<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12</volume><submitter>Feng S</submitter><pubmed_abstract>The AlkB family of Fe (II) and α-ketoglutarate-dependent dioxygenases works by removing alkyl substituents from alkylation-damaged nucleic acid bases through oxidative dealkylation, subsequently affecting tumor progression and patient prognosis. However, the specific roles of the AlkB family in Glioblastoma remain to be elucidated. By taking advantage of the abundant bioinformatics databases, such as GEPIA2, cBioPortal and TIMER, we performed a comprehensive analysis of the AlkB family in GBM, and managed to identify the significant prognostic hallmarks and therapeutic targets within this family. We found that the expression levels of ALKBH2 and ALKBH8 were significantly up-regulated in GBM compared with normal tissues. Meanwhile, the patients with high levels of ALKBH2 and ALKBH8 possesse</pubmed_abstract><journal>Frontiers in oncology</journal><pagination>847821</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8965608</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The AlkB Family: Potential Prognostic Biomarkers and Therapeutic Targets in Glioblastoma.</pubmed_title><pmcid>PMC8965608</pmcid><pubmed_authors>Zhang M</pubmed_authors><pubmed_authors>Feng S</pubmed_authors><pubmed_authors>Xu Z</pubmed_authors><pubmed_authors>Peng J</pubmed_authors></additional><is_claimable>false</is_claimable><name>The AlkB Family: Potential Prognostic Biomarkers and Therapeutic Targets in Glioblastoma.</name><description>The AlkB family of Fe (II) and α-ketoglutarate-dependent dioxygenases works by removing alkyl substituents from alkylation-damaged nucleic acid bases through oxidative dealkylation, subsequently affecting tumor progression and patient prognosis. However, the specific roles of the AlkB family in Glioblastoma remain to be elucidated. By taking advantage of the abundant bioinformatics databases, such as GEPIA2, cBioPortal and TIMER, we performed a comprehensive analysis of the AlkB family in GBM, and managed to identify the significant prognostic hallmarks and therapeutic targets within this family. We found that the expression levels of ALKBH2 and ALKBH8 were significantly up-regulated in GBM compared with normal tissues. Meanwhile, the patients with high levels of ALKBH2 and ALKBH8 possesse</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2026-04-08T17:27:15.772Z</modification><creation>2025-04-04T23:03:17.241Z</creation></dates><accession>S-EPMC8965608</accession><cross_references><pubmed>35371987</pubmed><doi>10.3389/fonc.2022.847821</doi></cross_references></HashMap>