ArticleAnnals of hematology2026
The novel ETV6::RARA fusion gene, identified in acute promyelocytic leukemia, is sensitive to invitro all-tans retinoic acid and arsenic trioxide administrations.
Article in Annals of hematology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Acute promyelocytic leukemia (APL) is characterized by the presence of PML::RARA fusion gene, and a favorable response to all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) administration. Here, we studied the leukemogenic properties of a novel fusion gene, ETV6::RARA t(12;17)(p13;q21), identified in an APL patient lacking the PML::RARA rearrangement. The ETV6-RARA fusion protein was over-expressed via lentiviral transfection in leukemia cells and its effects on cell growth were evaluated with cell counting kit 8 (CCK8) assay and on apoptosis and cellular differentiation with flow cytometry. The expression features induced by ETV6-RARA were studied by whole transcriptomic RNA sequencing analysis. ETV6-RARA over-expression enhanced the differentiation of U937 and HL60 cells to ATRA administration. ATRA, but not ATO, decreased the in-vitro levels of ETV6-RARA protein. ETV6-RARA significantly reduced the proliferation rates of U937 cells as compared to the control. Apoptosis in U937 ETV6-RARA+ cells was induced with combined ATRA and ATO administration. Differential gene expression analysis showed significant up-regulation of RARA in U937 ETV6-RARA+ cells, and gene set enrichment analysis revealed similarity between cells with ETV6::RARA and patients with PML::RARA based on their total RNA expression profiles. Furthermore, the expression profiles of U937 ETV6-RARA+ cells presented the activated enrichment of HALLMARK_EPITHELIAL_MESENCHYMAL_TRANSITION, and inhibited enrichment of HALLMARK_E2F_TARGETS pathways compared to the control cells. ETV6::RARA is an ATRA/ATO sensitive fusion gene.
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