<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>10</volume><submitter>Bewarder M</submitter><pubmed_abstract>Recently, neurabin-I and SAMD14 have been described as the autoantigenic target of approximately 66% of B-cell receptors (BCRs) of primary central nervous system lymphomas (PCNSL). Neurabin-I and SAMD14 share a highly homologous SAM domain that becomes immunogenic after atypical hyper-N-glycosylation (SAMD14 at ASN339 and neurabin-I at ASN1277). This post-translational modification of neurabin-I and SAMD14 seems to lead to a chronic immune reaction with B-cell receptor activation contributing to lymphoma genesis of PCNSLs. The selective tropism of PCNSL to the CNS corresponds well to the neurabin-I and SAMD14 protein expression pattern. When conjugated to Pseudomonas Exotoxin A (ETA´), the PCNSL reactive epitope exerts cytotoxic effects on lymphoma cells expressing a SAMD14/neurabin-I reac</pubmed_abstract><journal>Frontiers in oncology</journal><pagination>580364</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7689012</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Integration of the B-Cell Receptor Antigen Neurabin-I/SAMD14 Into an Antibody Format as New Therapeutic Approach for the Treatment of Primary CNS Lymphoma.</pubmed_title><pmcid>PMC7689012</pmcid><pubmed_authors>Pfreundschuh M</pubmed_authors><pubmed_authors>Hoth M</pubmed_authors><pubmed_authors>Bewarder M</pubmed_authors><pubmed_authors>Moelle C</pubmed_authors><pubmed_authors>Preuss KD</pubmed_authors><pubmed_authors>Neumann F</pubmed_authors><pubmed_authors>Kiefer M</pubmed_authors><pubmed_authors>Regitz E</pubmed_authors><pubmed_authors>Kaddu-Mulindwa D</pubmed_authors><pubmed_authors>Christofyllakis K</pubmed_authors><pubmed_authors>Thurner L</pubmed_authors><pubmed_authors>Stilgenbauer S</pubmed_authors><pubmed_authors>Fadle N</pubmed_authors><pubmed_authors>Goerens L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Integration of the B-Cell Receptor Antigen Neurabin-I/SAMD14 Into an Antibody Format as New Therapeutic Approach for the Treatment of Primary CNS Lymphoma.</name><description>Recently, neurabin-I and SAMD14 have been described as the autoantigenic target of approximately 66% of B-cell receptors (BCRs) of primary central nervous system lymphomas (PCNSL). Neurabin-I and SAMD14 share a highly homologous SAM domain that becomes immunogenic after atypical hyper-N-glycosylation (SAMD14 at ASN339 and neurabin-I at ASN1277). This post-translational modification of neurabin-I and SAMD14 seems to lead to a chronic immune reaction with B-cell receptor activation contributing to lymphoma genesis of PCNSLs. The selective tropism of PCNSL to the CNS corresponds well to the neurabin-I and SAMD14 protein expression pattern. When conjugated to Pseudomonas Exotoxin A (ETA´), the PCNSL reactive epitope exerts cytotoxic effects on lymphoma cells expressing a SAMD14/neurabin-I reac</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020</publication><modification>2025-04-25T20:43:07.98Z</modification><creation>2021-02-20T10:07:24Z</creation></dates><accession>S-EPMC7689012</accession><cross_references><pubmed>33282736</pubmed><doi>10.3389/fonc.2020.580364</doi></cross_references></HashMap>