Chiara Montironi

ORCID: 0000-0003-0753-231X
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About
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Research Areas
  • Chronic Lymphocytic Leukemia Research
  • Cancer, Hypoxia, and Metabolism
  • Cancer Immunotherapy and Biomarkers
  • Cancer-related Molecular Pathways
  • Pancreatic function and diabetes
  • Epigenetics and DNA Methylation
  • Amino Acid Enzymes and Metabolism
  • Calcium signaling and nucleotide metabolism
  • Cytokine Signaling Pathways and Interactions
  • interferon and immune responses
  • CAR-T cell therapy research
  • PI3K/AKT/mTOR signaling in cancer
  • Adenosine and Purinergic Signaling
  • Glycosylation and Glycoproteins Research
  • Cell death mechanisms and regulation
  • Immune Cell Function and Interaction
  • Single-cell and spatial transcriptomics

University of Amsterdam
2021-2024

Amsterdam University Medical Centers
2021-2024

Cancer Center Amsterdam
2021-2024

Oncode Institute
2023-2024

Amsterdam Institute for Addiction Research
2021

Abstract Interleukin-8 (IL-8/CXCL8) is a pro-angiogenic and pro-inflammatory chemokine that plays role in cancer development. Non-small cell lung carcinoma (NSCLC) produces high amounts of IL-8, which associated with poor prognosis resistance to chemo-radio immunotherapy. However, the signaling pathways lead IL-8 production NSCLC are unresolved. Here, we show expression release regulated autonomously by TRAIL death receptors several squamous adenocarcinoma lines. constitutively secrete could...

10.1038/s41419-022-05495-0 article EN cc-by Cell Death and Disease 2022-12-15

Abstract Acquired T-cell dysfunction is common in chronic B-cell malignancies. Given the strong connection between metabolism and function, we investigated metabolic alterations as basis of induced by malignant cells. Using cell lines human peripheral blood mononuclear cells, first established a model that recapitulates major aspects cancer-induced dysfunction. Cell derived from lymphocytic leukemia (CLL) (PGA-1, CII, Mec-1), but not other malignancies, altered metabolome generating...

10.1182/bloodadvances.2023010305 article EN cc-by-nc-nd Blood Advances 2023-08-08

The tumor suppressor p53 has been described to control various aspects of metabolic reprogramming in solid tumors, but B cell malignancies that role is as yet unknown. We generated pairs functional and knockout (KO) clones from distinct (acute lymphoblastic leukemia, chronic lymphocytic diffuse large lymphoma, multiple myeloma). Metabolomics isotope tracing showed loss did not drive a common signature. Instead, lines segregated according origin. Next, we focused on glutamine crucial energy...

10.1016/j.isci.2024.109640 article EN cc-by-nc-nd iScience 2024-03-28

Background: Chronic lymphocytic leukemia (CLL) remains incurable despite availability of targeted therapies. Successful autologous cell-based anti-cancer therapies require functionality and longevity effector cells, features that highly depend on complex metabolic processes. A key feature CLL is the suppression T-cell function, but underlying mechanism still poorly understood. We previously found signs impaired plasticity upon stimulation T cells from patients (van Bruggen, Blood 2019)....

10.1097/01.hs9.0000969284.17602.7a article EN cc-by-nc-nd HemaSphere 2023-08-01

Background: Acquired T-cell dysfunction is a prominent feature in chronic B-cell malignancies, such as lymphocytic leukemia (CLL). This widely assumed to hinder the efficacy of based immunotherapy. T cells rely on metabolic switches initiate and sustain an immune response, namely rapid shift glycolysis accompanied by amplification OXPHOS capacity. Aims: Given link between metabolism function, we aimed at uncovering alterations induced malignant B basis dysfunction. Methods: Using cell lines...

10.1097/01.hs9.0000969276.84566.9e article EN cc-by-nc-nd HemaSphere 2023-08-01
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