<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hickey CJ</submitter><funding>European Hematology Association</funding><funding>NCI NIH HHS</funding><pagination>159-69</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3538328</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>121(1)</volume><pubmed_abstract>Recently, we showed that increased miR-181a expression was associated with improved outcomes in cytogenetically normal acute myeloid leukemia (CN-AML). Interestingly, miR-181a expression was increased in CN-AML patients harboring CEBPA mutations, which are usually biallelic and associate with better prognosis. CEBPA encodes the C/EBPα transcription factor. We demonstrate here that the presence of N-terminal CEBPA mutations and miR-181a expression are linked. Indeed, the truncated C/EBPα-p30 isoform, which is produced from the N-terminal mutant CEBPA gene or from the differential translation of wild-type CEBPA mRNA and is commonly believed to have no transactivation activity, binds to the miR-181a-1 promoter and up-regulates the microRNA expression. Furthermore, we show that lenalidomide, a</pubmed_abstract><journal>Blood</journal><pubmed_title>Lenalidomide-mediated enhanced translation of C/EBPα-p30 protein up-regulates expression of the antileukemic microRNA-181a in acute myeloid leukemia.</pubmed_title><pmcid>PMC3538328</pmcid><funding_grant_id>CA35279</funding_grant_id><funding_grant_id>CA101140</funding_grant_id><funding_grant_id>U10 CA035279</funding_grant_id><funding_grant_id>U24 CA114725</funding_grant_id><funding_grant_id>CA114725</funding_grant_id><funding_grant_id>CA16058</funding_grant_id><funding_grant_id>CA33601</funding_grant_id><funding_grant_id>U10 CA003927</funding_grant_id><funding_grant_id>CA31946</funding_grant_id><funding_grant_id>U10 CA031946</funding_grant_id><funding_grant_id>P30 CA016058</funding_grant_id><funding_grant_id>U10 CA077658</funding_grant_id><funding_grant_id>U10 CA101140</funding_grant_id><funding_grant_id>TRTH68</funding_grant_id><funding_grant_id>CA03927</funding_grant_id><funding_grant_id>CA41287</funding_grant_id><funding_grant_id>CA77658</funding_grant_id><funding_grant_id>R01 CA095512</funding_grant_id><funding_grant_id>U10 CA033601</funding_grant_id><funding_grant_id>U10 CA041287</funding_grant_id><funding_grant_id>P50 CA140158</funding_grant_id><pubmed_authors>Vij R</pubmed_authors><pubmed_authors>Whitman SP</pubmed_authors><pubmed_authors>Becker H</pubmed_authors><pubmed_authors>Santhanam R</pubmed_authors><pubmed_authors>Zhao X</pubmed_authors><pubmed_authors>Mrozek K</pubmed_authors><pubmed_authors>Nicolet D</pubmed_authors><pubmed_authors>Perrotti D</pubmed_authors><pubmed_authors>Radomska HS</pubmed_authors><pubmed_authors>Walker A</pubmed_authors><pubmed_authors>Bloomfield CD</pubmed_authors><pubmed_authors>Fehniger TA</pubmed_authors><pubmed_authors>Byrd JC</pubmed_authors><pubmed_authors>Lee LJ</pubmed_authors><pubmed_authors>Marcucci G</pubmed_authors><pubmed_authors>Alachkar H</pubmed_authors><pubmed_authors>Eiring AM</pubmed_authors><pubmed_authors>Maharry K</pubmed_authors><pubmed_authors>Wu LC</pubmed_authors><pubmed_authors>Hickey CJ</pubmed_authors><pubmed_authors>Schwind S</pubmed_authors><pubmed_authors>Garzon R</pubmed_authors><pubmed_authors>Blum W</pubmed_authors><pubmed_authors>Mishra A</pubmed_authors><pubmed_authors>Dorrance AM</pubmed_authors><pubmed_authors>Wu YZ</pubmed_authors><pubmed_authors>Caligiuri MA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Lenalidomide-mediated enhanced translation of C/EBPα-p30 protein up-regulates expression of the antileukemic microRNA-181a in acute myeloid leukemia.</name><description>Recently, we showed that increased miR-181a expression was associated with improved outcomes in cytogenetically normal acute myeloid leukemia (CN-AML). Interestingly, miR-181a expression was increased in CN-AML patients harboring CEBPA mutations, which are usually biallelic and associate with better prognosis. CEBPA encodes the C/EBPα transcription factor. We demonstrate here that the presence of N-terminal CEBPA mutations and miR-181a expression are linked. Indeed, the truncated C/EBPα-p30 isoform, which is produced from the N-terminal mutant CEBPA gene or from the differential translation of wild-type CEBPA mRNA and is commonly believed to have no transactivation activity, binds to the miR-181a-1 promoter and up-regulates the microRNA expression. Furthermore, we show that lenalidomide, a</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Jan</publication><modification>2026-05-02T09:11:42.839Z</modification><creation>2026-04-07T17:47:39.408Z</creation></dates><accession>S-EPMC3538328</accession><cross_references><pubmed>23100311</pubmed><doi>10.1182/blood-2012-05-428573</doi></cross_references></HashMap>