<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12(7)</volume><submitter>Laranjeira ABA</submitter><funding>Division of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, MD, USA</funding><pubmed_abstract>&lt;h4>Background&lt;/h4>Ten-eleven-translocation (TET) 2 is a member of the TET family of proteins (TET1-3). &lt;i>DNMT1&lt;/i> gene deletion confers resistance to DNA methyltransferase (DNMT) inhibitors in colorectal, breast, and ovarian cancer cells. Currently, the effect of &lt;i>DNMT1&lt;/i> gene status on TET2 phenotype following DNMT inhibitor treatment is unclear in human malignancies.&lt;h4>Methods&lt;/h4>Human colorectal carcinoma HCT116 cells (&lt;i>DNMT&lt;sup>+/+&lt;/sup>&lt;/i>) and their isogenic DNMT1 knockout (&lt;i>DNMT1&lt;sup>-/-&lt;/sup>&lt;/i>) counterpart were treated with DNMT inhibitors. Expression of TET2 and tumor suppressor (p16&lt;sup>ink4A&lt;/sup> and p15&lt;sup>ink4B&lt;/sup>) proteins were examined by Western blot. Apoptosis and &lt;i>CDKN2A&lt;/i> promoter demethylation following drug treatment were detected by Annexin-V</pubmed_abstract><journal>Diseases (Basel, Switzerland)</journal><pagination>163</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11276550</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Upregulation of TET2 and Resistance to DNA Methyltransferase (DNMT) Inhibitors in &lt;i>DNMT1&lt;/i>-Deleted Cancer Cells.</pubmed_title><pmcid>PMC11276550</pmcid><pubmed_authors>Doroshow JH</pubmed_authors><pubmed_authors>Nguyen D</pubmed_authors><pubmed_authors>Laranjeira ABA</pubmed_authors><pubmed_authors>Yang SX</pubmed_authors><pubmed_authors>Pelosof LC</pubmed_authors></additional><is_claimable>false</is_claimable><name>Upregulation of TET2 and Resistance to DNA Methyltransferase (DNMT) Inhibitors in &lt;i>DNMT1&lt;/i>-Deleted Cancer Cells.</name><description>&lt;h4>Background&lt;/h4>Ten-eleven-translocation (TET) 2 is a member of the TET family of proteins (TET1-3). &lt;i>DNMT1&lt;/i> gene deletion confers resistance to DNA methyltransferase (DNMT) inhibitors in colorectal, breast, and ovarian cancer cells. Currently, the effect of &lt;i>DNMT1&lt;/i> gene status on TET2 phenotype following DNMT inhibitor treatment is unclear in human malignancies.&lt;h4>Methods&lt;/h4>Human colorectal carcinoma HCT116 cells (&lt;i>DNMT&lt;sup>+/+&lt;/sup>&lt;/i>) and their isogenic DNMT1 knockout (&lt;i>DNMT1&lt;sup>-/-&lt;/sup>&lt;/i>) counterpart were treated with DNMT inhibitors. Expression of TET2 and tumor suppressor (p16&lt;sup>ink4A&lt;/sup> and p15&lt;sup>ink4B&lt;/sup>) proteins were examined by Western blot. Apoptosis and &lt;i>CDKN2A&lt;/i> promoter demethylation following drug treatment were detected by Annexin-V</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jul</publication><modification>2026-04-08T19:18:57.588Z</modification><creation>2026-04-08T12:59:24.196Z</creation></dates><accession>S-EPMC11276550</accession><cross_references><pubmed>39057134</pubmed><doi>10.3390/diseases12070163</doi></cross_references></HashMap>