<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ray AL</submitter><funding>American Cancer Society</funding><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><funding>NIGMS NIH HHS</funding><pagination>2158-2169</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10239359</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>29(11)</volume><pubmed_abstract>&lt;h4>Purpose&lt;/h4>G-CSF enhances colon cancer development. This study defines the prevalence and effects of increased G-CSF signaling in human colon cancers and investigates G-CSF inhibition as an immunotherapeutic strategy against metastatic colon cancer.&lt;h4>Experimental design&lt;/h4>Patient samples were used to evaluate G-CSF and G-CSF receptor (G-CSFR) levels by IHC with sera used to measure G-CSF levels. Peripheral blood mononuclear cells were used to assess the rate of G-CSFR+ T cells and IFNγ responses to chronic ex vivo G-CSF. An immunocompetent mouse model of peritoneal metastasis (MC38 cells in C57Bl/6J) was used to determine the effects of G-CSF inhibition (αG-CSF) on survival and the tumor microenvironment (TME) with flow and mass cytometry.&lt;h4>Results&lt;/h4>In human colon cancer samp</pubmed_abstract><journal>Clinical cancer research : an official journal of the American Association for Cancer Research</journal><pubmed_title>G-CSF Is a Novel Mediator of T-Cell Suppression and an Immunotherapeutic Target for Women with Colon Cancer.</pubmed_title><pmcid>PMC10239359</pmcid><funding_grant_id>P20GM103639-6146</funding_grant_id><funding_grant_id>MRSG 15-136-01-CCE</funding_grant_id><funding_grant_id>P30 CA225520</funding_grant_id><funding_grant_id>P20 GM103639</funding_grant_id><pubmed_authors>Fung KM</pubmed_authors><pubmed_authors>Lerner MR</pubmed_authors><pubmed_authors>Kamal M</pubmed_authors><pubmed_authors>Guo S</pubmed_authors><pubmed_authors>Urdaneta-Perez MG</pubmed_authors><pubmed_authors>Saunders AS</pubmed_authors><pubmed_authors>Lang ML</pubmed_authors><pubmed_authors>Nofchissey RA</pubmed_authors><pubmed_authors>Hanson JA</pubmed_authors><pubmed_authors>Cloyde M</pubmed_authors><pubmed_authors>Lewis SE</pubmed_authors><pubmed_authors>Reidy MA</pubmed_authors><pubmed_authors>Ray AL</pubmed_authors><pubmed_authors>Morris KT</pubmed_authors></additional><is_claimable>false</is_claimable><name>G-CSF Is a Novel Mediator of T-Cell Suppression and an Immunotherapeutic Target for Women with Colon Cancer.</name><description>&lt;h4>Purpose&lt;/h4>G-CSF enhances colon cancer development. This study defines the prevalence and effects of increased G-CSF signaling in human colon cancers and investigates G-CSF inhibition as an immunotherapeutic strategy against metastatic colon cancer.&lt;h4>Experimental design&lt;/h4>Patient samples were used to evaluate G-CSF and G-CSF receptor (G-CSFR) levels by IHC with sera used to measure G-CSF levels. Peripheral blood mononuclear cells were used to assess the rate of G-CSFR+ T cells and IFNγ responses to chronic ex vivo G-CSF. An immunocompetent mouse model of peritoneal metastasis (MC38 cells in C57Bl/6J) was used to determine the effects of G-CSF inhibition (αG-CSF) on survival and the tumor microenvironment (TME) with flow and mass cytometry.&lt;h4>Results&lt;/h4>In human colon cancer samp</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jun</publication><modification>2026-05-28T11:24:37.586Z</modification><creation>2024-11-12T08:29:29.986Z</creation></dates><accession>S-EPMC10239359</accession><cross_references><pubmed>36951682</pubmed><doi>10.1158/1078-0432.ccr-22-3918</doi><doi>10.1158/1078-0432.CCR-22-3918</doi></cross_references></HashMap>