ResearcherThe University of Texas MD Anderson Cancer CenterActive in the last 2 years
Giannicola Genovese
Matched on ORCID iD 0000-0003-1392-9954; OpenAlex author ID A5046740782. Sources: OpenAlex.
Their work
- Papers
- 18 (first author 4, last author 0)
- Trials
- 0
- Grants
- 0
- Labs led
- 0
- Collaborators
- 55
2014: 1 paper · 2015: 1 paper · 2016: 1 paper · 2017: 2 papers · 2018: none · 2019: none · 2020: 2 papers · 2021: 1 paper · 2022: none · 2023: 1 paper · 2024: 3 papers · 2025: 1 paper · 2026: 5 papers
Papers 18
- Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. Co-author DOI 10.1038/s41586-026-10488-6↗
- Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. Co-author DOI 10.1038/s41586-026-10995-6↗
- Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. Co-author DOI 10.1038/s41586-026-11134-x↗
- GFER Represents a Target for Dual Disruption of Redox Homeostasis and Reactivation of the Immune Response in Pancreatic Adenocarcinoma. Co-author DOI 10.1158/0008-5472.can-24-4211↗
- DPY30 Is an Epigenetic Decoupler Linking Replication Stress to Immunoediting in Pancreatic Cancer. Co-author DOI 10.1158/0008-5472.can-25-3849↗
- Switching on the evolutionary potential of pancreatic cancer: the tumor suppressor functions of PBRM1. First author DOI 10.1172/jci193205↗
- The KRAS mutational spectrum and its clinical implications in pancreatic cancer. First author DOI 10.1016/j.ccell.2024.08.001↗
- WRAD core perturbation impairs DNA replication fidelity promoting immunoediting in pancreatic cancer Co-author DOI 10.1101/2024.10.21.619543↗
- Clonal dominance defines metastatic dissemination in pancreatic cancer. Co-author DOI 10.1126/sciadv.add9342↗
- KRAS-Dependency in Pancreatic Ductal Adenocarcinoma: Mechanisms of Escaping in Resistance to KRAS Inhibitors and Perspectives of Therapy. First author DOI 10.3390/ijms24119313↗
- PRMT1-dependent regulation of RNA metabolism and DNA damage response sustains pancreatic ductal adenocarcinoma. Co-author DOI 10.1038/s41467-021-24798-y↗
- Diversity Across the Pancreatic Ductal Adenocarcinoma Disease Spectrum Revealed by Network-Anchored Functional Genomics Co-author DOI 10.1101/2020.09.17.302034↗
- Oncogenic KRAS-Driven Metabolic Reprogramming in Pancreatic Cancer Cells Utilizes Cytokines from the Tumor Microenvironment. Co-author DOI 10.1158/2159-8290.cd-19-0297↗
- Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. Co-author DOI 10.1038/nature21052↗
- Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. Co-author DOI 10.1038/nature21064↗
- In Vivo Functional Platform Targeting Patient-Derived Xenografts Identifies WDR5-Myc Association as a Critical Determinant of Pancreatic Cancer. First author DOI 10.1016/j.celrep.2016.05.063↗
- Genetic events that limit the efficacy of MEK and RTK inhibitor therapies in a mouse model of KRAS-driven pancreatic cancer. Co-author DOI 10.1158/0008-5472.can-14-1854↗
- Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. Co-author DOI 10.1038/nature13611↗
Closest collaborators
The 25 strongest of 55 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Giulio Francesco Draetta · 15 shared papers, 2014–2026 · strength 1.97
- Paper The KRAS mutational spectrum and its clinical implications in pancreatic cancer. DOI 10.1016/j.ccell.2024.08.001↗
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper GFER Represents a Target for Dual Disruption of Redox Homeostasis and Reactivation of the Immune Response in Pancreatic… DOI 10.1158/0008-5472.can-24-4211↗
- Andrea Viale · 14 shared papers, 2014–2026 · strength 1.61
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper GFER Represents a Target for Dual Disruption of Redox Homeostasis and Reactivation of the Immune Response in Pancreatic… DOI 10.1158/0008-5472.can-24-4211↗
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Luigi Perelli · 5 shared papers, 2023–2026 · strength 1.42
- Paper Switching on the evolutionary potential of pancreatic cancer: the tumor suppressor functions of PBRM1. DOI 10.1172/jci193205↗
- Paper The KRAS mutational spectrum and its clinical implications in pancreatic cancer. DOI 10.1016/j.ccell.2024.08.001↗
- Paper KRAS-Dependency in Pancreatic Ductal Adenocarcinoma: Mechanisms of Escaping in Resistance to KRAS Inhibitors and Perspe… DOI 10.3390/ijms24119313↗
- Huamin Wang · 11 shared papers, 2014–2026 · strength 1.26
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper GFER Represents a Target for Dual Disruption of Redox Homeostasis and Reactivation of the Immune Response in Pancreatic… DOI 10.1158/0008-5472.can-24-4211↗
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Haoqiang Ying · 11 shared papers, 2014–2026 · strength 1.26
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper GFER Represents a Target for Dual Disruption of Redox Homeostasis and Reactivation of the Immune Response in Pancreatic… DOI 10.1158/0008-5472.can-24-4211↗
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Alessandro Carugo · 11 shared papers, 2014–2026 · strength 1.14
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper DPY30 Is an Epigenetic Decoupler Linking Replication Stress to Immunoediting in Pancreatic Cancer. DOI 10.1158/0008-5472.can-25-3849↗
- Timothy Paul Heffernan · 11 shared papers, 2014–2026 · strength 1.14
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper DPY30 Is an Epigenetic Decoupler Linking Replication Stress to Immunoediting in Pancreatic Cancer. DOI 10.1158/0008-5472.can-25-3849↗
- Virginia Giuliani · 9 shared papers, 2014–2026 · strength 1.03
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper DPY30 Is an Epigenetic Decoupler Linking Replication Stress to Immunoediting in Pancreatic Cancer. DOI 10.1158/0008-5472.can-25-3849↗
- Wantong Yao · 8 shared papers, 2014–2026 · strength 0.91
- Paper GFER Represents a Target for Dual Disruption of Redox Homeostasis and Reactivation of the Immune Response in Pancreatic… DOI 10.1158/0008-5472.can-24-4211↗
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper DPY30 Is an Epigenetic Decoupler Linking Replication Stress to Immunoediting in Pancreatic Cancer. DOI 10.1158/0008-5472.can-25-3849↗
- Anirban Maitra · 9 shared papers, 2016–2026 · strength 0.90
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper Clonal dominance defines metastatic dissemination in pancreatic cancer. DOI 10.1126/sciadv.add9342↗
- Jason B. Fleming · 9 shared papers, 2014–2026 · strength 0.87
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Ronald Anthony Depinho · 9 shared papers, 2014–2026 · strength 0.87
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- I-Lin Ho · 5 shared papers, 2020–2026 · strength 0.74
- Paper GFER Represents a Target for Dual Disruption of Redox Homeostasis and Reactivation of the Immune Response in Pancreatic… DOI 10.1158/0008-5472.can-24-4211↗
- Paper DPY30 Is an Epigenetic Decoupler Linking Replication Stress to Immunoediting in Pancreatic Cancer. DOI 10.1158/0008-5472.can-25-3849↗
- Paper Clonal dominance defines metastatic dissemination in pancreatic cancer. DOI 10.1126/sciadv.add9342↗
- Francesca Citron · 4 shared papers, 2024–2026 · strength 0.66
- Paper GFER Represents a Target for Dual Disruption of Redox Homeostasis and Reactivation of the Immune Response in Pancreatic… DOI 10.1158/0008-5472.can-24-4211↗
- Paper DPY30 Is an Epigenetic Decoupler Linking Replication Stress to Immunoediting in Pancreatic Cancer. DOI 10.1158/0008-5472.can-25-3849↗
- Paper Clonal dominance defines metastatic dissemination in pancreatic cancer. DOI 10.1126/sciadv.add9342↗
- Ziheng Chen · 4 shared papers, 2024–2026 · strength 0.66
- Paper GFER Represents a Target for Dual Disruption of Redox Homeostasis and Reactivation of the Immune Response in Pancreatic… DOI 10.1158/0008-5472.can-24-4211↗
- Paper DPY30 Is an Epigenetic Decoupler Linking Replication Stress to Immunoediting in Pancreatic Cancer. DOI 10.1158/0008-5472.can-25-3849↗
- Paper Clonal dominance defines metastatic dissemination in pancreatic cancer. DOI 10.1126/sciadv.add9342↗
- Prasenjit Dey · 5 shared papers, 2017–2026 · strength 0.57
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper Oncogenic KRAS-Driven Metabolic Reprogramming in Pancreatic Cancer Cells Utilizes Cytokines from the Tumor Microenviron… DOI 10.1158/2159-8290.cd-19-0297↗
- Ya’an Kang · 5 shared papers, 2014–2026 · strength 0.53
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/nature21052↗
- Tony Gutschner · 4 shared papers, 2017–2026 · strength 0.49
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/nature21052↗
- Johnathon Lynn Rose · 4 shared papers, 2016–2026 · strength 0.41
- Paper GFER Represents a Target for Dual Disruption of Redox Homeostasis and Reactivation of the Immune Response in Pancreatic… DOI 10.1158/0008-5472.can-24-4211↗
- Paper PRMT1-dependent regulation of RNA metabolism and DNA damage response sustains pancreatic ductal adenocarcinoma. DOI 10.1038/s41467-021-24798-y↗
- Paper Diversity Across the Pancreatic Ductal Adenocarcinoma Disease Spectrum Revealed by Network-Anchored Functional Genomics DOI 10.1101/2020.09.17.302034↗
- Piergiorgio Pettazzoni · 5 shared papers, 2014–2026 · strength 0.34
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/nature21064↗
- Paper In Vivo Functional Platform Targeting Patient-Derived Xenografts Identifies WDR5-Myc Association as a Critical Determin… DOI 10.1016/j.celrep.2016.05.063↗
- Chiara Bonini · 2 shared papers, 2024–2026 · strength 0.31
- Michael P. Kim · 3 shared papers, 2020–2024 · strength 0.30
- Paper Clonal dominance defines metastatic dissemination in pancreatic cancer. DOI 10.1126/sciadv.add9342↗
- Paper PRMT1-dependent regulation of RNA metabolism and DNA damage response sustains pancreatic ductal adenocarcinoma. DOI 10.1038/s41467-021-24798-y↗
- Paper Diversity Across the Pancreatic Ductal Adenocarcinoma Disease Spectrum Revealed by Network-Anchored Functional Genomics DOI 10.1101/2020.09.17.302034↗
- Avnish Kapoor · 3 shared papers, 2014–2026 · strength 0.26
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper Genetic events that limit the efficacy of MEK and RTK inhibitor therapies in a mouse model of KRAS-driven pancreatic ca… DOI 10.1158/0008-5472.can-14-1854↗
- Paper Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/nature13611↗
- Lynda Chin · 3 shared papers, 2016–2026 · strength 0.26
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/nature21064↗
- Paper In Vivo Functional Platform Targeting Patient-Derived Xenografts Identifies WDR5-Myc Association as a Critical Determin… DOI 10.1016/j.celrep.2016.05.063↗
- Lifeng Yang · 2 shared papers, 2017–2026 · strength 0.26
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.