is associated with breast cancer and is required for mammary placode formation in the mouse. In this study, we employed a genetic mosaic analysis based on Cre-mediated recombination to investigate FGF receptor 2 (Fgfr2) function in the postnatal mammary gland. Mosaic inactivation of Fgfr2 by the MMTV-Cre transgene enabled us to compare the behavior of Fgfr2 null and Fgfr2 heterozygous cells in the same gland. Fgfr2 null cells were at a competitive disadvantage to their Fgfr2 heterozygous neighbors in the highly proliferative terminal end buds (TEBs) at the invasion front, owing to a negative effect of loss of Fgfr2 function on cell proliferation. However, Fgfr2 null cells were tolerated in mature ducts. In these genetic mosaic mammary glands, the epithelial network is apparen</pubmed_abstract><journal>Developmental biology</journal><pubmed_title>Genetic mosaic analysis reveals FGF receptor 2 function in terminal end buds during mammary gland branching morphogenesis.</pubmed_title><pmcid>PMC2582391</pmcid><funding_grant_id>CA057621</funding_grant_id><funding_grant_id>U01 ES012801</funding_grant_id><funding_grant_id>HD025331</funding_grant_id><funding_grant_id>HL07731</funding_grant_id><funding_grant_id>R01 CA057621</funding_grant_id><funding_grant_id>R37 HD025331-20</funding_grant_id><funding_grant_id>T32 HL007731-09</funding_grant_id><funding_grant_id>T32 HL007731</funding_grant_id><funding_grant_id>R01 CA057621-14</funding_grant_id><funding_grant_id>R37 HD025331</funding_grant_id><funding_grant_id>ES012801</funding_grant_id><funding_grant_id>U01 ES012801-05</funding_grant_id><pubmed_authors>Werb Z</pubmed_authors><pubmed_authors>Martin GR</pubmed_authors><pubmed_authors>Lu P</pubmed_authors><pubmed_authors>Ewald AJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genetic mosaic analysis reveals FGF receptor 2 function in terminal end buds during mammary gland branching morphogenesis.</name><description>FGF signaling is associated with breast cancer and is required for mammary placode formation in the mouse. In this study, we employed a genetic mosaic analysis based on Cre-mediated recombination to investigate FGF receptor 2 (Fgfr2) function in the postnatal mammary gland. Mosaic inactivation of Fgfr2 by the MMTV-Cre transgene enabled us to compare the behavior of Fgfr2 null and Fgfr2 heterozygous cells in the same gland. Fgfr2 null cells were at a competitive disadvantage to their Fgfr2 heterozygous neighbors in the highly proliferative terminal end buds (TEBs) at the invasion front, owing to a negative effect of loss of Fgfr2 function on cell proliferation. However, Fgfr2 null cells were tolerated in mature ducts. In these genetic mosaic mammary glands, the epithelial network is apparen</description><dates><release>2008-01-01T00:00:00Z</release><publication>2008 Sep</publication><modification>2025-04-20T02:07:43.355Z</modification><creation>2019-03-27T00:19:20Z</creation></dates><accession>S-EPMC2582391</accession><cross_references><pubmed>18585375</pubmed><doi>10.1016/j.ydbio.2008.06.005</doi></cross_references></HashMap>