<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Matsumoto T</submitter><funding>JSPS KAKENHI Grant-in-Aid for Early-Career Scientists</funding><funding>JSPS KAKENHI Grant-in-Aid for Scientific Research (C)</funding><funding>Japan Society for the Promotion of Science</funding><pagination>4583</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11083213</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>25(9)</volume><pubmed_abstract>5-azacytidine (AZA), a representative DNA-demethylating drug, has been widely used to treat myelodysplastic syndromes (MDS). However, it remains unclear whether AZA's DNA demethylation of any specific gene is correlated with clinical responses to AZA. In this study, we investigated genes that could contribute to the development of evidence-based epigenetic therapeutics with AZA. A DNA microarray identified that AZA specifically upregulated the expression of 438 genes in AZA-sensitive MDS-L cells but not in AZA-resistant counterpart MDS-L/CDA cells. Of these 438 genes, the &lt;i>ALOX12&lt;/i> gene was hypermethylated in MDS-L cells but not in MDS-L/CDA cells. In addition, we further found that (1) the &lt;i>ALOX12&lt;/i> gene was hypermethylated in patients with MDS compared to healthy controls; (2) MD</pubmed_abstract><journal>International journal of molecular sciences</journal><pubmed_title>Enhanced ALOX12 Gene Expression Predicts Therapeutic Susceptibility to 5-Azacytidine in Patients with Myelodysplastic Syndromes.</pubmed_title><pmcid>PMC11083213</pmcid><funding_grant_id>24K18567</funding_grant_id><funding_grant_id>21K06703</funding_grant_id><pubmed_authors>Matsumoto T</pubmed_authors><pubmed_authors>Ono M</pubmed_authors><pubmed_authors>Murakami Y</pubmed_authors><pubmed_authors>Yoshida-Sakai N</pubmed_authors><pubmed_authors>Kanazawa K</pubmed_authors><pubmed_authors>Katsuchi D</pubmed_authors><pubmed_authors>Imamura Y</pubmed_authors><pubmed_authors>Okamura T</pubmed_authors><pubmed_authors>Kuwano M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Enhanced ALOX12 Gene Expression Predicts Therapeutic Susceptibility to 5-Azacytidine in Patients with Myelodysplastic Syndromes.</name><description>5-azacytidine (AZA), a representative DNA-demethylating drug, has been widely used to treat myelodysplastic syndromes (MDS). However, it remains unclear whether AZA's DNA demethylation of any specific gene is correlated with clinical responses to AZA. In this study, we investigated genes that could contribute to the development of evidence-based epigenetic therapeutics with AZA. A DNA microarray identified that AZA specifically upregulated the expression of 438 genes in AZA-sensitive MDS-L cells but not in AZA-resistant counterpart MDS-L/CDA cells. Of these 438 genes, the &lt;i>ALOX12&lt;/i> gene was hypermethylated in MDS-L cells but not in MDS-L/CDA cells. In addition, we further found that (1) the &lt;i>ALOX12&lt;/i> gene was hypermethylated in patients with MDS compared to healthy controls; (2) MD</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Apr</publication><modification>2026-05-26T20:10:44.385Z</modification><creation>2026-05-26T03:07:08.737Z</creation></dates><accession>S-EPMC11083213</accession><cross_references><pubmed>38731802</pubmed><doi>10.3390/ijms25094583</doi></cross_references></HashMap>