Giovanni Gambi

ORCID: 0000-0002-2318-0003
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About
Contact & Profiles
Research Areas
  • melanin and skin pigmentation
  • RNA regulation and disease
  • Cytokine Signaling Pathways and Interactions
  • CRISPR and Genetic Engineering
  • Melanoma and MAPK Pathways
  • Cutaneous Melanoma Detection and Management
  • Cancer-related molecular mechanisms research
  • Lung Cancer Treatments and Mutations
  • RNA modifications and cancer
  • Genomics and Chromatin Dynamics
  • Immunodeficiency and Autoimmune Disorders
  • Epigenetics and DNA Methylation
  • Immune cells in cancer
  • Ubiquitin and proteasome pathways
  • Cancer, Hypoxia, and Metabolism
  • Mycobacterium research and diagnosis
  • Tuberculosis Research and Epidemiology
  • Chromatin Remodeling and Cancer
  • Protein Degradation and Inhibitors
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • interferon and immune responses
  • Cancer-related gene regulation
  • Redox biology and oxidative stress
  • Circular RNAs in diseases
  • Genomics, phytochemicals, and oxidative stress

New York University
2024-2025

Institut de génétique et de biologie moléculaire et cellulaire
2019-2023

Centre National de la Recherche Scientifique
2017-2023

Inserm
2017-2023

Université de Strasbourg
2017-2023

La Ligue Contre le Cancer
2017-2023

Istituto di Ricovero e Cura a Carattere Scientifico San Raffaele
2019

Vita-Salute San Raffaele University
2019

Istituti di Ricovero e Cura a Carattere Scientifico
2019

Institut de Biologie Moléculaire et Cellulaire
2019

Purpose: Understanding tumor heterogeneity is an important challenge in current cancer research. Transcription and epigenetic profiling of cultured melanoma cells have defined at least two distinct cell phenotypes characterized by distinctive gene expression signatures associated with high or low/absent microphthalmia-associated transcription factor (MITF). Nevertheless, populations primary human tumors much less well characterized.Experimental Design: We performed single-cell analyses on...

10.1158/1078-0432.ccr-17-0010 article EN Clinical Cancer Research 2017-08-29

Chromodomain helicase DNA binding protein 4 (CHD4) is an ATPase subunit of the Nucleosome Remodelling and Deacetylation (NuRD) complex that regulates gene expression. CHD4 essential for growth multiple patient derived melanoma xenografts breast cancer. Here we show expression PADI1 (Protein Arginine Deiminase 1) PADI3 in cancer cell types modulating citrullination arginine residues allosterically-regulated glycolytic enzyme pyruvate kinase M2 (PKM2). Citrullination PKM2 R106 reprogrammes...

10.1038/s41467-021-21960-4 article EN cc-by Nature Communications 2021-03-19

Epigenetic silencing of promoter and enhancer regions is a common phenomenon in malignant cells. The transcription factor STAT3 aberrantly activated several tumors, where its constitutive acetylation accounts for the transcriptional repression number tumor suppressor genes (TSG) via molecular mechanisms that remain to be understood. Using nucleophosmin-anaplastic lymphoma kinase-positive (NPM-ALK+) anaplastic large-cell (ALCL) as model system, we found cells patient-derived xenografts...

10.1158/0008-5472.can-18-0359 article EN Cancer Research 2019-01-28

Abstract Tumor heterogeneity is a key feature of melanomas that hinders development effective treatments. Aiming to overcome this, we identified LINC00518 (LENOX; lincRNA-enhancer oxidative phosphorylation) as melanoma-specific lncRNA expressed in all known melanoma cell states and essential for survival vitro vivo. Mechanistically, LENOX promoted association the RAP2C GTPase with mitochondrial fission regulator DRP1, increasing DRP1 S637 phosphorylation, fusion, phosphorylation. expression...

10.1158/0008-5472.can-22-0959 article EN cc-by-nc-nd Cancer Research 2022-10-10

The melanocyte lineage determining Microphthalmia-associated transcription factor (MITF) drives proliferation and survival of melanocytic melanoma cells through regulation both coding genes long non-coding RNAs (LncRNAs). Here we characterize LINC00520 (hereafter called LncRNA ENhancer Translation, LENT) regulated by MITF strongly expressed in cells. LENT is essential for cultured xenograft tumours. interacts with the G4 quadruplex resolvase DHX36 associate ribosome 80S light polysome...

10.1101/2025.02.03.636228 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2025-02-08

While the mutational landscape across early T-cell precursor acute lymphoblastic leukemia (ETP-ALL) and ETP-like is known, establishing a unified framework that activates stem cell genes characteristic of these tumors remains elusive. Using complementary mouse human models, chromatin mapping, enhancer profiling, we show coactivator ZMIZ1 promotes normal malignant ETP population growth by inducing transcription factor MYB in feedforward circuits to convergently activate oncogenes (MEF2C,...

10.1084/jem.20231349 article EN The Journal of Experimental Medicine 2025-02-19

Super-enhancers (SEs) are stretches of enhancers ensuring a high level expression key genes associated with cell function. The identification cancer-specific SE-driven is powerful means for the development innovative therapeutic strategies. Here, we identify MITF/SOX10/TFIIH-dependent SE promoting BAHCC1 in broad panel melanoma cells. highly expressed metastatic and required tumor engraftment, growth, dissemination. Integrative genomics analyses reveal that transcriptional regulator...

10.1016/j.celrep.2023.113363 article EN cc-by-nc-nd Cell Reports 2023-11-01

Abstract Super enhancers (SE) are stretches of active ensuring high expression levels key genes associated with cell function and survival. The identification cancer-specific SE-driven their functional characterization may prove to be a powerful means for the development innovative therapeutic strategies. By performing epigenomic profiling in patient-derived short-term melanoma cultures, we identify SE promoting specific BAHCC1 broad panel cutaneous uveal cells. is highly expressed...

10.1101/2023.01.18.524519 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-01-20

<div>Abstract<p>Tumor heterogeneity is a key feature of melanomas that hinders development effective treatments. Aiming to overcome this, we identified LINC00518 (LENOX; lincRNA-enhancer oxidative phosphorylation) as melanoma-specific lncRNA expressed in all known melanoma cell states and essential for survival <i>in vitro</i> vivo</i>. Mechanistically, LENOX promoted association the RAP2C GTPase with mitochondrial fission regulator DRP1, increasing DRP1 S637...

10.1158/0008-5472.c.6514419.v1 preprint EN 2023-03-31

Abstract CHD3 and CHD4 are mutually exclusive ATPase subunits of the Nucleosome Remodelling Deacetylation (NuRD) complex that regulates gene expression. is essential for growth multiple patient derived melanoma xenografts breast cancer. Here we show expression PADI1 (Protein Arginine Deiminase 1) PADI3 in cancer cell types modulating citrullination three arginines allosterically-regulated glycolytic enzyme pyruvate kinase M2 (PKM2). Citrullination reprograms cross-talk between PKM2 ligands...

10.1101/718486 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2019-08-04

<div>Abstract<p>Epigenetic silencing of promoter and enhancer regions is a common phenomenon in malignant cells. The transcription factor STAT3 aberrantly activated several tumors, where its constitutive acetylation accounts for the transcriptional repression number tumor suppressor genes (TSG) via molecular mechanisms that remain to be understood. Using nucleophosmin-anaplastic lymphoma kinase–positive (NPM-ALK<sup>+</sup>) anaplastic large-cell (ALCL) as model...

10.1158/0008-5472.c.6510984.v1 preprint EN 2023-03-31

<div>Abstract<p>Tumor heterogeneity is a key feature of melanomas that hinders development effective treatments. Aiming to overcome this, we identified LINC00518 (LENOX; lincRNA-enhancer oxidative phosphorylation) as melanoma-specific lncRNA expressed in all known melanoma cell states and essential for survival <i>in vitro</i> vivo</i>. Mechanistically, LENOX promoted association the RAP2C GTPase with mitochondrial fission regulator DRP1, increasing DRP1 S637...

10.1158/0008-5472.c.6514419 preprint EN 2023-03-31
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