ResearcherUniversity of MinnesotaActive in the last 2 years
Phoebe A. Phillips
Matched on ORCID iD 0000-0002-4481-8782; OpenAlex author ID A5014082005, A5054435062. Sources: OpenAlex.
Their work
- Papers
- 22 (first author 2, last author 11)
- Trials
- 0
- Grants
- 0
- Labs led
- 1
- Collaborators
- 45
2011: 1 paper · 2012: none · 2013: 1 paper · 2014: 3 papers · 2015: 1 paper · 2016: 1 paper · 2017: 2 papers · 2018: none · 2019: none · 2020: 1 paper · 2021: 4 papers · 2022: 2 papers · 2023: 1 paper · 2024: none · 2025: 1 paper · 2026: 4 papers
Papers 22
- Efficacy and Safety Assessment of 5-Fluorouracil, Irinotecan and Oxaliplatin-Loaded Implants in Mouse and Pig Models for Pancreatic Cancer Therapy. Co-author DOI 10.1002/adma.202522617↗
- HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. Last author DOI 10.1038/s41388-026-03865-y↗
- βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. Last author DOI 10.1038/s41419-026-08657-6↗
- Pulsed priming with the FAK inhibitor narmafotinib enhances both gemcitabine/Abraxane and FOLFIRINOX chemotherapy response in pancreatic cancer Co-author DOI 10.64898/2026.07.23.740234↗
- MYH knockdown in pancreatic cancer cells creates an exploitable DNA repair vulnerability. Co-author DOI 10.1016/j.neo.2025.101138↗
- A first-in-class pan-lysyl oxidase inhibitor impairs stromal remodeling and enhances gemcitabine response and survival in pancreatic cancer. Co-author DOI 10.1038/s43018-023-00614-y↗
- βIII-Tubulin is a Brake on Extrinsic Cell-Death in Pancreatic Cancer Last author DOI 10.1101/2022.09.29.510034↗
- Imaging Modalities for Early Detection of Pancreatic Cancer: Current State and Future Research Opportunities. Co-author DOI 10.3390/cancers14102539↗
- Interfacial Curvature in Confined Coculture Directs Stromal Cell Activity with Spatial Corralling of Pancreatic Cancer Cells. Co-author DOI 10.1002/adbi.202000525↗
- Cancer-Associated Fibroblasts in Pancreatic Ductal Adenocarcinoma Determine Response to SLC7A11 Inhibition. Last author DOI 10.1158/0008-5472.can-20-2496↗
- ROR1 and ROR2 expression in pancreatic cancer. Co-author DOI 10.1186/s12885-021-08952-9↗
- Does the Microenvironment Hold the Hidden Key for Functional Precision Medicine in Pancreatic Cancer? Last author DOI 10.3390/cancers13102427↗
- Targeting the undruggable in pancreatic cancer using nano-based gene silencing drugs. Last author DOI 10.1016/j.biomaterials.2019.119742↗
- Inhibition of group 1 p21-activated kinases suppresses pancreatic stellate cell activation and increases survival of mice with pancreatic cancer. First author DOI 10.1002/ijc.30615↗
- MutY-Homolog (MYH) inhibition reduces pancreatic cancer cell growth and increases chemosensitivity. Last author DOI 10.18632/oncotarget.13985↗
- Delineating the Role of βIV-Tubulins in Pancreatic Cancer: βIVb-Tubulin Inhibition Sensitizes Pancreatic Cancer Cells to Vinca Alkaloids. Last author DOI 10.1016/j.neo.2016.10.011↗
- βIII-tubulin: a novel mediator of chemoresistance and metastases in pancreatic cancer. Last author DOI 10.18632/oncotarget.2946↗
- Fruit-derived phenolic compounds and pancreatic cancer: perspectives from Australian native fruits. Co-author DOI 10.1016/j.jep.2013.12.023↗
- Potential applications of nanotechnology for the diagnosis and treatment of pancreatic cancer. Last author DOI 10.3389/fphys.2014.00002↗
- Role of pancreatic stellate cells in chemoresistance in pancreatic cancer. Last author DOI 10.3389/fphys.2014.00141↗
- Therapeutic perspectives on pancreatic cancer. First author DOI 10.2174/1568009611313040004↗
- Myricetin induces pancreatic cancer cell death via the induction of apoptosis and inhibition of the phosphatidylinositol 3-kinase (PI3K) signaling pathway. Co-author DOI 10.1016/j.canlet.2011.05.002↗
Closest collaborators
The 25 strongest of 45 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- George Sharbeen · 13 shared papers, 2014–2026 · strength 1.62
- Paper Efficacy and Safety Assessment of 5-Fluorouracil, Irinotecan and Oxaliplatin-Loaded Implants in Mouse and Pig Models fo… DOI 10.1002/adma.202522617↗
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- David Goldstein · 12 shared papers, 2014–2026 · strength 1.31
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper MYH knockdown in pancreatic cancer cells creates an exploitable DNA repair vulnerability. DOI 10.1016/j.neo.2025.101138↗
- Joshua A. McCarroll · 12 shared papers, 2014–2026 · strength 1.31
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper MYH knockdown in pancreatic cancer cells creates an exploitable DNA repair vulnerability. DOI 10.1016/j.neo.2025.101138↗
- Koroush Shahsavar Haghighi · 7 shared papers, 2021–2026 · strength 1.12
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper MYH knockdown in pancreatic cancer cells creates an exploitable DNA repair vulnerability. DOI 10.1016/j.neo.2025.101138↗
- John Kokkinos · 7 shared papers, 2020–2026 · strength 1.05
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper MYH knockdown in pancreatic cancer cells creates an exploitable DNA repair vulnerability. DOI 10.1016/j.neo.2025.101138↗
- Amber L. Johns · 8 shared papers, 2015–2026 · strength 0.96
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper MYH knockdown in pancreatic cancer cells creates an exploitable DNA repair vulnerability. DOI 10.1016/j.neo.2025.101138↗
- Mert Erkan · 6 shared papers, 2015–2026 · strength 0.83
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper MYH knockdown in pancreatic cancer cells creates an exploitable DNA repair vulnerability. DOI 10.1016/j.neo.2025.101138↗
- Anthony James Gill · 5 shared papers, 2021–2026 · strength 0.79
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper MYH knockdown in pancreatic cancer cells creates an exploitable DNA repair vulnerability. DOI 10.1016/j.neo.2025.101138↗
- Val Gebski · 4 shared papers, 2021–2026 · strength 0.59
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper βIII-Tubulin is a Brake on Extrinsic Cell-Death in Pancreatic Cancer DOI 10.1101/2022.09.29.510034↗
- Jennifer P. Morton · 4 shared papers, 2021–2026 · strength 0.59
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper βIII-Tubulin is a Brake on Extrinsic Cell-Death in Pancreatic Cancer DOI 10.1101/2022.09.29.510034↗
- Marina Pajic · 4 shared papers, 2021–2026 · strength 0.58
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper MYH knockdown in pancreatic cancer cells creates an exploitable DNA repair vulnerability. DOI 10.1016/j.neo.2025.101138↗
- Paper βIII-Tubulin is a Brake on Extrinsic Cell-Death in Pancreatic Cancer DOI 10.1101/2022.09.29.510034↗
- Australian Pancreatic Cancer Genome Initiative · 3 shared papers, 2020–2026 · strength 0.50
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper MYH knockdown in pancreatic cancer cells creates an exploitable DNA repair vulnerability. DOI 10.1016/j.neo.2025.101138↗
- Paper Targeting the undruggable in pancreatic cancer using nano-based gene silencing drugs. DOI 10.1016/j.biomaterials.2019.119742↗
- Paul Timpson · 3 shared papers, 2021–2026 · strength 0.42
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper Interfacial Curvature in Confined Coculture Directs Stromal Cell Activity with Spatial Corralling of Pancreatic Cancer … DOI 10.1002/adbi.202000525↗
- Paper Cancer-Associated Fibroblasts in Pancreatic Ductal Adenocarcinoma Determine Response to SLC7A11 Inhibition. DOI 10.1158/0008-5472.can-20-2496↗
- Minoti Vivek Apte · 2 shared papers, 2021–2026 · strength 0.29
- Kara L. Vine · 1 shared paper, 2026 · strength 0.23
- Ashna A. Kumar · 1 shared paper, 2026 · strength 0.23
- Elahe Minaei · 1 shared paper, 2026 · strength 0.23
- Samantha J. Wade · 1 shared paper, 2026 · strength 0.23
- Kendelle Joan Murphy · 1 shared paper, 2026 · strength 0.21
- James Ephraums · 1 shared paper, 2025 · strength 0.19
- Katherina Podlekareva Farr · 1 shared paper, 2022 · strength 0.19
- Boon Hui Chua · 1 shared paper, 2022 · strength 0.19
- Andrew Victor Biankin · 3 shared papers, 2015–2017 · strength 0.17
- Paper MutY-Homolog (MYH) inhibition reduces pancreatic cancer cell growth and increases chemosensitivity. DOI 10.18632/oncotarget.13985↗
- Paper Delineating the Role of βIV-Tubulins in Pancreatic Cancer: βIVb-Tubulin Inhibition Sensitizes Pancreatic Cancer Cells t… DOI 10.1016/j.neo.2016.10.011↗
- Paper βIII-tubulin: a novel mediator of chemoresistance and metastases in pancreatic cancer. DOI 10.18632/oncotarget.2946↗
- Kristopher Alan Kilian · 1 shared paper, 2021 · strength 0.13
- Stephanie R. Nemec · 1 shared paper, 2021 · strength 0.13
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.