<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ruiz-Ciancio D</submitter><funding>NHLBI NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>698-712</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10469072</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>33</volume><pubmed_abstract>Despite improvements in B cell acute lymphoblastic leukemia (B-ALL) treatment, a significant number of patients experience relapse of the disease, resulting in poor prognosis and high mortality. One of the drawbacks of current B-ALL treatments is the high toxicity associated with the non-specificity of chemotherapeutic drugs. Targeted therapy is an appealing strategy to treat B-ALL to mitigate these toxic off-target effects. One such target is the B cell surface protein CD22. The restricted expression of CD22 on the B-cell lineage and its ligand-induced internalizing properties make it an attractive target in cases of B cell malignancies. To target B-ALL and the CD22 protein, we performed cell internalization SELEX (Systematic Evolution of Ligands by EXponential enrichment) followed by molecular docking to identify internalizing aptamers specific for B-ALL cells that bind the CD22 cell-surface receptor. We identified two RNA aptamers, B-ALL1 and B-ALL2, that target human malignant B cells, with B-ALL1 the first documented RNA aptamer interacting with the CD22 antigen. These B-ALL-specific aptamers represent an important first step toward developing novel targeted therapies for B cell malignancy treatments.</pubmed_abstract><journal>Molecular therapy. Nucleic acids</journal><pubmed_title>Selection of a novel cell-internalizing RNA aptamer specific for CD22 antigen in B cell acute lymphoblastic leukemia.</pubmed_title><pmcid>PMC10469072</pmcid><funding_grant_id>R01 CA138503</funding_grant_id><funding_grant_id>R01 HL139581</funding_grant_id><funding_grant_id>P30 CA086862</funding_grant_id><pubmed_authors>Di Bartolo AL</pubmed_authors><pubmed_authors>Lin LH</pubmed_authors><pubmed_authors>Sanchez D</pubmed_authors><pubmed_authors>Mestre MB</pubmed_authors><pubmed_authors>Ruiz-Ciancio D</pubmed_authors><pubmed_authors>Barros MN</pubmed_authors><pubmed_authors>Masone D</pubmed_authors><pubmed_authors>Giangrande PH</pubmed_authors><pubmed_authors>Veeramani S</pubmed_authors><pubmed_authors>Thiel WH</pubmed_authors></additional><is_claimable>false</is_claimable><name>Selection of a novel cell-internalizing RNA aptamer specific for CD22 antigen in B cell acute lymphoblastic leukemia.</name><description>Despite improvements in B cell acute lymphoblastic leukemia (B-ALL) treatment, a significant number of patients experience relapse of the disease, resulting in poor prognosis and high mortality. One of the drawbacks of current B-ALL treatments is the high toxicity associated with the non-specificity of chemotherapeutic drugs. Targeted therapy is an appealing strategy to treat B-ALL to mitigate these toxic off-target effects. One such target is the B cell surface protein CD22. The restricted expression of CD22 on the B-cell lineage and its ligand-induced internalizing properties make it an attractive target in cases of B cell malignancies. To target B-ALL and the CD22 protein, we performed cell internalization SELEX (Systematic Evolution of Ligands by EXponential enrichment) followed by molecular docking to identify internalizing aptamers specific for B-ALL cells that bind the CD22 cell-surface receptor. We identified two RNA aptamers, B-ALL1 and B-ALL2, that target human malignant B cells, with B-ALL1 the first documented RNA aptamer interacting with the CD22 antigen. These B-ALL-specific aptamers represent an important first step toward developing novel targeted therapies for B cell malignancy treatments.</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Sep</publication><modification>2026-06-23T03:17:42.06Z</modification><creation>2025-04-20T03:47:16.728Z</creation></dates><accession>S-EPMC10469072</accession><cross_references><pubmed>37662970</pubmed><doi>10.1016/j.omtn.2023.07.028</doi></cross_references></HashMap>