<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Nyland SB</submitter><funding>NCRR NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>581-7</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3312981</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>36(5)</volume><pubmed_abstract>Large granular lymphocyte (LGL) leukemia is characterized by clonal expansion of antigen-activated cytotoxic T cells (CTL). Patients frequently exhibit seroreactivity against a human T-cell leukemia virus (HTLV) epitope, BA21. Aplastic anemia, paroxysmal nocturnal hemoglobinuria and myelodysplastic syndrome are bone marrow failure diseases that can also be associated with similar aberrant CTL activation (LGL-BMF). We identified a BA21 peptide that was specifically reactive with LGL leukemia sera and found significantly elevated antibody reactivity against the same peptide in LGL-BMF sera. This finding of shared seroreactivity in LGL-BMF conditions and LGL leukemia suggests that these diseases might share a common pathogenesis.</pubmed_abstract><journal>Leukemia research</journal><pubmed_title>Seroreactivity to LGL leukemia-specific epitopes in aplastic anemia, myelodysplastic syndrome and paroxysmal nocturnal hemoglobinuria: results of a bone marrow failure consortium study.</pubmed_title><pmcid>PMC3312981</pmcid><funding_grant_id>U54RR019397</funding_grant_id><funding_grant_id>CA133525</funding_grant_id><funding_grant_id>R01 CA133525-05</funding_grant_id><funding_grant_id>CA112112</funding_grant_id><funding_grant_id>R01 CA098472</funding_grant_id><funding_grant_id>U54 RR019397</funding_grant_id><funding_grant_id>R01 CA112112</funding_grant_id><funding_grant_id>CA 94872</funding_grant_id><funding_grant_id>U54 RR019397-01</funding_grant_id><funding_grant_id>R01 CA098472-09</funding_grant_id><funding_grant_id>R01 CA133525</funding_grant_id><funding_grant_id>R01 CA112112-04</funding_grant_id><pubmed_authors>Clemente MJ</pubmed_authors><pubmed_authors>Loughran TP</pubmed_authors><pubmed_authors>Jarbadan NR</pubmed_authors><pubmed_authors>Baab KT</pubmed_authors><pubmed_authors>Krissinger DJ</pubmed_authors><pubmed_authors>Liao J</pubmed_authors><pubmed_authors>Nyland SB</pubmed_authors><pubmed_authors>Paquette R</pubmed_authors><pubmed_authors>Cuthbertson D</pubmed_authors><pubmed_authors>List AF</pubmed_authors><pubmed_authors>Irby RB</pubmed_authors><pubmed_authors>Epling-Burnette P</pubmed_authors><pubmed_authors>Maciejewski JP</pubmed_authors><pubmed_authors>Sokol L</pubmed_authors><pubmed_authors>Schaefer E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Seroreactivity to LGL leukemia-specific epitopes in aplastic anemia, myelodysplastic syndrome and paroxysmal nocturnal hemoglobinuria: results of a bone marrow failure consortium study.</name><description>Large granular lymphocyte (LGL) leukemia is characterized by clonal expansion of antigen-activated cytotoxic T cells (CTL). Patients frequently exhibit seroreactivity against a human T-cell leukemia virus (HTLV) epitope, BA21. Aplastic anemia, paroxysmal nocturnal hemoglobinuria and myelodysplastic syndrome are bone marrow failure diseases that can also be associated with similar aberrant CTL activation (LGL-BMF). We identified a BA21 peptide that was specifically reactive with LGL leukemia sera and found significantly elevated antibody reactivity against the same peptide in LGL-BMF sera. This finding of shared seroreactivity in LGL-BMF conditions and LGL leukemia suggests that these diseases might share a common pathogenesis.</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 May</publication><modification>2020-10-29T14:20:30Z</modification><creation>2019-03-27T00:51:37Z</creation></dates><accession>S-EPMC3312981</accession><cross_references><pubmed>22386729</pubmed><doi>10.1016/j.leukres.2012.02.001</doi></cross_references></HashMap>