A5053870246- RNA modifications and cancer
- Cancer-related molecular mechanisms research
- Melanoma and MAPK Pathways
- Epigenetics and DNA Methylation
- RNA Research and Splicing
- Acute Myeloid Leukemia Research
- CRISPR and Genetic Engineering
- Immunotherapy and Immune Responses
- Congenital heart defects research
- Single-cell and spatial transcriptomics
- Protein Degradation and Inhibitors
- Genetics and Neurodevelopmental Disorders
- MicroRNA in disease regulation
- CAR-T cell therapy research
- Cancer, Lipids, and Metabolism
- Genomics and Chromatin Dynamics
- Cancer Genomics and Diagnostics
- Advanced biosensing and bioanalysis techniques
- Cell Adhesion Molecules Research
- Plant and Fungal Interactions Research
- Genomics and Rare Diseases
- Cancer Cells and Metastasis
- Metabolism, Diabetes, and Cancer
- S100 Proteins and Annexins
- Cutaneous Melanoma Detection and Management
Institut d'Investigació Biomédica de Bellvitge
2022-2025
VIB-KU Leuven Center for Cancer Biology
2018-2025
Institute of Predictive and Personalized Medicine of Cancer
2023
KU Leuven
2018-2022
Universidad de Navarra
2011-2020
Navarre Institute of Health Research
2016-2020
Abstract Background The p53 transcription factor is located at the core of a complex wiring signaling pathways that are critical for preservation cellular homeostasis. Only recently it has become clear regulates expression several long intergenic noncoding RNAs (lincRNAs). However, relatively little known about role lincRNAs play in this pathway. Results Here we characterize lincRNA named Pint (p53 induced transcript). We show ubiquitously expressed finely regulated by p53. In mouse cells,...
It is now obvious that the majority of cellular transcripts do not code for proteins, and a significant subset them are long non-coding RNAs (lncRNAs). Many lncRNAs show aberrant expression in cancer, some have been linked to cell transformation. However, underlying mechanisms remain poorly understood it unknown how sequences lncRNA dictate their function. Here we characterize function p53-regulated human LINC-PINT cancer. We find downregulated multiple types cancer acts as tumor suppressor...
Despite the inarguable relevance of p53 in cancer, genome-wide studies relating endogenous activity to expression lncRNAs human cells are still missing. Here, by integrating RNA-seq with ChIP-seq analyses a cancer cell line under DNA damage, we define high-confidence set 18 that transcriptional targets. We demonstrate two p53-regulated required for efficient binding some its target genes, modulating network and contributing apoptosis induction damage. also show p53-lncRNAs is lowered...
Induction and reversal of chromatin silencing is critical for successful development, tissue homeostasis, the derivation induced pluripotent stem cells (iPSCs). X-Chromosome inactivation (XCI) reactivation (XCR) in female represent chromosome-wide transitions between active inactive states. Although XCI has long been studied, providing important insights into gene regulation, dynamics mechanisms underlying stable X-linked genes are much less understood. Here, we use allele-specific...
Cancer is characterized by genomic instability leading to deletion or amplification of oncogenes tumor suppressors. However, most the altered regions are devoid known cancer drivers. Here, we identify lncRNAs frequently lost amplified in cancer. Among them, found lncRNA associated with lung cancer-1 (ALAL-1) as adenocarcinomas. ALAL-1 also overexpressed additional types, such squamous carcinoma. The RNA product able promote proliferation and tumorigenicity cells. a TNFα- NF-κB-induced...
Abstract Single-cell multi-omics methods enable the study of cell state diversity, which is largely determined by interplay genome, epigenome, and transcriptome. Here, we describe Gtag&T-seq, a genome-and-transcriptome sequencing (G&T-seq) protocol same single cells that omits whole-genome amplification (WGA) using direct genomic tagmentation (Gtag). Gtag drastically decreases cost improves coverage uniformity at single-cell pseudo-bulk levels compared to WGA-based G&T-seq. We...
Background The EVI1 gene (3q26) codes for a zinc finger transcription factor with important roles in both mammalian development and leukemogenesis. Over-expression of through either 3q26 rearrangements, MLL fusions, or other unknown mechanisms confers poor prognosis acute myeloid leukemia.Design Methods We analyzed the prevalence prognostic impact over-expression series 476 patients leukemia, investigated epigenetic modifications locus which could be involved transcriptional regulation this...
Article14 February 2022Open Access Source DataTransparent process Blockade of the pro-fibrotic reaction mediated by miR-143/-145 cluster enhances responses to targeted therapy in melanoma Serena Diazzi Université Côte d'Azur, INSERM, C3M, Nice, France CNRS, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Sophia Antipolis, Equipe labellisée Ligue Contre le Cancer, Contribution: Conceptualization, Formal analysis, Investigation, Methodology, Writing - original draft, review &...
Glioblastoma, the most aggressive primary brain tumor, is genetically heterogeneous. Alternative splicing (AS) plays a key role in numerous pathologies, including cancer. The objectives of our study were to determine whether aberrant AS could play malignant phenotype glioma and understand mechanism underlying its regulation.We obtained surgical samples from patients with glioblastoma who underwent 5-aminolevulinic fluorescence-guided surgery. Biopsies taken tumor center as well adjacent...
Abstract: The complex universe of RNA transcribed by mammalian cells includes thousands large molecules that do not encode for proteins. Despite their lack coding capacity and relatively low conservation, many noncoding (lncRNAs) have been shown to be functional, adding a new level complexity on the structural organization, function, evolution genome. Here, we summarize current knowledge lncRNAs, starting from methodologies led identification genomic evolutive features. We discuss diverse...
Summary The ability to predict the future behaviour of an individual cancer is crucial for precision medicine and, in particular, development strategies that prevent acquisition resistance anti-cancer drugs. Therapy resistance, which often develops from a heterogeneous pool drug-tolerant cells known as minimal residual disease (MRD), thought mainly occur through genetic alterations. Increasing evidence, however, indicates drug might also be acquired though nongenetic mechanisms. A key...
<title>Abstract</title> Patients with GATA2 deficiency are predisposed to developing myelodysplastic syndrome (MDS), which can progress acute myeloid leukemia (AML). This progression is often associated the acquisition of additional cytogenetic and somatic alterations. Mutations in SETBP1 ASXL1 genes frequently observed pediatric patients, but their roles disease remain poorly understood. Genome editing induced pluripotent stem cells (iPSCs) enabled precise reconstruction mutation...
ABSTRACT Single-cell multi-omics methods are enabling the study of cell state diversity, which is largely determined by interplay genome, epigenome, and transcriptome. Here, we describe Gtag&T-seq, a genome-and-transcriptome sequencing (G&T-seq) protocol same single cells that omits whole-genome amplification (WGA) using direct genomic tagmentation (Gtag). Gtag drastically decreases cost improves coverage uniformity at both single-cell pseudo-bulk level when compared to WGA-based...
Background: GATA2 deficiency has been identified as a common hereditary cause of myelodysplastic syndromes (MDS) and acute myeloid leukemia in children. Penetrance expressivity within affected families is often variable, suggesting that cooperating factors are required to trigger the disease. Somatic mutations MDS driver genes (i.e. SETBP1, ASXL1) have GATA2-MDS. Despite recent studies identifying germline genetics acquired deficiency, understanding molecular mechanism triggers leukemic...