A5038904654- Melanoma and MAPK Pathways
- Cellular Mechanics and Interactions
- Cytokine Signaling Pathways and Interactions
- Cell Adhesion Molecules Research
- Cutaneous lymphoproliferative disorders research
- Eosinophilic Disorders and Syndromes
- Hippo pathway signaling and YAP/TAZ
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Synthesis of Tetrazole Derivatives
- Skin and Cellular Biology Research
- melanin and skin pigmentation
- Cancer Immunotherapy and Biomarkers
- HER2/EGFR in Cancer Research
- bioluminescence and chemiluminescence research
- Immunotherapy and Immune Responses
- Immune cells in cancer
- Immune Cell Function and Interaction
- Advanced Breast Cancer Therapies
- Mycobacterium research and diagnosis
- Protein Tyrosine Phosphatases
- Cutaneous Melanoma Detection and Management
- Colorectal Cancer Treatments and Studies
- Phagocytosis and Immune Regulation
- Cancer Cells and Metastasis
- Cancer Mechanisms and Therapy
Inserm
2019-2024
University of California, San Francisco
2022-2024
Centre Méditerranéen de Médecine Moléculaire
2022-2023
Université Côte d'Azur
2019-2023
La Ligue Contre le Cancer
2019-2023
Institut de Chimie de Nice
2019
Aberrant extracellular matrix (ECM) deposition and stiffening is a physical hallmark of several solid cancers associated with therapy failure. BRAF-mutant melanomas treated BRAF MEK inhibitors almost invariably develop resistance that frequently transcriptional reprogramming de-differentiated cell state. Melanoma cells secrete their own ECM proteins, an event promoted by oncogenic inhibition. Yet, the contribution cancer cell-derived tumor mechanics to drug adaptation remains poorly...
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 &...
Fibroblastic reticular cells (FRC) are immunologically specialized myofibroblasts that control the elasticity of lymph node, in part through their contractile properties. Swelling tumor-draining nodes is a hallmark lymphophilic cancers such as cutaneous melanoma. Melanoma displays high intratumoral heterogeneity with coexistence melanoma variable differentiation phenotypes from melanocytic to dedifferentiated states. Factors secreted by promote premetastatic node reprograming and tumor...
Cladribine is an oral synthetic purine analog that depletes lymphocytes and induces a dose-dependent reduction of T B cells. It was approved for the therapy highly active relapsing-remitting multiple sclerosis. Given cladribine's mechanism action, increased risk malignancies suspected from number cancers occurred in 3.5 mg/kg-treated arm (CLARITY study). We showed cladribine inhibits cell proliferation on three melanoma lines tested, irrespectively their mutational oncogenic status...
Abstract Extracellular matrix (ECM) stiffening, resulting from increased collagen deposition and cross-linking, is a key biophysical factor of the tumor microenvironment. Cutaneous melanoma deadly metastatic cancer. Its aggressiveness stems high intratumoral heterogeneity, plasticity cells, which transit melanocytic state to dedifferentiated therapy-resistant invasive phenotypes, characterized by mesenchymal and/or neural crest stem cell-like features. Phenotypic regulated stroma-derived...
<title>Abstract</title> Tumor progression is accompanied by fibrosis, which associated with diminished anti-tumor immune infiltrate. Here, we demonstrate that tumor infiltrating myeloid cells respond to the stiffened fibrotic microenvironment (TME) initiating a TGF-beta (TGFβ)-directed, collagen biosynthesis program. A collateral effect of this programming an untenable metabolic milieu for productive CD8 T cell responses, as collagen-synthesizing macrophages consume environmental arginine,...
Abstract Resistance to BRAF and MEK inhibitors in V600E mutant melanomas remains a major obstacle that limits patient benefit. Microenvironment components including the extracellular matrix (ECM) can support tumor cell adaptation tolerance targeted therapies, however underlying mechanisms remain poorly understood. Here, we investigated process of matrix-mediated drug resistance (MM-DR) response inhibition melanoma. We demonstrate physical structural cues from fibroblast-derived ECM abrogate...
Supplementary Figure from Secretion of IL1 by Dedifferentiated Melanoma Cells Inhibits JAK1-STAT3–Driven Actomyosin Contractility Lymph Node Fibroblastic Reticular
Supplementary Figure from Secretion of IL1 by Dedifferentiated Melanoma Cells Inhibits JAK1-STAT3–Driven Actomyosin Contractility Lymph Node Fibroblastic Reticular
<div>Abstract<p>Fibroblastic reticular cells (FRC) are immunologically specialized myofibroblasts that control the elasticity of lymph node, in part through their contractile properties. Swelling tumor-draining nodes is a hallmark lymphophilic cancers such as cutaneous melanoma. Melanoma displays high intratumoral heterogeneity with coexistence melanoma variable differentiation phenotypes from melanocytic to dedifferentiated states. Factors secreted by promote premetastatic node...
<p>F-actin and fibronectin stainings in M238P M238R cells</p>
<p>BRAF inhibition drives collagen deposition and stiffening in M229 xenograft melanoma tumor</p>
<div>Abstract<p>Aberrant extracellular matrix (ECM) deposition and stiffening is a physical hallmark of several solid cancers associated with therapy failure. BRAF-mutant melanomas treated BRAF MEK inhibitors almost invariably develop resistance that frequently transcriptional reprogramming de-differentiated cell state. Melanoma cells secrete their own ECM proteins, an event promoted by oncogenic inhibition. Yet, the contribution cancer cell–derived tumor mechanics to drug...
<div>Abstract<p>Aberrant extracellular matrix (ECM) deposition and stiffening is a physical hallmark of several solid cancers associated with therapy failure. BRAF-mutant melanomas treated BRAF MEK inhibitors almost invariably develop resistance that frequently transcriptional reprogramming de-differentiated cell state. Melanoma cells secrete their own ECM proteins, an event promoted by oncogenic inhibition. Yet, the contribution cancer cell–derived tumor mechanics to drug...
<p>Mesenchymal signature of BRAFi resistant melanoma cells</p>
<p>Mesenchymal signature of BRAFi resistant melanoma cells</p>
<p>Supplementary Methods</p>
<p>Morphology and focal adhesions complexes of parental BRAFi-resistant cells on hydrogels various stiffness</p>
<p>F-actin and fibronectin stainings in M238P M238R cells</p>
<p>BRAF and MEK inhibition induces F-actin remodeling, YAP/MRTF activation focal adhesion assembly in BRAF-mutant melanoma cells</p>
<p>Morphology and focal adhesions complexes of parental BRAFi-resistant cells on hydrogels various stiffness</p>
<p>BRAF inhibition drives collagen deposition and stiffening in M229 xenograft melanoma tumor</p>
<p>Drug-protective effect of M229R melanoma cells-derived ECM</p>