<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liu YT</submitter><funding>NIH National Eye Institute</funding><funding>NEI NIH HHS</funding><funding>National Cancer Institute</funding><funding>NCI NIH HHS</funding><funding>Cancer Prevention and Research Institute of Texas</funding><pagination>1854-1866</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6726575</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>17(9)</volume><pubmed_abstract>Disruption of the &lt;i>CDKN2A&lt;/i> (&lt;i>INK4A/ARF&lt;/i>) and &lt;i>B&lt;/i> (&lt;i>INK4B&lt;/i>) genes, which encode three function-independent tumor suppressors, is one of the most common events in human cancer. Because their relative importance in tumor prevention appears to be species- and context-specific, studying their regulation can shed light on mechanisms by which they are bypassed in malignant transformation. We previously unveiled a new pathway in which TGFβ selectively induces &lt;i>Arf&lt;/i> at mouse &lt;i>Cdkn2a&lt;/i> in eye development and cultured fibroblasts. As TGFβ signaling is often derailed in cancer development or progression, we investigated its control of &lt;i>CDKN2A/B&lt;/i> in human cancer. Computational analyses of sequencing and array data from nearly 11,000 patients with cancer in TCGA showed </pubmed_abstract><journal>Molecular cancer research : MCR</journal><pubmed_title>Identification of &lt;i>De Novo&lt;/i> Enhancers Activated by TGFβ to Drive Expression of &lt;i>CDKN2A&lt;/i> and &lt;i>B&lt;/i> in HeLa Cells.</pubmed_title><pmcid>PMC6726575</pmcid><funding_grant_id>R01 EY019942</funding_grant_id><funding_grant_id>CA142543</funding_grant_id><funding_grant_id>RP120685-P2</funding_grant_id><funding_grant_id>RP180319</funding_grant_id><funding_grant_id>P30 CA142543</funding_grant_id><pubmed_authors>Xu L</pubmed_authors><pubmed_authors>Skapek SX</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Liem P</pubmed_authors><pubmed_authors>Zheng Y</pubmed_authors><pubmed_authors>Hooks JC</pubmed_authors><pubmed_authors>Zhou Q</pubmed_authors><pubmed_authors>Bennett L</pubmed_authors><pubmed_authors>Liu YT</pubmed_authors></additional><is_claimable>false</is_claimable><name>Identification of &lt;i>De Novo&lt;/i> Enhancers Activated by TGFβ to Drive Expression of &lt;i>CDKN2A&lt;/i> and &lt;i>B&lt;/i> in HeLa Cells.</name><description>Disruption of the &lt;i>CDKN2A&lt;/i> (&lt;i>INK4A/ARF&lt;/i>) and &lt;i>B&lt;/i> (&lt;i>INK4B&lt;/i>) genes, which encode three function-independent tumor suppressors, is one of the most common events in human cancer. Because their relative importance in tumor prevention appears to be species- and context-specific, studying their regulation can shed light on mechanisms by which they are bypassed in malignant transformation. We previously unveiled a new pathway in which TGFβ selectively induces &lt;i>Arf&lt;/i> at mouse &lt;i>Cdkn2a&lt;/i> in eye development and cultured fibroblasts. As TGFβ signaling is often derailed in cancer development or progression, we investigated its control of &lt;i>CDKN2A/B&lt;/i> in human cancer. Computational analyses of sequencing and array data from nearly 11,000 patients with cancer in TCGA showed </description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Sep</publication><modification>2026-05-04T10:08:50.899Z</modification><creation>2020-05-22T11:28:10Z</creation></dates><accession>S-EPMC6726575</accession><cross_references><pubmed>31189690</pubmed><doi>10.1158/1541-7786.mcr-19-0289</doi><doi>10.1158/1541-7786.MCR-19-0289</doi></cross_references></HashMap>