ResearcherWayne State UniversityActive in the last 2 years
Boris Pasche
Matched on ORCID iD 0000-0002-3750-7898; OpenAlex author ID A5042254050. Sources: OpenAlex.
Their work
- Papers
- 7 (first author 0, last author 1)
- Trials
- 0
- Grants
- 0
- Labs led
- 0
- Collaborators
- 25
2017: 1 paper · 2018: none · 2019: none · 2020: none · 2021: 1 paper · 2022: none · 2023: 1 paper · 2024: 1 paper · 2025: 2 papers · 2026: 1 paper
Papers 7
- XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant pancreatic ductal adenocarcinoma. Co-author DOI 10.1016/j.canlet.2026.218804↗
- Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcinoma Co-author DOI 10.1101/2025.11.21.689857↗
- PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer Co-author DOI 10.64898/2025.12.06.692635↗
- RCC1 regulation of subcellular protein localization via Ran GTPase drives pancreatic ductal adenocarcinoma growth. Co-author DOI 10.1016/j.canlet.2024.217275↗
- Regulator of Chromosome Condensation (RCC1) a novel therapeutic target in pancreatic ductal adenocarcinoma drives tumor progression via the c-Myc-RCC1-Ran axis Co-author DOI 10.1101/2023.12.18.572102↗
- IGFBP2 promotes tumor progression by inducing alternative polarization of macrophages in pancreatic ductal adenocarcinoma through the STAT3 pathway. Co-author DOI 10.1016/j.canlet.2020.12.008↗
- Safety and tolerability of the first-in-class agent CPI-613 in combination with modified FOLFIRINOX in patients with metastatic pancreatic cancer: a single-cen… Last author DOI 10.1016/s1470-2045(17)30314-5↗
Closest collaborators
The 25 strongest of 25 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Sahar F. Bannoura · 5 shared papers, 2023–2026 · strength 0.88
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper RCC1 regulation of subcellular protein localization via Ran GTPase drives pancreatic ductal adenocarcinoma growth. DOI 10.1016/j.canlet.2024.217275↗
- Md. Hafiz Uddin · 5 shared papers, 2023–2026 · strength 0.88
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper RCC1 regulation of subcellular protein localization via Ran GTPase drives pancreatic ductal adenocarcinoma growth. DOI 10.1016/j.canlet.2024.217275↗
- Mohammed Najeeb Al Hallak · 5 shared papers, 2023–2026 · strength 0.88
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper RCC1 regulation of subcellular protein localization via Ran GTPase drives pancreatic ductal adenocarcinoma growth. DOI 10.1016/j.canlet.2024.217275↗
- Husain Yar Khan · 5 shared papers, 2023–2026 · strength 0.88
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper RCC1 regulation of subcellular protein localization via Ran GTPase drives pancreatic ductal adenocarcinoma growth. DOI 10.1016/j.canlet.2024.217275↗
- Amro Aboukameel · 5 shared papers, 2023–2026 · strength 0.88
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper RCC1 regulation of subcellular protein localization via Ran GTPase drives pancreatic ductal adenocarcinoma growth. DOI 10.1016/j.canlet.2024.217275↗
- Asfar Sohail Azmi · 5 shared papers, 2023–2026 · strength 0.88
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper RCC1 regulation of subcellular protein localization via Ran GTPase drives pancreatic ductal adenocarcinoma growth. DOI 10.1016/j.canlet.2024.217275↗
- Muhammad Wasif Saif · 4 shared papers, 2024–2026 · strength 0.72
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper RCC1 regulation of subcellular protein localization via Ran GTPase drives pancreatic ductal adenocarcinoma growth. DOI 10.1016/j.canlet.2024.217275↗
- Ramzi M. Mohammad · 4 shared papers, 2024–2026 · strength 0.72
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper RCC1 regulation of subcellular protein localization via Ran GTPase drives pancreatic ductal adenocarcinoma growth. DOI 10.1016/j.canlet.2024.217275↗
- Bassel F. El‐Rayes · 4 shared papers, 2024–2026 · strength 0.72
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper RCC1 regulation of subcellular protein localization via Ran GTPase drives pancreatic ductal adenocarcinoma growth. DOI 10.1016/j.canlet.2024.217275↗
- Eliza Wright Beal · 4 shared papers, 2023–2026 · strength 0.70
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper RCC1 regulation of subcellular protein localization via Ran GTPase drives pancreatic ductal adenocarcinoma growth. DOI 10.1016/j.canlet.2024.217275↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Bin Bao · 3 shared papers, 2025–2026 · strength 0.55
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- P. A. Philip · 2 shared papers, 2025–2026 · strength 0.37
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Anthony Frank Shields · 2 shared papers, 2025–2026 · strength 0.37
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Azeddine Atfi · 2 shared papers, 2025–2026 · strength 0.37
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Philip A. Philip · 2 shared papers, 2024–2025 · strength 0.35
- Kay‐Uwe Wagner · 2 shared papers, 2023–2024 · strength 0.33
- Paper RCC1 regulation of subcellular protein localization via Ran GTPase drives pancreatic ductal adenocarcinoma growth. DOI 10.1016/j.canlet.2024.217275↗
- Paper Regulator of Chromosome Condensation (RCC1) a novel therapeutic target in pancreatic ductal adenocarcinoma drives tumor… DOI 10.1101/2023.12.18.572102↗
- Wei Zhang · 2 shared papers, 2017–2021 · strength 0.17
- Paper IGFBP2 promotes tumor progression by inducing alternative polarization of macrophages in pancreatic ductal adenocarcino… DOI 10.1016/j.canlet.2020.12.008↗
- Paper Safety and tolerability of the first-in-class agent CPI-613 in combination with modified FOLFIRINOX in patients with me… DOI 10.1016/s1470-2045(17)30314-5↗
- Steve H. Kim · 1 shared paper, 2025 · strength 0.17
- Longhao Sun · 1 shared paper, 2021 · strength 0.12
- Liang Liu · 1 shared paper, 2021 · strength 0.12
- Huamin Wang · 1 shared paper, 2021 · strength 0.12
- Ya’an Kang · 1 shared paper, 2021 · strength 0.12
- Jason B. Fleming · 1 shared paper, 2021 · strength 0.12
- Clancy J. Clark · 1 shared paper, 2017 · strength 0.05
- Angela Tatiana Alistar · 1 shared paper, 2017 · strength 0.05
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.