Publications by authors named "V Rondeau"
Article Synopsis
- T-lineage acute lymphoblastic leukemia (ALL) presents as an aggressive cancer with diverse subtypes, making traditional classification difficult.
- A multiomics analysis of bone marrow samples revealed a specific subset of T-lineage ALL with active inflammatory and stem gene programs, showing unique biological and treatment response characteristics.
- A computational inflammatory gene signature scoring system was developed to better classify patients, identifying a high-risk subtype that could guide targeted therapies for more effective treatment approaches.
Background: WHIM (Warts, Hypogammaglobulinemia, Infections, and Myelokathexis) syndrome is an ultra-rare, combined primary immunodeficiency and chronic neutropenic disorder characterized by a range of clinical presentations, including peripheral neutropenia, lymphopenia, and recurrent infections. WHIM syndrome is most often caused by gain-of-function mutations in the gene encoding C-X-C chemokine receptor 4 (CXCR4). As such, inhibition of CXCR4 with XOLREMDI (mavorixafor), an orally bioavailable CXCR4 antagonist, demonstrated clinically meaningful increases in absolute neutrophil and lymphocyte counts and concomitant reduction in infections in patients with WHIM syndrome, resulting in its recent U.
View Article and Find Full Text PDFArticle Synopsis
- Hematopoietic multipotent progenitors (MPPs) in the bone marrow can differentiate into various cell types, influenced by both intrinsic and extrinsic signals, with WHIM syndrome patients exhibiting an excess of myeloid cells due to CXCR4 signaling mutations.
- Research using knock-in mice with WHIM-associated mutations showed that MPP4 cells, which usually develop into lymphoid cells, instead skewed towards myeloid differentiation due to increased mTOR signaling and altered oxidative phosphorylation.
- Treatment with CXCR4 antagonist AMD3100 or mTOR inhibitor rapamycin reversed this myeloid bias, indicating that normal CXCR4 function is crucial for maintaining the lymphoid potential of MPP4 cells by regulating
2-Aminoethanethiol dioxygenase (ADO) is a thiol dioxygenase that sulfinylates cysteamine and amino-terminal cysteines in polypeptides. The pathophysiological roles of ADO remain largely unknown. Here, we demonstrate that ADO expression represents a vulnerability in cancer cells, as ADO depletion led to loss of proliferative capacity and survival in cancer cells and reduced xenograft growth.
View Article and Find Full Text PDFAcute myeloid leukemia (AML) is a devastating disease initiated and maintained by a rare subset of cells called leukemia stem cells (LSCs). LSCs are responsible for driving disease relapse, making the development of new therapeutic strategies to target LSCs urgently needed. The use of mass spectrometry-based metabolomics profiling has enabled the discovery of unique and targetable metabolic properties in LSCs.
View Article and Find Full Text PDF