<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Devall MAM</submitter><funding>NIDDK NIH HHS</funding><funding>NIH NIDDK</funding><funding>NCI NIH HHS</funding><funding>NIH NCI</funding><pagination>1089-1100</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8639779</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(12)</volume><pubmed_abstract>Mechanisms underlying aspirin chemoprevention of colorectal cancer remain unclear. Prior studies have been limited because of the inability of preclinical models to recapitulate human normal colon epithelium or cellular heterogeneity present in mucosal biopsies. To overcome some of these obstacles, we performed &lt;i>in vitro&lt;/i> aspirin treatment of colon organoids derived from normal mucosal biopsies to reveal transcriptional networks relevant to aspirin chemoprevention. Colon organoids derived from 38 healthy individuals undergoing endoscopy were treated with 50 μmol/L aspirin or vehicle control for 72 hours and subjected to bulk RNA sequencing. Paired regression analysis using DESeq2 identified differentially expressed genes (DEG) associated with aspirin treatment. Cellular composition wa</pubmed_abstract><journal>Cancer prevention research (Philadelphia, Pa.)</journal><pubmed_title>Transcriptome-wide &lt;i>In Vitro&lt;/i> Effects of Aspirin on Patient-derived Normal Colon Organoids.</pubmed_title><pmcid>PMC8639779</pmcid><funding_grant_id>K01 DK120742</funding_grant_id><funding_grant_id>R01 CA211184</funding_grant_id><funding_grant_id>R01 CA257523</funding_grant_id><funding_grant_id>R01 CA201407</funding_grant_id><funding_grant_id>R01 CA137178</funding_grant_id><funding_grant_id>R35 CA253185</funding_grant_id><funding_grant_id>L30 CA209764</funding_grant_id><funding_grant_id>CA254314</funding_grant_id><funding_grant_id>R01 CA143237</funding_grant_id><funding_grant_id>F32 CA254314</funding_grant_id><funding_grant_id>R01 CA204279</funding_grant_id><funding_grant_id>R01 CA245314</funding_grant_id><pubmed_authors>Eaton S</pubmed_authors><pubmed_authors>Ali MW</pubmed_authors><pubmed_authors>Chan AT</pubmed_authors><pubmed_authors>Takacsi-Nagy O</pubmed_authors><pubmed_authors>Mo J</pubmed_authors><pubmed_authors>Powell SM</pubmed_authors><pubmed_authors>Drew DA</pubmed_authors><pubmed_authors>Devall MAM</pubmed_authors><pubmed_authors>Bryant J</pubmed_authors><pubmed_authors>Jennelle LT</pubmed_authors><pubmed_authors>Dampier CH</pubmed_authors><pubmed_authors>Diez-Obrero V</pubmed_authors><pubmed_authors>Moreno V</pubmed_authors><pubmed_authors>Peters U</pubmed_authors><pubmed_authors>Plummer SJ</pubmed_authors><pubmed_authors>Kedrin D</pubmed_authors><pubmed_authors>Yilmaz OH</pubmed_authors><pubmed_authors>Casey G</pubmed_authors><pubmed_authors>Zerjav DC</pubmed_authors></additional><is_claimable>false</is_claimable><name>Transcriptome-wide &lt;i>In Vitro&lt;/i> Effects of Aspirin on Patient-derived Normal Colon Organoids.</name><description>Mechanisms underlying aspirin chemoprevention of colorectal cancer remain unclear. Prior studies have been limited because of the inability of preclinical models to recapitulate human normal colon epithelium or cellular heterogeneity present in mucosal biopsies. To overcome some of these obstacles, we performed &lt;i>in vitro&lt;/i> aspirin treatment of colon organoids derived from normal mucosal biopsies to reveal transcriptional networks relevant to aspirin chemoprevention. Colon organoids derived from 38 healthy individuals undergoing endoscopy were treated with 50 μmol/L aspirin or vehicle control for 72 hours and subjected to bulk RNA sequencing. Paired regression analysis using DESeq2 identified differentially expressed genes (DEG) associated with aspirin treatment. Cellular composition wa</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Dec</publication><modification>2026-05-09T20:13:38.679Z</modification><creation>2025-02-19T00:56:31.267Z</creation></dates><accession>S-EPMC8639779</accession><cross_references><pubmed>34389629</pubmed><doi>10.1158/1940-6207.capr-21-0041</doi><doi>10.1158/1940-6207.CAPR-21-0041</doi></cross_references></HashMap>