Noemi Reyes
A5060283962- Acute Lymphoblastic Leukemia research
- Chronic Myeloid Leukemia Treatments
- CAR-T cell therapy research
- Acute Myeloid Leukemia Research
- Cancer therapeutics and mechanisms
- Biochemical and Molecular Research
- Immune Cell Function and Interaction
- Lung Cancer Research Studies
- Childhood Cancer Survivors' Quality of Life
- Protein Degradation and Inhibitors
- Renal and related cancers
- Epigenetics and DNA Methylation
- Neuroblastoma Research and Treatments
St. Jude Children's Research Hospital
2022-2025
Abstract Acute lymphoblastic leukemia expressing the gamma delta T-cell receptor (γδ T-ALL) is a poorly understood disease. We studied 200 children with γδ T-ALL from 13 clinical study groups to understand and genetic features of this found age drivers were significantly associated outcome. diagnosed in under 3 years was extremely high-risk enriched for alterations that result both LMO2 activation STAG2 inactivation. Mechanistically, using patient samples isogenic cell lines, we show...
T cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy, and there unmet need for targeted therapies, especially patients with relapsed disease. We have recently identified pre-T receptor lymphocyte-specific protein tyrosine kinase (LCK) signaling as a common therapeutic vulnerability in T-ALL. LCK inhibitor dasatinib showed efficacy against T-ALL preclinical studies T-ALL; however, this transient most cases. Leveraging the proteolysis targeting chimera (PROTAC)...
Abstract Chimeric antigen receptor (CAR)-T cell therapies, while promising for CD19+ hematological malignancies, often face setbacks due to relapses. Our research identifies GPR65 as a tumor-specific determinant affecting the efficacy of CAR-T therapy. In human patients and an immune-competent mouse model B-cell acute lymphoblastic leukemia (B-ALL), low expression correlates with resistance treatment. knockout (GPR65 KO) tumors in mice similarly exhibit resistance. Through single-cell...
Abstract FLT3 is an attractive therapeutic target in acute lymphoblastic leukemia (ALL) but the mechanism for its activation this cancer incompletely understood. Profiling global gene expression large ALL cohorts, we identify over-expression of ZNF384 -rearranged ALL, consistently across cases harboring different fusion partners with . Mechanistically, discover intergenic enhancer element at locus that exclusively activated enhancer-promoter looping directly mediated by protein. There also a...
Resistance of acute lymphoblastic leukemia (ALL) cells to chemotherapy, whether present at diagnosis or acquired during treatment, is a major cause treatment failure. Primary ALL are accessible for drug sensitivity testing the time new relapse, but there limitations with current methods determining ex vivo. Here, we describe functional precision medicine method using fluorescence imaging platform test profiles primary cells. Leukemia co-cultured mesenchymal stromal and tested panel 40...
<p>The gene expression profiles of γδ T-ALL.</p>
<p>The genomic features of LMO2::STAG2 translocations.</p>
<p>The clinical features of γδ T-ALL.</p>
<p>Coverage of ATAC seq, H3K27ac ChIP and RNAseq at the LIN28B ID1 locus.</p>
<div>Abstract<p>Acute lymphoblastic leukemia expressing the gamma delta T-cell receptor (γδ T-ALL) is a poorly understood disease. We studied 200 children with γδ T-ALL from 13 clinical study groups to understand and genetic features of this found age drivers were significantly associated outcome. diagnosed in under 3 years was extremely high-risk enriched for alterations that result both <i>LMO2</i> activation <i>STAG2</i> inactivation. Mechanistically,...
<p>Supplementary Methods, Supplementary Results, Data Figures 1 and 2</p>
<p>ChIP-seq coverage at the CD34 locus showing effects of STAG2 inactivation.</p>
<p>The genomic feature of LMO2 γδ-like T-ALL.</p>