Marta Coscia

ORCID: 0000-0003-2123-7675
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About
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Research Areas
  • Chronic Lymphocytic Leukemia Research
  • Lymphoma Diagnosis and Treatment
  • Immunodeficiency and Autoimmune Disorders
  • Advanced Breast Cancer Therapies
  • Immune Cell Function and Interaction
  • Acute Lymphoblastic Leukemia research
  • Immunotherapy and Immune Responses
  • T-cell and B-cell Immunology
  • Cancer-related Molecular Pathways
  • Monoclonal and Polyclonal Antibodies Research
  • Multiple Myeloma Research and Treatments
  • CAR-T cell therapy research
  • Chronic Myeloid Leukemia Treatments
  • Gastrointestinal Tumor Research and Treatment
  • Phagocytosis and Immune Regulation
  • Cancer, Hypoxia, and Metabolism
  • Calcium signaling and nucleotide metabolism
  • Galectins and Cancer Biology
  • Bone health and treatments
  • Cancer Immunotherapy and Biomarkers
  • Cancer, Lipids, and Metabolism
  • Adenosine and Purinergic Signaling
  • PI3K/AKT/mTOR signaling in cancer
  • Glycosylation and Glycoproteins Research
  • Acute Myeloid Leukemia Research

University of Turin
2016-2025

University of Insubria
2024-2025

Aziende Socio Sanitarie Territoriale dei Sette Laghi
2024-2025

Azienda Ospedaliera Citta' della Salute e della Scienza di Torino
2015-2024

Ospedale di Circolo e Fondazione Macchi
2024

Fred Hutch Cancer Center
2023

University of Washington
2023

University of Medical Sciences and Technology
2023

National Research Council
2023

Neuroscience Institute
2023

Chronic lymphocytic leukemia (CLL) is a disease of the elderly, characterized by immunodeficiency. Hence, patients with CLL might be considered more susceptible to severe complications from COVID-19. We undertook this retrospective international multicenter study characterize course COVID-19 in and identify potential predictors outcome. Of 190 confirmed diagnosed between 28/03/2020 22/05/2020, 151 (79%) presented (need oxygen and/or intensive care admission). Severe was associated advanced...

10.1038/s41375-020-0959-x article EN other-oa Leukemia 2020-07-09

Chronic lymphocytic leukemia is marked by profound defects in T-cell function. Programmed death-1 a receptor involved tumor-mediated immunosuppression through binding of the PD-L1 ligand. Multiparametric flow cytometry and immunohistochemistry were used to study PD-1/PD-L1 expression. Functional assays determine involvement axis responses. PD-1 expression CD4+ CD8+ T lymphocytes was significantly higher 117 chronic patients than 33 donors comparable age. from displayed increased numbers...

10.3324/haematol.2012.077537 article EN cc-by-nc Haematologica 2013-01-08

Abstract Patients with chronic lymphocytic leukemia (CLL) progressing on ibrutinib constitute an unmet need. Though Bruton tyrosine kinase (BTK) and PLCG2 mutations are associated resistance, their frequency relevance to progression not fully understood. In this multicenter retrospective observational study, we analyzed 98 patients CLL (49 relapsing after initial response 49 still responding ≥1 year of continuous treatment) using a next-generation sequencing (NGS) panel (1% sensitivity)...

10.1182/bloodadvances.2022008821 article EN cc-by-nc-nd Blood Advances 2023-01-25

It is unknown whether zoledronic acid (ZA) at clinically relevant doses active against tumours not located in bone. Mice transgenic for the activated ErbB-2 oncogene were treated with a cumulative number of equivalent to that recommended human beings. A significant increase tumour-free and overall survival was observed mice ZA. At compatible concentrations, ZA modulated mevalonate pathway affected protein prenylation both tumour cells macrophages. marked reduction tumour-associated...

10.1111/j.1582-4934.2009.00926.x article EN Journal of Cellular and Molecular Medicine 2009-10-10

Abstract Vγ9Vδ2 T cells play a major role as effector of innate immune responses against microbes, stressed cells, and tumor cells. They constitute <5% PBLs but can be expanded by zoledronic acid (ZA)-treated monocytes or dendritic (DC). Much less is known about their ability to act cellular adjuvants bridging adaptive immunity, especially in patients with cancer. We have addressed this issue multiple myeloma (MM), prototypic disease several dysfunctions that also affect γδ DC....

10.4049/jimmunol.1002514 article EN The Journal of Immunology 2011-07-14

Vγ9Vδ2 T cells have a natural inclination to recognize malignant B in vitro via receptors for stress-induced self-ligands and TCR-dependent recognition of phosphoantigens (pAgs) generated the mevalonate (Mev) pathway. This is continuously challenged vivo by immune suppression operated tumor cells. Multiple myeloma (MM) prototypic B-cell malignancy which subvert local microenvironment reshape antitumor responses. In this study, we investigated competence bone marrow (BM) large series MM...

10.1080/2162402x.2015.1047580 article EN OncoImmunology 2015-05-26

Chronic lymphocytic leukemia (CLL) is a variable disease; therefore, markers to identify aggressive forms are essential for patient management. Here, we have shown that expression of the costimulatory molecule and microbial sensor SLAMF1 (also known as CD150) lost in subset patients with an CLL associates shorter time first treatment reduced overall survival. silencing CLL-like Mec-1 cells, which constitutively express SLAMF1, modulated pathways related cell migration, cytoskeletal...

10.1172/jci83013 article EN Journal of Clinical Investigation 2015-11-29

Key Points Hypoxia shapes the CLL lymph node microenvironment by acting through A2A adenosine receptor. Inhibiting receptor counteracts effects of hypoxia on cells, macrophages, and T lymphocytes.

10.1182/bloodadvances.2016000984 article EN cc-by-nc-nd Blood Advances 2016-11-22

In chronic lymphocytic leukemia (CLL), the hypoxia-inducible factor 1 (HIF-1) regulates response of tumor cells to hypoxia and their protective interactions with leukemic microenvironment. this study, we demonstrate that CLL from TP53-disrupted (TP53dis) patients have constitutively higher expression levels α-subunit HIF-1 (HIF-1α) increased transcriptional activity compared wild-type counterpart. TP53dis subset, HIF-1α upregulation is due reduced ubiquitin ligase von Hippel-Lindau protein...

10.3324/haematol.2019.217430 article EN cc-by-nc Haematologica 2019-07-09
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