A5047008191- Acute Myeloid Leukemia Research
- Histone Deacetylase Inhibitors Research
- T-cell and Retrovirus Studies
- Acute Lymphoblastic Leukemia research
- Cancer therapeutics and mechanisms
- Immune Cell Function and Interaction
- Chronic Myeloid Leukemia Treatments
- Chronic Lymphocytic Leukemia Research
- Cancer Genomics and Diagnostics
- Signaling Pathways in Disease
- RNA Interference and Gene Delivery
- RNA modifications and cancer
- DNA Repair Mechanisms
- Protein Degradation and Inhibitors
- PI3K/AKT/mTOR signaling in cancer
- Peptidase Inhibition and Analysis
- CRISPR and Genetic Engineering
- Cancer-related gene regulation
- RNA and protein synthesis mechanisms
- Cancer-related Molecular Pathways
- Synthetic Organic Chemistry Methods
- Macrophage Migration Inhibitory Factor
- Genomics and Chromatin Dynamics
- Galectins and Cancer Biology
- CAR-T cell therapy research
Université Paris Cité
2016-2023
Institut de recherche Saint-Louis
2023
Hôpital Saint-Louis
2016-2023
Assistance Publique – Hôpitaux de Paris
2023
Centre National pour la Recherche Scientifique et Technique (CNRST)
2023
Inserm
2015-2023
Délégation Paris 7
2016-2023
Sorbonne Paris Cité
2016-2023
Centre National de la Recherche Scientifique
2008-2023
Université Paris-Saclay
2020-2021
Fanconi anemia (FA) is a recessive genetic disease characterized by congenital abnormalities, chromosome instability, progressive bone marrow failure (BMF), and strong predisposition to cancer. Twenty FA genes have been identified, the FANC proteins they encode cooperate in common pathway that regulates DNA crosslink repair replication fork stability. We identified child with severe BMF who harbored biallelic inactivating mutations of translesion synthesis (TLS) gene REV7 (also known as...
Abstract Acute myeloid leukemia (AML) pathogenesis often involves a mutation in the NPM1 nucleolar chaperone, but bases for its transforming properties and overall association with favorable therapeutic responses remain incompletely understood. Here we demonstrate that an oncogenic mutant form of (NPM1c) impairs mitochondrial function. NPM1c also hampers formation promyelocytic (PML) nuclear bodies (NB), which are regulators fitness key senescence effectors. Actinomycin D (ActD), antibiotic...
Abstract Low hypodiploidy defines a rare subtype of B-cell acute lymphoblastic leukemia (B-ALL) with dismal outcome. To investigate the genomic basis low-hypodiploid ALL (LH-ALL) in adults, we analyzed copy-number aberrations, loss heterozygosity, mutations, and cytogenetics data prospective cohort Philadelphia (Ph)-negative B-ALL patients (n = 591, ages 18–84 years), allowing us to identify 80 LH-ALL cases (14%). Genomic analysis was critical for evidencing low many missed by cytogenetics....
Circular RNAs (circRNAs) are stable RNA molecules that can drive cancer through interactions with microRNAs and proteins by the expression of circRNA encoded peptides. The aim study was to define landscape potential impact in T-cell acute lymphoblastic leukemia (T-ALL). Analysis CirComPara RNA-sequencing data from 25 T-ALL patients, immature, HOXA overexpressing, TLX1, TLX3, TAL1, or LMO2 rearranged, thymocyte populations human healthy donors disclosed 68 554 circRNAs. Study top 3447 highly...
Oncogenic alterations underlying B-cell acute lymphoblastic leukemia (B-ALL) in adults remain incompletely elucidated. To uncover novel oncogenic drivers, we performed RNA sequencing and whole-genome analyses a large cohort of unresolved B-ALL. We identified subtype characterized by distinct gene expression signature the unique association 2 genomic microdeletions. The 17q21.31 microdeletion resulted UBTF::ATXN7L3 fusion transcript encoding chimeric protein. 13q12.2 deletion monoallelic...
Deletion of chromosome 6q is a well-recognized abnormality found in poor-prognosis T-cell acute lymphoblastic leukemia (T-ALL). Using integrated genomic approaches, we identified two candidate haploinsufficient genes contiguous at 6q14, SYNCRIP (encoding hnRNP-Q) and SNHG5 (that hosts snoRNAs), both involved regulating RNA maturation translation. Combined silencing genes, but not either gene alone, accelerated leukemogeneis Tal1/Lmo1/Notch1-driven mouse model, demonstrating the...
The Rel/NF-kappaB transcription factors are often activated in solid or hematological malignancies. In most cases, NF-kappaB activation is found malignant cells and results from of the canonical pathway, leading to RelA and/or c-Rel activation. Recently, activity inflammatory infiltrating tumors has been shown contribute tumor initiation progression. Noncanonical activation, which leads RelB also reported breast carcinoma, prostate cancer, lymphoid leukemia.Here we report a novel role for...
Long-range oncogenic enhancers play an important role in cancer. Yet, whether similar regulation of tumor suppressor genes is relevant remains unclear. Loss expression PTEN associated with the pathogenesis various cancers, including T-cell leukemia (T-ALL). Here, we identify a highly conserved distal enhancer (PE) that interacts promoter multiple hematopoietic populations, T-cells, and acts as hub transcription factors T-ALL. Consistently, loss PE leads to reduced levels T-ALL cells....
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy with few available targeted therapies. We previously reported that the phosphatase calcineurin (Cn) required for LIC (leukemia Initiating Capacity) potential of T-ALL pointing to Cn as interesting therapeutic target. Calcineurin inhibitors have however unwanted side effect. NFAT transcription factors play crucial roles downstream during thymocyte development, T cell differentiation, activation and anergy. Here we...
ABSTRACT T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy with few available targeted therapies. We previously reported that the phosphatase calcineurin (Cn) required for LIC (leukemia Initiating Capacity) potential of T-ALL pointing to Cn as interesting therapeutic target. Calcineurin inhibitors have however unwanted side effect. NFAT transcription factors play crucial roles downstream during thymocyte development, T cell differentiation, activation and anergy. Here...
<p>Supp Fig. S1-6, Supp Tables S1-S3, Methods and References</p>
<div>Abstract<p>Deletion of chromosome 6q is a well-recognized abnormality found in poor-prognosis T-cell acute lymphoblastic leukemia (T-ALL). Using integrated genomic approaches, we identified two candidate haploinsufficient genes contiguous at 6q14, <i>SYNCRIP</i> (encoding hnRNP-Q) and <i>SNHG5</i> (that hosts snoRNAs), both involved regulating RNA maturation translation. Combined silencing genes, but not either gene alone, accelerated leukemogeneis...
<p>Differentially Expressed Proteins Deleted versus non-deleted clones</p>
<p>Differentially expressed genes in Xenograted T-ALL shSYNCRIP-SNHG5 versus ShCtrl</p>
<p>Differentially Expressed Proteins Deleted versus non-deleted clones</p>
<div>Abstract<p>Deletion of chromosome 6q is a well-recognized abnormality found in poor-prognosis T-cell acute lymphoblastic leukemia (T-ALL). Using integrated genomic approaches, we identified two candidate haploinsufficient genes contiguous at 6q14, <i>SYNCRIP</i> (encoding hnRNP-Q) and <i>SNHG5</i> (that hosts snoRNAs), both involved regulating RNA maturation translation. Combined silencing genes, but not either gene alone, accelerated leukemogeneis...
<p>Differentially translated transcripts - translatome</p>