<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Swanton C</submitter><funding>Cancer Research UK</funding><funding>Rosetrees Trust</funding><funding>European Research Council</funding><funding>The Francis Crick Institute</funding><pagination>704-12</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4497973</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>5(7)</volume><pubmed_abstract>&lt;h4>Unlabelled&lt;/h4>Deep sequencing technologies are revealing the complexities of cancer evolution, casting light on mutational processes fueling tumor adaptation, immune escape, and treatment resistance. Understanding mechanisms driving cancer diversity is a critical step toward developing strategies to attenuate tumor evolution and adaptation. One emerging mechanism fueling tumor diversity and subclonal evolution is genomic DNA cytosine deamination catalyzed by APOBEC3B and at least one other APOBEC family member. Deregulation of APOBEC3 enzymes causes a general mutator phenotype that manifests as diverse and heterogeneous tumor subclones. Here, we summarize knowledge of the APOBEC DNA deaminase family in cancer, and their role as driving forces for intratumor heterogeneity and a therape</pubmed_abstract><journal>Cancer discovery</journal><pubmed_title>APOBEC Enzymes: Mutagenic Fuel for Cancer Evolution and Heterogeneity.</pubmed_title><pmcid>PMC4497973</pmcid><funding_grant_id>A19310</funding_grant_id><funding_grant_id>17786</funding_grant_id><funding_grant_id>M179</funding_grant_id><funding_grant_id>19310</funding_grant_id><funding_grant_id>A17786</funding_grant_id><funding_grant_id>10169</funding_grant_id><funding_grant_id>M391</funding_grant_id><funding_grant_id>617844</funding_grant_id><funding_grant_id>A11590</funding_grant_id><pubmed_authors>Swanton C</pubmed_authors><pubmed_authors>Harris RS</pubmed_authors><pubmed_authors>McGranahan N</pubmed_authors><pubmed_authors>Starrett GJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>APOBEC Enzymes: Mutagenic Fuel for Cancer Evolution and Heterogeneity.</name><description>&lt;h4>Unlabelled&lt;/h4>Deep sequencing technologies are revealing the complexities of cancer evolution, casting light on mutational processes fueling tumor adaptation, immune escape, and treatment resistance. Understanding mechanisms driving cancer diversity is a critical step toward developing strategies to attenuate tumor evolution and adaptation. One emerging mechanism fueling tumor diversity and subclonal evolution is genomic DNA cytosine deamination catalyzed by APOBEC3B and at least one other APOBEC family member. Deregulation of APOBEC3 enzymes causes a general mutator phenotype that manifests as diverse and heterogeneous tumor subclones. Here, we summarize knowledge of the APOBEC DNA deaminase family in cancer, and their role as driving forces for intratumor heterogeneity and a therape</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Jul</publication><modification>2025-04-05T13:09:31.555Z</modification><creation>2019-06-06T14:36:09Z</creation></dates><accession>S-EPMC4497973</accession><cross_references><pubmed>26091828</pubmed><doi>10.1158/2159-8290.cd-15-0344</doi><doi>10.1158/2159-8290.CD-15-0344</doi></cross_references></HashMap>