<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Shan NL</submitter><funding>National Institute of Environmental Health Sciences</funding><funding>NCCIH NIH HHS</funding><funding>NIEHS NIH HHS</funding><funding>NCI NIH HHS</funding><funding>National Center for Complementary and Integrative Health of the NIH</funding><pagination>673-686</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7415686</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(8)</volume><pubmed_abstract>Ductal carcinoma &lt;i>in situ&lt;/i> (DCIS), which accounts for one out of every five new breast cancer diagnoses, will progress to potentially lethal invasive ductal carcinoma (IDC) in about 50% of cases. Vitamin D compounds have been shown to inhibit progression to IDC in the MCF10DCIS model. This inhibition appears to involve a reduction in the cancer stem cell-like population in MCF10DCIS tumors. To identify genes that are involved in the vitamin D effects, a global transcriptomic analysis was undertaken of MCF10DCIS cells grown in mammosphere cultures, in which cancer stem-like cells grow preferentially and produce colonies by self-renewal and maturation, in the presence and absence of 1α25(OH)&lt;sub>2&lt;/sub>D&lt;sub>3&lt;/sub> and a vitamin D analog, BXL0124. Using next-generation RNA-sequencing, </pubmed_abstract><journal>Cancer prevention research (Philadelphia, Pa.)</journal><pubmed_title>Analysis of the Transcriptome: Regulation of Cancer Stemness in Breast Ductal Carcinoma &lt;i>In Situ&lt;/i> by Vitamin D Compounds.</pubmed_title><pmcid>PMC7415686</pmcid><funding_grant_id>R01 AT009152</funding_grant_id><funding_grant_id>ES005022</funding_grant_id><funding_grant_id>R01 CA127645</funding_grant_id><funding_grant_id>P30 ES005022</funding_grant_id><funding_grant_id>R01 AT007036</funding_grant_id><pubmed_authors>Furmanski P</pubmed_authors><pubmed_authors>Cheng D</pubmed_authors><pubmed_authors>Li SN</pubmed_authors><pubmed_authors>Sargsyan D</pubmed_authors><pubmed_authors>Maehr H</pubmed_authors><pubmed_authors>Wernyj R</pubmed_authors><pubmed_authors>Kuo HD</pubmed_authors><pubmed_authors>Cai L</pubmed_authors><pubmed_authors>Kong AN</pubmed_authors><pubmed_authors>Minden A</pubmed_authors><pubmed_authors>Bak MJ</pubmed_authors><pubmed_authors>Wu R</pubmed_authors><pubmed_authors>Shan NL</pubmed_authors><pubmed_authors>Fang M</pubmed_authors><pubmed_authors>Suh N</pubmed_authors></additional><is_claimable>false</is_claimable><name>Analysis of the Transcriptome: Regulation of Cancer Stemness in Breast Ductal Carcinoma &lt;i>In Situ&lt;/i> by Vitamin D Compounds.</name><description>Ductal carcinoma &lt;i>in situ&lt;/i> (DCIS), which accounts for one out of every five new breast cancer diagnoses, will progress to potentially lethal invasive ductal carcinoma (IDC) in about 50% of cases. Vitamin D compounds have been shown to inhibit progression to IDC in the MCF10DCIS model. This inhibition appears to involve a reduction in the cancer stem cell-like population in MCF10DCIS tumors. To identify genes that are involved in the vitamin D effects, a global transcriptomic analysis was undertaken of MCF10DCIS cells grown in mammosphere cultures, in which cancer stem-like cells grow preferentially and produce colonies by self-renewal and maturation, in the presence and absence of 1α25(OH)&lt;sub>2&lt;/sub>D&lt;sub>3&lt;/sub> and a vitamin D analog, BXL0124. Using next-generation RNA-sequencing, </description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Aug</publication><modification>2026-05-03T04:59:02.586Z</modification><creation>2021-02-21T05:14:11Z</creation></dates><accession>S-EPMC7415686</accession><cross_references><pubmed>32467291</pubmed><doi>10.1158/1940-6207.capr-19-0566</doi><doi>10.1158/1940-6207.CAPR-19-0566</doi></cross_references></HashMap>