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Filippo Veglia, Ph.D.

  • Assistant Professor, Genome Regulation and Cell Signaling Program, Ellen and Ronald Caplan Cancer Center

Dr. Filippo Veglia is an expert in myeloid cell biology, cancer immunology, and tumor metabolism. He is dedicated to advancing cancer research by developing innovative, immune-based approaches to improve treatment and patient outcomes.

Dr. Veglia earned his Ph.D. in Immunology and Applied Biotechnology from Tor Vergata University in Rome, Italy. He completed his postdoctoral training in the lab of Dr. Dmitry Gabrilovich at The Wistar Institute. In 2020, he was appointed Assistant Member at Moffitt Cancer Center in the Department of Immuno-Oncology and joined the Neuro-Oncology Program. He returned to Wistar in December 2023 as an Assistant Professor in the Immunology, Microenvironment and Metastasis Program and, in 2024, also became part of the Genome Regulation and Cell Signaling Program.

The Veglia Laboratory

The Veglia Laboratory

Veglia’s laboratory focuses on tumor microenvironment-driven mechanisms that reprogram myeloid cells toward immunosuppressive and pro-tumoral phenotypes. His team demonstrated that both monocyte-derived macrophages (De Leo A et al., Immunity 2024) and neutrophils (Ugolini A et al., Cancer Discovery 2025) undergo profound functional transformation in the glioblastoma (GBM) microenvironment, driven by glucose-induced histone lactylation. These groundbreaking studies reveal novel metabolic-epigenetic targets with the potential to improve immunotherapy outcomes for highly resistant tumors such as Glioblastoma (GBM).

The laboratory is actively working on the following areas:

  1. Metabolic and epigenetic determinants of immune cell reprogramming within the tumor microenvironment (TME).
  2. Understanding and harnessing anti-tumor neutrophils and macrophages in brain tumors.
  3. Investigating trained immunity and its implications for cancer therapy.
  4. Elucidating the role of microglia during tumor progression.
  5. Developing CAR-based products to overcome resistance mechanisms in solid tumors.
Staff
  • Staff Scientist

    Alessandra De Leo, Ph.D.

  • Postdoctoral Fellows

    Barbara Peixoto, Ph.D.
    Alessio Ugolini, Ph.D.

Available Positions
  • Postdoctoral fellow and research assistant positions are available in the Veglia Laboratory. Candidates should have recently received or be close to obtaining their Ph.D. degree or equivalent (for postdoc) or B.S. degree or equivalent (for RA) and have a strong background in in immunology, tumor microenvironment, and molecular biology. Interested applicants are invited to email: fveglia@wistar.org

Staff
  • Staff Scientist

    Alessandra De Leo, Ph.D.

  • Postdoctoral Fellows

    Haksoo Lee, Ph.D.
    Alessio Ugolini, Ph.D.

  • Predoctoral Trainees

    Filippo Badii

Available Positions
  • Learn about job opportunities at The Wistar Institute here.

Lab Photos


spring lab team
2025
2025

    Selected Publications

    Protocol to study the genomic profile of histone lactylation with CUT&RUN assay in tumor-associated macrophages

    Alessandra De Leo, Alessio Ugolini, Filippo Veglia. Protocol to study the genomic profile of histone lactylation with CUT&RUN assay in tumor-associated macrophages. STAR Protocols. doi: 10.1016/j.xpro.2025.103766. PMID: 40220301 PMCID: PMC12018546

    Functional Reprogramming of Neutrophils within the Brain Tumor Microenvironment by Hypoxia-Driven Histone Lactylation

    Alessio Ugolini, Alessandra De Leo, Xiaoqing Yu, Fabio Scirocchi, Xiaoxian Liu; Barbara Peixoto, Delia Scocozza, Angelica Pace, Michela Perego, Alessandro Gardini, Luca D’Angelo, James K.C. Liu, Arnold B. Etame, Aurelia Rughetti, Marianna Nuti, Antonio Santoro, Michael A. Vogelbaum, Jose R. Conejo-Garcia, Paulo C. Rodriguez, Filippo Veglia. Functional Reprogramming of Neutrophils within the Brain Tumor Microenvironment by Hypoxia-Driven Histone Lactylation. Cancer Discov (2025) 15 (6): 1270–1296. doi: 10.1158/2159-8290.CD-24-1056. PMID: 40014923

    Glucose-driven histone lactylation promotes the immunosuppressive activity of monocyte-derived macrophages in glioblastoma

    De Leo A, Ugolini A, Yu X, Scirocchi F, Scocozza D, Peixoto B, Pace A, D’Angelo L, Liu JKC, Etame AB, Rughetti A, Nuti M, Santoro A, Vogelbaum MA, Conejo-Garcia JR, Rodriguez PC, Veglia F. Glucose-driven histone lactylation promotes the immunosuppressive activity of monocyte-derived macrophages in glioblastoma. Immunity. 2024 Apr 30:S1074-7613(24)00211-5. doi: 10.1016/j.immuni.2024.04.006. Epub ahead of print. PMID: 38703775.

    Analysis of classical neutrophils and polymorphonuclear myeloid-derived suppressor cells in cancer patients and tumor-bearing mice

    Veglia F, Hashimoto A, Dweep H, Sanseviero E, De Leo A, Tcyganov E, Kossenkov A, Mulligan C, Nam B, Masters G, Patel J, Bhargava V, Wilkinson P, Smirnov D, Sepulveda MA, Singhal S, Eruslanov EB, Cristescu R, Loboda A, Nefedova Y, Gabrilovich DI. Analysis of classical neutrophils and polymorphonuclear myeloid-derived suppressor cells in cancer patients and tumor-bearing mice. J Exp Med. 2021 Apr 5;218(4):e20201803. doi: 10.1084/jem.20201803. PMID: 33566112; PMCIDPMC7879582.

    Polymorphonuclear myeloid-derived suppressor cells limit antigen cross-presentation by dendritic cells in cancer

    Ugolini A, Tyurin VA, Tyurina YY, Tcyganov EN, Donthireddy L, Kagan VE, Gabrilovich DI, Veglia F. Polymorphonuclear myeloid-derived suppressor cells limit antigen cross-presentation by dendritic cells in cancer. JCI Insight. 2020 Aug 6;5(15):e138581. doi: 10.1172/jci.insight.138581. PMID: 32584791; PMCIDPMC7455061.

    Fatty acid transport protein 2 reprograms neutrophils in cancer

    Veglia F, Tyurin VA, Blasi M, De Leo A, Kossenkov AV, Donthireddy L, To TKJ, Schug Z, Basu S, Wang F, Ricciotti E, DiRusso C, Murphy ME, Vonderheide RH, Lieberman PM, Mulligan C, Nam B, Hockstein N, Masters G, Guarino M, Lin C, Nefedova Y, Black P, Kagan VE, Gabrilovich DI. Fatty acid transport protein 2 reprograms neutrophils in cancer. Nature. 2019 May;569(7754):73-78. doi: 10.1038/s41586-019-1118-2. Epub 2019 Apr 17. PMID: 30996346; PMCIDPMC6557120.