<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>32(3)</volume><submitter>Imbery JF</submitter><pubmed_abstract>Chronic lymphocytic leukemia (CLL) growth is dependent on both B cell receptor (BCR) signaling and signals from microenvironmental T helper (Th) cells. We previously described a mechanism where Th cells enhance BCR signaling and proliferation through CD45 phosphatase activity regulation via galectin-1 and CD43. The CLL negative prognostic indicator CD38 is linked to BCR signaling and proliferation, with its expression induced by Th cells. Here, we explore a link between CD38 and CD45 phosphatase activity regulation using patient-derived material in a Th-CLL cell co-culture model. Results demonstrate CD43 and galectin-1 are co-expressed with CD38, defining proliferative CLL cells with augmented CD45 activity. CD38 enzymatic and receptor inhibition regulated CD43 and galectin-1 expression, C</pubmed_abstract><journal>Molecular therapy. Oncology</journal><pagination>200841</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11519781</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>CD38 regulates chronic lymphocytic leukemia proliferation via CD45 phosphatase activity.</pubmed_title><pmcid>PMC11519781</pmcid><pubmed_authors>Bottini N</pubmed_authors><pubmed_authors>Imbery JF</pubmed_authors><pubmed_authors>Stanford SM</pubmed_authors><pubmed_authors>Wiik C</pubmed_authors><pubmed_authors>Dobbing MK</pubmed_authors><pubmed_authors>Heinzelbecker J</pubmed_authors><pubmed_authors>Szodoray P</pubmed_authors><pubmed_authors>Jebsen JK</pubmed_authors><pubmed_authors>Munthe LA</pubmed_authors><pubmed_authors>Nakken B</pubmed_authors><pubmed_authors>Tjonnfjord GE</pubmed_authors><pubmed_authors>Tveita A</pubmed_authors></additional><is_claimable>false</is_claimable><name>CD38 regulates chronic lymphocytic leukemia proliferation via CD45 phosphatase activity.</name><description>Chronic lymphocytic leukemia (CLL) growth is dependent on both B cell receptor (BCR) signaling and signals from microenvironmental T helper (Th) cells. We previously described a mechanism where Th cells enhance BCR signaling and proliferation through CD45 phosphatase activity regulation via galectin-1 and CD43. The CLL negative prognostic indicator CD38 is linked to BCR signaling and proliferation, with its expression induced by Th cells. Here, we explore a link between CD38 and CD45 phosphatase activity regulation using patient-derived material in a Th-CLL cell co-culture model. Results demonstrate CD43 and galectin-1 are co-expressed with CD38, defining proliferative CLL cells with augmented CD45 activity. CD38 enzymatic and receptor inhibition regulated CD43 and galectin-1 expression, C</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Sep</publication><modification>2026-07-16T07:19:00.278Z</modification><creation>2025-04-06T15:30:21.734Z</creation></dates><accession>S-EPMC11519781</accession><cross_references><pubmed>39474602</pubmed><doi>10.1016/j.omton.2024.200841</doi></cross_references></HashMap>