ResearcherUniversity of VeronaActive in the last 2 years
Vincenzo Bronte
Matched on ORCID iD 0000-0002-3741-5141; OpenAlex author ID A5052489243. Sources: OpenAlex.
Their work
- Papers
- 7 (first author 0, last author 2)
- Trials
- 0
- Grants
- 0
- Labs led
- 0
- Collaborators
- 46
2014: 1 paper · 2015: none · 2016: none · 2017: none · 2018: none · 2019: 1 paper · 2020: none · 2021: none · 2022: 1 paper · 2023: none · 2024: 2 papers · 2025: 1 paper · 2026: 1 paper
Papers 7
- Transcriptional and Epigenetic Plasticity Drive an Alternative Non-clonal Mechanism of Resistance to Kras G12D Inhibition in Pancreatic Cancer Co-author DOI 10.34133/cancomm.0030↗
- Local ablation disrupts immune evasion in pancreatic cancer. Co-author DOI 10.1016/j.canlet.2024.217327↗
- Expression of the membrane tetraspanin claudin 18 on cancer cells promotes T lymphocyte infiltration and antitumor immunity in pancreatic cancer. Last author DOI 10.1016/j.immuni.2024.04.021↗
- Axon guidance cue SEMA3A promotes the aggressive phenotype of basal-like PDAC. Co-author DOI 10.1136/gutjnl-2023-329807↗
- Interrupting the nitrosative stress fuels tumor-specific cytotoxic T lymphocytes in pancreatic cancer. Last author DOI 10.1136/jitc-2021-003549↗
- MAP Kinase inhibition reshapes tumor microenvironment of mouse pancreatic cancer by depleting anti-inflammatory macrophages Co-author DOI 10.1101/759779↗
- Interfacing polymeric scaffolds with primary pancreatic ductal adenocarcinoma cells to develop 3D cancer models. Co-author DOI 10.4161/21592527.2014.955386↗
Closest collaborators
The 25 strongest of 46 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Vincenzo Corbo · 6 shared papers, 2019–2026 · strength 0.88
- Paper Transcriptional and Epigenetic Plasticity Drive an Alternative Non-clonal Mechanism of Resistance to Kras G12D Inhibiti… DOI 10.34133/cancomm.0030↗
- Paper Local ablation disrupts immune evasion in pancreatic cancer. DOI 10.1016/j.canlet.2024.217327↗
- Paper Axon guidance cue SEMA3A promotes the aggressive phenotype of basal-like PDAC. DOI 10.1136/gutjnl-2023-329807↗
- Francesco De Sanctis · 6 shared papers, 2019–2026 · strength 0.88
- Paper Transcriptional and Epigenetic Plasticity Drive an Alternative Non-clonal Mechanism of Resistance to Kras G12D Inhibiti… DOI 10.34133/cancomm.0030↗
- Paper Local ablation disrupts immune evasion in pancreatic cancer. DOI 10.1016/j.canlet.2024.217327↗
- Paper Axon guidance cue SEMA3A promotes the aggressive phenotype of basal-like PDAC. DOI 10.1136/gutjnl-2023-329807↗
- Aldo Scarpa Scarpa · 5 shared papers, 2019–2025 · strength 0.65
- Paper Local ablation disrupts immune evasion in pancreatic cancer. DOI 10.1016/j.canlet.2024.217327↗
- Paper Axon guidance cue SEMA3A promotes the aggressive phenotype of basal-like PDAC. DOI 10.1136/gutjnl-2023-329807↗
- Paper Expression of the membrane tetraspanin claudin 18 on cancer cells promotes T lymphocyte infiltration and antitumor immu… DOI 10.1016/j.immuni.2024.04.021↗
- Geny Piro · 3 shared papers, 2024–2026 · strength 0.56
- Paper Transcriptional and Epigenetic Plasticity Drive an Alternative Non-clonal Mechanism of Resistance to Kras G12D Inhibiti… DOI 10.34133/cancomm.0030↗
- Paper Local ablation disrupts immune evasion in pancreatic cancer. DOI 10.1016/j.canlet.2024.217327↗
- Paper Axon guidance cue SEMA3A promotes the aggressive phenotype of basal-like PDAC. DOI 10.1136/gutjnl-2023-329807↗
- Carmine Carbone · 3 shared papers, 2024–2026 · strength 0.56
- Paper Transcriptional and Epigenetic Plasticity Drive an Alternative Non-clonal Mechanism of Resistance to Kras G12D Inhibiti… DOI 10.34133/cancomm.0030↗
- Paper Local ablation disrupts immune evasion in pancreatic cancer. DOI 10.1016/j.canlet.2024.217327↗
- Paper Axon guidance cue SEMA3A promotes the aggressive phenotype of basal-like PDAC. DOI 10.1136/gutjnl-2023-329807↗
- Rita Teresa Lawlor · 4 shared papers, 2019–2024 · strength 0.48
- Paper Axon guidance cue SEMA3A promotes the aggressive phenotype of basal-like PDAC. DOI 10.1136/gutjnl-2023-329807↗
- Paper Expression of the membrane tetraspanin claudin 18 on cancer cells promotes T lymphocyte infiltration and antitumor immu… DOI 10.1016/j.immuni.2024.04.021↗
- Paper Interrupting the nitrosative stress fuels tumor-specific cytotoxic T lymphocytes in pancreatic cancer. DOI 10.1136/jitc-2021-003549↗
- Antonio Agostini · 2 shared papers, 2025–2026 · strength 0.40
- Giampaolo Tortora · 2 shared papers, 2025–2026 · strength 0.40
- Francesca Lupo · 3 shared papers, 2019–2025 · strength 0.40
- Paper Local ablation disrupts immune evasion in pancreatic cancer. DOI 10.1016/j.canlet.2024.217327↗
- Paper Axon guidance cue SEMA3A promotes the aggressive phenotype of basal-like PDAC. DOI 10.1136/gutjnl-2023-329807↗
- Paper MAP Kinase inhibition reshapes tumor microenvironment of mouse pancreatic cancer by depleting anti-inflammatory macroph… DOI 10.1101/759779↗
- Peter J. Bailey · 2 shared papers, 2024 · strength 0.30
- Chiara Musiu · 2 shared papers, 2022–2025 · strength 0.27
- Claudio Bassi · 2 shared papers, 2022–2025 · strength 0.27
- Salvatore Paiella · 2 shared papers, 2022–2025 · strength 0.27
- Roberto Salvia · 2 shared papers, 2022–2025 · strength 0.27
- David Arthur Tuveson · 2 shared papers, 2022–2024 · strength 0.26
- Alessia Caggiano · 1 shared paper, 2026 · strength 0.23
- Claudio Sette · 1 shared paper, 2026 · strength 0.23
- Gian Luca Rampioni Vinciguerra · 1 shared paper, 2026 · strength 0.23
- Pietro Delfino · 2 shared papers, 2019–2024 · strength 0.22
- Sabrina L. D’Agosto · 2 shared papers, 2019–2024 · strength 0.22
- Elena Fiorini · 2 shared papers, 2019–2024 · strength 0.22
- Matteo Fassan · 2 shared papers, 2019–2022 · strength 0.17
- Giuseppe Malleo · 1 shared paper, 2025 · strength 0.17
- Pasquina Marzola · 1 shared paper, 2025 · strength 0.17
- Mirko D’Onofrio · 1 shared paper, 2025 · strength 0.17
How to reach this person
A chain of introductions through people who have published, run trials or held grants together (warm_path@1: fewest links first, then the strongest). Built from public records only; no contact details are kept.