<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wang Z</submitter><funding>National Natural Science Foundation of China</funding><pagination>738</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7483467</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(9)</volume><pubmed_abstract>Histone deacetylase 7 (HDAC7), a member of class IIa HDACs, has been described to be an important regulator for B cell development and has a potential role in B cell acute lymphoblastic leukemia (B-ALL). CC1007, a BML-210 analog, is designed to indirectly inhibit class IIa HDACs by binding to myocyte enhancer factor-2 (MEF2) and blocking the recruitment of class IIa HDACs to MEF2-targeted genes to enhance the expression of these targets. In this study, we investigated the anticancer effects of CC1007 in breakpoint cluster region-Abelson 1 fusion gene-negative (BCR-ABL1&lt;sup>-&lt;/sup>) pre-B-ALL cell lines and primary patient-derived BCR-ABL1&lt;sup>-&lt;/sup> pre-B-ALL cells. CC1007 had obvious antileukemic activity toward pre-B-ALL cells in vitro and in vivo; it also significantly prolonged median</pubmed_abstract><journal>Cell death &amp; disease</journal><pubmed_title>A small molecular compound CC1007 induces cross-lineage differentiation by inhibiting HDAC7 expression and HDAC7/MEF2C interaction in BCR-ABL1&lt;sup>-&lt;/sup> pre-B-ALL.</pubmed_title><pmcid>PMC7483467</pmcid><funding_grant_id>81500171</funding_grant_id><funding_grant_id>81600183</funding_grant_id><funding_grant_id>81470323</funding_grant_id><pubmed_authors>Zhang G</pubmed_authors><pubmed_authors>Chen L</pubmed_authors><pubmed_authors>Liu S</pubmed_authors><pubmed_authors>Li R</pubmed_authors><pubmed_authors>Deng M</pubmed_authors><pubmed_authors>Cheng Z</pubmed_authors><pubmed_authors>Peng H</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Hu G</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Luo Y</pubmed_authors><pubmed_authors>Wang Z</pubmed_authors><pubmed_authors>Zhu S</pubmed_authors><pubmed_authors>Xu Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>A small molecular compound CC1007 induces cross-lineage differentiation by inhibiting HDAC7 expression and HDAC7/MEF2C interaction in BCR-ABL1&lt;sup>-&lt;/sup> pre-B-ALL.</name><description>Histone deacetylase 7 (HDAC7), a member of class IIa HDACs, has been described to be an important regulator for B cell development and has a potential role in B cell acute lymphoblastic leukemia (B-ALL). CC1007, a BML-210 analog, is designed to indirectly inhibit class IIa HDACs by binding to myocyte enhancer factor-2 (MEF2) and blocking the recruitment of class IIa HDACs to MEF2-targeted genes to enhance the expression of these targets. In this study, we investigated the anticancer effects of CC1007 in breakpoint cluster region-Abelson 1 fusion gene-negative (BCR-ABL1&lt;sup>-&lt;/sup>) pre-B-ALL cell lines and primary patient-derived BCR-ABL1&lt;sup>-&lt;/sup> pre-B-ALL cells. CC1007 had obvious antileukemic activity toward pre-B-ALL cells in vitro and in vivo; it also significantly prolonged median</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Sep</publication><modification>2025-04-18T18:31:22.506Z</modification><creation>2020-09-25T07:03:21Z</creation></dates><accession>S-EPMC7483467</accession><cross_references><pubmed>32913188</pubmed><doi>10.1038/s41419-020-02949-1</doi></cross_references></HashMap>