Publications by authors named "F Pflumio"
Pediatric acute myeloid leukemia frequently harbor fusion oncogenes associated with poor prognosis, including KMT2A, NUP98 and GLIS2 rearrangements. While murine models have demonstrated their leukemogenic activities, the steps from a normal human cell to leukemic blasts remain unclear. Here, we precisely reproduced the inversion of chromosome 16 resulting in ETO2::GLIS2 fusion in human induced pluripotent stem cells (iPSC).
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- * Research using single-cell RNA sequencing identified a specific group of chemotherapy-resistant leukemic cells (CLCs) that are quiescent and marked by high CD44 expression, allowing them to evade treatment.
- * The study found that these CLCs exhibit unique gene activity and enhanced E-selectin binding during relapse, suggesting potential pathways for improving prognosis and developing new therapies.
Article Synopsis
- The study investigates the role of the ETO2::GLIS2 fusion oncogene in pediatric acute myeloid leukemia (AML), highlighting its connection to worse outcomes in patients.
- The researchers developed models using lentiviral transduction and CRISPR-Cas9 to explore how ETO2::GLIS2 influences leukemia development in human fetal versus post-natal hematopoietic stem cells.
- They found that the presence of specific human cytokines like IL3 and SCF is crucial for leukemogenesis, suggesting that a combination treatment targeting MEK and BCL2 could effectively reduce leukemia progression.
T-cell acute lymphoblastic leukemia (T-ALL) is a malignant hematological disorder characterized by an increased proliferation of immature T lymphocytes precursors. T-ALL treatment includes chemotherapy with strong side effects, and patients that undergo relapse display poor prognosis. Although cell-intrinsic oncogenic pathways are well-studied, the tumor microenvironment, like inflammatory cellular and molecular components is less explored in T-ALL.
View Article and Find Full Text PDFTranscriptional cofactors of the ETO family are recurrent fusion partners in acute leukemia. We characterized the ETO2 regulome by integrating transcriptomic and chromatin binding analyses in human erythroleukemia xenografts and controlled ETO2 depletion models. We demonstrate that beyond its well-established repressive activity, ETO2 directly activates transcription of MYB, among other genes.
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