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                <term xml:lang="en">B-cell acute lymphoblastic leukemia</term>
                <term xml:lang="en">PAX5 alterations</term>
                <term xml:lang="en">primary oncogenic event</term>
                <term xml:lang="en">PAX5 P80R mutation</term>
                <term xml:lang="en">leukemia initiation</term>
                <term xml:lang="en">oncogenic transformation</term>
                <term xml:lang="en">Hif2</term>
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              <p>Abstract The transcription factor PAX5 is a major target of genetic alterations in human B-cell precursor acute lymphoblastic leukemia (B-ALL). Among the alterations, the P80R mutation affecting the DNA-binding domain represents the most frequent PAX5 point mutation in B-ALL. In contrast to other somatic PAX5 mutations, PAX5P80R defines a distinct B-ALL subtype characterized by a unique transcriptional program. In this study, we aimed to develop a model to elucidate the mechanism by which PAX5P80R perturbs normal B-cell differentiation and the oncogenic relays involved in PAX5P80R-driven malignant progression. A retroviral complementation approach of Pax5-deficient murine fetal liver cells demonstrated at the functional and molecular levels that PAX5P80R failed to rescue definitive B-cell commitment but maintained the repression of T-cell development. Moreover, PAX5P80R eventually led to clonal B-ALL transformation after transplantation through the acquisition of secondary mutations in genes involved in the JAK/STAT and RAS/MAPK pathways. Finally, transcriptomic analyses combined with pharmacologic investigation revealed ectopic activation of HIF2α as a common feature of B-ALL and identified acriflavine as a potent drug against B-ALL. Hence, this study provides a strategy to model the multistep process of B-ALL and sheds light on the biological mechanism by which the PAX5P80R mutation leads to leukemia. Significance: PAX5P80R perturbs normal B-cell development, leads to clonal transformation, and activates HIF2α as an oncogenic relay, providing mechanistic insights that could improve treatment of B-cell acute lymphoblastic leukemia.</p>
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          <idno type="anr">ANR-23-IAHU-0005</idno>
          <orgName>Institut de la leucémie Paris Saint-Louis</orgName>
          <desc>Institut de la leucémie Paris Saint-Louis</desc>
          <date type="start">2023</date>
        </org>
      </listOrg>
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</TEI>