Pancreatic Cancer Research

ResearcherUniversity of VeronaActive in the last 2 years

Vincenzo Corbo

ORCID-verified (high confidence, 0.95), identity_conf@1As of 7 November 2026

Matched on ORCID iD 0000-0002-6340-8009; OpenAlex author ID A5024767391. Sources: OpenAlex.

Their work

Papers
53 (first author 4, last author 7)
Trials
0
Grants
0
Labs led
1
Collaborators
202
Papers, trials and grants by year

2012: 2 papers · 2013: none · 2014: 1 paper · 2015: 2 papers · 2016: 2 papers · 2017: 4 papers · 2018: none · 2019: 3 papers · 2020: 2 papers · 2021: 5 papers · 2022: 6 papers · 2023: 8 papers · 2024: 4 papers · 2025: 8 papers · 2026: 6 papers

Papers 50 of 53

  1. Deciphering transcriptional plasticity in pancreatic ductal adenocarcinoma reveals alterations in sensory neuron innervation. Co-author DOI 10.1002/1878-0261.70233↗
  2. Tumor-specific targeting of a mitochondrial Kv1.3 channel inhibitor through conjugation to gastrin/cholecystokinin B receptor ligand strongly reduces pancreati… Co-author DOI 10.1016/j.phrs.2026.108150↗
  3. Fra-2 controls the response to the KRAS inhibitor MRTX-1133 in pancreatic ductal adenocarcinoma. Co-author DOI 10.1073/pnas.2601788123↗
  4. Estrogen Shapes Fibroblast States to Limit Pancreatic Cancer Aggressiveness. First author DOI 10.1158/0008-5472.can-25-4671↗
  5. Multinucleated Giant Cells in Human Pancreatic Cancer Are a Distinct Macrophage Population Undergoing a DNA Damage Response and Associated with an Aggressive T… Co-author DOI 10.1158/2326-6066.cir-25-1602↗
  6. 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↗
  7. Mucinous cystic neoplasms and simple mucinous cysts are two distinct precursors of pancreatic cancer: clinicopathological, genomic, and transcriptomic characte… Co-author DOI 10.1002/path.6437↗
  8. Local ablation disrupts immune evasion in pancreatic cancer. Co-author DOI 10.1016/j.canlet.2024.217327↗
  9. Advancing pancreatic cancer research and therapeutics: the transformative role of organoid technology. Co-author DOI 10.1038/s12276-024-01378-w↗
  10. MYC ecDNA promotes intratumour heterogeneity and plasticity in PDAC. Last author DOI 10.1038/s41586-025-08721-9↗
  11. SMAD4 and KRAS Status Shapes Cancer Cell-Stromal Cross-Talk and Therapeutic Response in Pancreatic Cancer. Co-author DOI 10.1158/0008-5472.can-24-2330↗
  12. Antibody-based delivery of interleukin-2 modulates the immunosuppressive tumor microenvironment and achieves cure in pancreatic ductal adenocarcinoma syngeneic… Co-author DOI 10.1186/s13046-024-03238-x↗
  13. The GLP-1R agonist semaglutide reshapes pancreatic cancer associated fibroblasts reducing collagen proline hydroxylation and favoring T lymphocyte infiltration. Co-author DOI 10.1186/s13046-024-03263-w↗
  14. A first-in-class inhibitor of homologous recombination DNA repair counteracts tumour growth, metastasis and therapeutic resistance in pancreatic cancer. Co-author DOI 10.1186/s13046-025-03389-5↗
  15. Expression of the membrane tetraspanin claudin 18 on cancer cells promotes T lymphocyte infiltration and antitumor immunity in pancreatic cancer. Co-author DOI 10.1016/j.immuni.2024.04.021↗
  16. Differential activity of MAPK signalling defines fibroblast subtypes in pancreatic cancer. Last author DOI 10.1038/s41467-024-54975-8↗
  17. Axon guidance cue SEMA3A promotes the aggressive phenotype of basal-like PDAC. Last author DOI 10.1136/gutjnl-2023-329807↗
  18. Cellular collusion: cracking the code of immunosuppression and chemo resistance in PDAC. Co-author DOI 10.3389/fimmu.2024.1341079↗
  19. Overcoming therapeutic resistance in pancreatic cancer: Emerging opportunities by targeting BRCAs and p53. First author DOI 10.1016/j.bbcan.2023.188914↗
  20. Clinical and Genomic Characterization of Pancreatic Ductal Adenocarcinoma with Signet-Ring/Poorly Cohesive Cells. Co-author DOI 10.1016/j.modpat.2023.100251↗
  21. CXCR1/2 dual-inhibitor ladarixin reduces tumour burden and promotes immunotherapy response in pancreatic cancer. Co-author DOI 10.1038/s41416-022-02028-6↗
  22. IL-1β+ macrophages fuel pathogenic inflammation in pancreatic cancer. Co-author DOI 10.1038/s41586-023-06685-2↗
  23. Lysosomal lipid switch sensitises to nutrient deprivation and mTOR targeting in pancreatic cancer. Co-author DOI 10.1136/gutjnl-2021-325117↗
  24. LAMC2 Regulates Key Transcriptional and Targetable Effectors to Support Pancreatic Cancer Growth. Co-author DOI 10.1158/1078-0432.ccr-22-0794↗
  25. Talniflumate abrogates mucin immune suppressive barrier improving efficacy of gemcitabine and nab-paclitaxel treatment in pancreatic cancer. Co-author DOI 10.1186/s12967-023-04733-z↗
  26. The tumor stroma influences immune cell distribution and recruitment in a PDAC-on-a-chip model. Co-author DOI 10.3389/fimmu.2023.1155085↗
  27. p53 mutations define the chromatin landscape to confer drug tolerance in pancreatic cancer. Co-author DOI 10.1002/1878-0261.13161↗
  28. Loss of FGFR4 promotes the malignant phenotype of PDAC. Last author DOI 10.1038/s41388-022-02432-5↗
  29. Refining targeted therapeutic approaches in pancreatic cancer: from histology and molecular pathology to the clinic. Co-author DOI 10.1080/14728222.2022.2021397↗
  30. Interrupting the nitrosative stress fuels tumor-specific cytotoxic T lymphocytes in pancreatic cancer. Co-author DOI 10.1136/jitc-2021-003549↗
  31. Spatial transcriptomics identified mucin-specific O-glycosylation as a key pathway in pancreatic cancer development and a promising therapeutic target Co-author DOI 10.21203/rs.3.rs-2095432/v1↗
  32. Germline Aberrations in Pancreatic Cancer: Implications for Clinical Care. First author DOI 10.3390/cancers14133239↗
  33. Impact of COVID-19 on Pancreatic Cancer Research and the Path Forward. Co-author DOI 10.1053/j.gastro.2021.06.080↗
  34. Intratumoral injection of TLR9 agonist promotes an immunopermissive microenvironment transition and causes cooperative antitumor activity in combination with a… Co-author DOI 10.1136/jitc-2021-002876↗
  35. ROR1 and ROR2 expression in pancreatic cancer. Co-author DOI 10.1186/s12885-021-08952-9↗
  36. Homologous Recombination Deficiency in Pancreatic Cancer: A Systematic Review and Prevalence Meta-Analysis. Co-author DOI 10.1200/jco.20.03238↗
  37. Cell Lineage Infidelity in PDAC Progression and Therapy Resistance. Last author DOI 10.3389/fcell.2021.795251↗
  38. Combinatorial Effect of Magnetic Field and Radiotherapy in PDAC Organoids: A Pilot Study. Co-author DOI 10.3390/biomedicines8120609↗
  39. From Genetic Alterations to Tumor Microenvironment: The Ariadne's String in Pancreatic Cancer. Co-author DOI 10.3390/cells9020309↗
  40. CAF hierarchy driven by pancreatic cancer cell p53-status creates a pro-metastatic and chemoresistant environment via perlecan. Last author DOI 10.1038/s41467-019-10968-6↗
  41. MAP Kinase inhibition reshapes tumor microenvironment of mouse pancreatic cancer by depleting anti-inflammatory macrophages Last author DOI 10.1101/759779↗
  42. Identification of Resistance Pathways Specific to Malignancy Using Organoid Models of Pancreatic Cancer. First author DOI 10.1158/1078-0432.ccr-19-1398↗
  43. Hypermutation In Pancreatic Cancer. Co-author DOI 10.1053/j.gastro.2016.09.060↗
  44. Distinct populations of inflammatory fibroblasts and myofibroblasts in pancreatic cancer. Co-author DOI 10.1084/jem.20162024↗
  45. Lack of growth inhibitory synergism with combined MAPK/PI3K inhibition in preclinical models of pancreatic cancer. Co-author DOI 10.1093/annonc/mdx335↗
  46. Lack of Association for Reported Endocrine Pancreatic Cancer Risk Loci in the PANDoRA Consortium. Co-author DOI 10.1158/1055-9965.epi-17-0075↗
  47. Genomic analyses identify molecular subtypes of pancreatic cancer. Co-author DOI 10.1038/nature16965↗
  48. Functional single nucleotide polymorphisms within the cyclin-dependent kinase inhibitor 2A/2B region affect pancreatic cancer risk. Co-author DOI 10.18632/oncotarget.10935↗
  49. Organoid models of human and mouse ductal pancreatic cancer. Co-author DOI 10.1016/j.cell.2014.12.021↗
  50. Whole genomes redefine the mutational landscape of pancreatic cancer. Co-author DOI 10.1038/nature14169↗

Closest collaborators

The 25 strongest of 202 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.

  1. Aldo Scarpa · 22 shared papers, 2012–2025 · strength 2.60
  2. Carmine Carbone · 14 shared papers, 2021–2026 · strength 2.36
  3. Lisa Veghini · 10 shared papers, 2021–2026 · strength 2.20
  4. Geny Piro · 12 shared papers, 2021–2026 · strength 1.98
  5. Antonio Agostini · 11 shared papers, 2021–2026 · strength 1.88
  6. Francesco De Sanctis · 11 shared papers, 2019–2026 · strength 1.69
  7. Rita Teresa Lawlor · 14 shared papers, 2014–2025 · strength 1.67
  8. Giampaolo Tortora · 9 shared papers, 2012–2026 · strength 1.39
  9. Elena Fiorini · 7 shared papers, 2019–2026 · strength 1.09
  10. Francesca Lupo · 7 shared papers, 2019–2025 · strength 1.04
  11. Sabrina L. D’Agosto · 7 shared papers, 2019–2025 · strength 1.00
  12. Claudio Luchini · 7 shared papers, 2020–2025 · strength 0.97
  13. Michèle Milella · 8 shared papers, 2017–2025 · strength 0.93
  14. Vincenzo Bronte · 6 shared papers, 2019–2026 · strength 0.88
  15. Salvatore Paiella · 6 shared papers, 2021–2025 · strength 0.87
  16. Pietro Delfino · 7 shared papers, 2019–2024 · strength 0.87
  17. Alessia Caggiano · 5 shared papers, 2022–2026 · strength 0.86
  18. Roberto Salvia · 6 shared papers, 2021–2025 · strength 0.83
  19. Antonia Malinova · 5 shared papers, 2021–2025 · strength 0.76
  20. Chang‐Il Hwang · 6 shared papers, 2015–2025 · strength 0.76
  21. Giuseppe Malleo · 5 shared papers, 2021–2025 · strength 0.73
  22. Antonio Pea · 6 shared papers, 2020–2025 · strength 0.70
  23. Peter J. Bailey · 5 shared papers, 2014–2025 · strength 0.61
  24. Claudio Bassi · 5 shared papers, 2021–2025 · strength 0.59
  25. David Arthur Tuveson · 6 shared papers, 2015–2025 · strength 0.58

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.