<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yustein JT</submitter><funding>NCI NIH HHS</funding><funding>NINDS NIH HHS</funding><pagination>3534-9</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2840500</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>107(8)</volume><pubmed_abstract>Ectopic Myc expression plays a key role in human tumorigenesis, and Myc dose-dependent tumorigenesis has been well established in transgenic mice, but the Myc target genes that are dependent on Myc levels have not been well characterized. In this regard, we used the human P493-6 B cells, which have a preneoplastic state dependent on the Epstein-Barr viral EBNA2 protein and a neoplastic state with ectopic inducible Myc, to identify putative ectopic Myc target genes. Among the ectopic targets, JAG2 that encodes a Notch receptor ligand Jagged2, was directly induced by Myc. Inhibition of Notch signaling through RNAi targeting JAG2 or the gamma-secretase Notch inhibitor N-[N-(3,5-difluorophenacetyl)-L-alanyl]-(S)-phenylglycine t-butyl ester (DAPT) preferentially inhibited the neoplastic state i</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>Induction of ectopic Myc target gene JAG2 augments hypoxic growth and tumorigenesis in a human B-cell model.</pubmed_title><pmcid>PMC2840500</pmcid><funding_grant_id>R01 NS055089</funding_grant_id><funding_grant_id>R01 CA051497</funding_grant_id><funding_grant_id>T32CA60441</funding_grant_id><funding_grant_id>R01 CA57341</funding_grant_id><funding_grant_id>R01 CA51497</funding_grant_id><funding_grant_id>T32 CA060441</funding_grant_id><funding_grant_id>R01 CA057341</funding_grant_id><pubmed_authors>Yustein JT</pubmed_authors><pubmed_authors>Gao P</pubmed_authors><pubmed_authors>Chng WJ</pubmed_authors><pubmed_authors>Dang CV</pubmed_authors><pubmed_authors>Vuica-Ross M</pubmed_authors><pubmed_authors>Jie C</pubmed_authors><pubmed_authors>Le A</pubmed_authors><pubmed_authors>Eberhart CG</pubmed_authors><pubmed_authors>Liu YC</pubmed_authors><pubmed_authors>Bergsagel PL</pubmed_authors></additional><is_claimable>false</is_claimable><name>Induction of ectopic Myc target gene JAG2 augments hypoxic growth and tumorigenesis in a human B-cell model.</name><description>Ectopic Myc expression plays a key role in human tumorigenesis, and Myc dose-dependent tumorigenesis has been well established in transgenic mice, but the Myc target genes that are dependent on Myc levels have not been well characterized. In this regard, we used the human P493-6 B cells, which have a preneoplastic state dependent on the Epstein-Barr viral EBNA2 protein and a neoplastic state with ectopic inducible Myc, to identify putative ectopic Myc target genes. Among the ectopic targets, JAG2 that encodes a Notch receptor ligand Jagged2, was directly induced by Myc. Inhibition of Notch signaling through RNAi targeting JAG2 or the gamma-secretase Notch inhibitor N-[N-(3,5-difluorophenacetyl)-L-alanyl]-(S)-phenylglycine t-butyl ester (DAPT) preferentially inhibited the neoplastic state i</description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 Feb</publication><modification>2026-05-01T16:58:14.11Z</modification><creation>2026-04-18T03:08:35.571Z</creation></dates><accession>S-EPMC2840500</accession><cross_references><pubmed>20133585</pubmed><doi>10.1073/pnas.0901230107</doi></cross_references></HashMap>