Publications by authors named "S Hebrard"
B cell acute lymphoblastic leukemia (B-ALL) is a multistep disease characterized by the hierarchical acquisition of genetic alterations. However, the question of how a primary oncogene reprograms stem cell-like properties in committed B cells and leads to a preneoplastic population remains unclear. Here, we used the PAX5::ELN oncogenic model to demonstrate a causal link between the differentiation blockade, the self-renewal, and the emergence of preleukemic stem cells (pre-LSCs).
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- * The study analyzed 113 cases of del(11q) MDS, highlighting features like a predominance in females, survival rates similar to other MDS cases, and a specific genetic deletion affecting key genes associated with hematopoiesis.
- * Findings suggest that the loss of the CADM1 gene, along with other genetic mutations, may play a significant role in the development of del(11q) MDS, indicating its potential as
PAX5-ELN oncoprotein promotes multistep B-cell acute lymphoblastic leukemia in mice.
Proc Natl Acad Sci U S A
October 2018
is a well-known haploinsufficient tumor suppressor gene in human B-cell precursor acute lymphoblastic leukemia (B-ALL) and is involved in various chromosomal translocations that fuse a part of PAX5 with other partners. However, the role of PAX5 fusion proteins in B-ALL initiation and transformation is ill-known. We previously reported a new recurrent t(7;9)(q11;p13) chromosomal translocation in human B-ALL that juxtaposed to the coding sequence of elastin ().
View Article and Find Full Text PDFPax5 is the guardian of the B cell identity since it primes or enhances the expression of B cell specific genes and concomitantly represses the expression of B cell inappropriate genes. The tight regulation of is therefore required for an efficient B cell differentiation. A defect in its dosage can translate into immunodeficiency or malignant disorders such as leukemia or lymphoma.
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