ResearcherPurdue University West LafayetteActive in the last 2 years
Melissa L. Fishel
Matched on ORCID iD 0000-0002-9436-6382; OpenAlex author ID A5055500811; NIH RePORTER profile ID 7580025. Sources: OpenAlex.
Their work
- Papers
- 31 (first author 0, last author 9)
- Trials
- 0
- Grants
- 5
- Labs led
- 2
- Collaborators
- 56
2012: 1 paper · 2013: none · 2014: none · 2015: none · 2016: 3 papers · 2017: 3 papers · 2018: 2 papers · 2019: 1 paper · 2020: none · 2021: 1 paper · 2022: 1 paper, 2 grants · 2023: 8 papers · 2024: 2 papers · 2025: 2 papers, 1 grant · 2026: 7 papers, 2 grants
Papers 31
- Ketogenic supplementation enhances KRASG12D inhibitor efficacy in pancreatic ductal adenocarcinoma Co-author DOI 10.1016/j.canlet.2026.218490↗
- Depletion of Fibrinogen Suppresses Growth of Primary Tumors and Metastasis of Pancreatic Ductal Adenocarcinoma. Last author DOI 10.1053/j.gastro.2025.09.024↗
- Beyond Cys65: Redox Effector Factor-1 CRISPR-Engineered Cys93 and Cys99 Mutants Reveal Cooperative and Secondary Roles of Redox Signaling and Pancreatic Ductal… Last author DOI 10.1177/15230864261489484↗
- Targeting APE1 endonuclease activity impairs metastasis and enhances genotoxic therapy response in pancreatic cancer. Co-author DOI 10.1186/s13046-026-03705-7↗
- Integrated Post-Translational Modification (PTM) Proteomics Reveals Early Redox and Mitochondrial Remodeling Following Ref-1 Inhibition in Pancreatic Cancer Co-author DOI 10.2139/ssrn.7345898↗
- Correction: Cui et al. Anticancer Peptides Derived from Aldolase A and Induced Tumor-Suppressing Cells Inhibit Pancreatic Ductal Adenocarcinoma Cells. Pharmace… Co-author DOI 10.3390/pharmaceutics18070808↗
- Extravascular coagulation stabilizes pro-fibrotic stromal states via tumor-intrinsic PAR1 signaling in pancreatic ductal adenocarcinoma Co-author DOI 10.64898/2026.06.25.734662↗
- The absence of Peroxiredoxin-1 in human pancreatic ductal adenocarcinoma (PDAC) markedly reduces cell survival and tumor growth when coupled with the inhibitio… Co-author DOI 10.1016/j.redox.2025.103848↗
- Fast-Relaxing Hydrogels Promote Pancreatic Adenocarcinoma Cell Aggressiveness through Integrin β1 Signaling. Co-author DOI 10.1021/acs.biomac.4c01441↗
- Plasminogen deficiency suppresses pancreatic ductal adenocarcinoma disease progression. Co-author DOI 10.1002/1878-0261.13552↗
- In vitro and In vivo evidence demonstrating chronic absence of Ref-1 Cysteine 65 impacts Ref-1 folding configuration, redox signaling, proliferation and metast… Co-author DOI 10.1016/j.redox.2023.102977↗
- Viscoelastic hydrogels for interrogating pancreatic cancer-stromal cell interactions. Co-author DOI 10.1016/j.mtbio.2023.100576↗
- Amplification-Free, High-Throughput Nanoplasmonic Quantification of Circulating MicroRNAs in Unprocessed Plasma Microsamples for Earlier Pancreatic Cancer Dete… Co-author DOI 10.1021/acssensors.2c02105↗
- The inhibition of pancreatic cancer progression by K-Ras-overexpressing mesenchymal stem cell-derived secretomes. Co-author DOI 10.1038/s41598-023-41835-6↗
- Gemcitabine plus nab-paclitaxel preserves skeletal and cardiac mass and function in a murine model of pancreatic cancer cachexia Co-author DOI 10.1101/2023.04.15.536434↗
- Activation of the integrated stress response (ISR) pathways in response to Ref-1 inhibition in human pancreatic cancer and its tumor microenvironment. Last author DOI 10.3389/fmed.2023.1146115↗
- Exploring the Tumor-Suppressing Potential of PSCA in Pancreatic Ductal Adenocarcinoma. Co-author DOI 10.3390/cancers15204917↗
- Anticancer Peptides Derived from Aldolase A and Induced Tumor-Suppressing Cells Inhibit Pancreatic Ductal Adenocarcinoma Cells. Co-author DOI 10.3390/pharmaceutics15102447↗
- A novel triptolide analog downregulates NF-κB and induces mitochondrial apoptosis pathways in human pancreatic cancer. Co-author DOI 10.7554/elife.85862↗
- RelA Is an Essential Target for Enhancing Cellular Responses to the DNA Repair/Ref-1 Redox Signaling Protein and Restoring Perturbated Cellular Redox Homeostas… Co-author DOI 10.3389/fonc.2022.826617↗
- Ref-1 redox activity alters cancer cell metabolism in pancreatic cancer: exploiting this novel finding as a potential target. Last author DOI 10.1186/s13046-021-02046-x↗
- Identification and Characterization of AES-135, a Hydroxamic Acid-Based HDAC Inhibitor That Prolongs Survival in an Orthotopic Mouse Model of Pancreatic Cancer. Co-author DOI 10.1021/acs.jmedchem.8b01957↗
- PTEN-Dependent Stabilization of MTSS1 Inhibits Metastatic Phenotype in Pancreatic Ductal Adenocarcinoma. Co-author DOI 10.1016/j.neo.2017.10.004↗
- Blocking HIF signaling via novel inhibitors of CA9 and APE1/Ref-1 dramatically affects pancreatic cancer cell survival. Last author DOI 10.1038/s41598-018-32034-9↗
- APE1/Ref-1 knockdown in pancreatic ductal adenocarcinoma - characterizing gene expression changes and identifying novel pathways using single-cell RNA sequenci… Last author DOI 10.1002/1878-0261.12138↗
- Cancer-associated fibroblast exosomes regulate survival and proliferation of pancreatic cancer cells. Co-author DOI 10.1038/onc.2016.353↗
- Loss of MTSS1 results in increased metastatic potential in pancreatic cancer. Co-author DOI 10.18632/oncotarget.14869↗
- Tissue Transglutaminase Activates Cancer-Associated Fibroblasts and Contributes to Gemcitabine Resistance in Pancreatic Cancer. Co-author DOI 10.1016/j.neo.2016.09.003↗
- Applying Small Molecule Signal Transducer and Activator of Transcription-3 (STAT3) Protein Inhibitors as Pancreatic Cancer Therapeutics. Last author DOI 10.1158/1535-7163.mct-15-0003↗
- Regulation of HIF1α under Hypoxia by APE1/Ref-1 Impacts CA9 Expression: Dual Targeting in Patient-Derived 3D Pancreatic Cancer Models. Last author DOI 10.1158/1535-7163.mct-16-0253↗
- APE1/Ref-1 regulates STAT3 transcriptional activity and APE1/Ref-1-STAT3 dual-targeting effectively inhibits pancreatic cancer cell survival. Last author DOI 10.1371/journal.pone.0047462↗
Grants 5
- Metabolic flux analysis and PDX models to understand therapeutic vulnerabilities following inhibition of Ref-1 redox signaling in pancreatic cancer R01CA282478↗
- Reprogramming PDAC Stroma by Targeting Coagulation in the Tumor Microenvironment U01CA274304↗
- Investigation of novel signaling protein in 3D and in vivo PDAC models using second generation Ref-1 inhibitors R01CA254110↗
- Exploiting the Ref-1 node in pancreatic cancer: tailoring new pancreatic cancer therapy using multi-targeted combinations R01CA167291↗
- Targeting the Plasminogen Activation System to Limit Pancreatic Cancer Progression and Associated Thrombosis U01HL143403↗
Closest collaborators
The 25 strongest of 56 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Mark R. Kelley · 13 shared papers, 2 shared grants, 2012–2026 · strength 3.98
- Grant Metabolic flux analysis and PDX models to understand therapeutic vulnerabilities following inhibition of Ref-1 redox si… R01CA282478↗
- Grant Exploiting the Ref-1 node in pancreatic cancer: tailoring new pancreatic cancer therapy using multi-targeted combinatio… R01CA167291↗
- Paper Integrated Post-Translational Modification (PTM) Proteomics Reveals Early Redox and Mitochondrial Remodeling Following … DOI 10.2139/ssrn.7345898↗
- Bumsoo Han · 2 shared papers, 3 shared grants, 2021–2026 · strength 2.88
- Grant Investigation of novel signaling protein in 3D and in vivo PDAC models using second generation Ref-1 inhibitors R01CA254110↗
- Grant Reprogramming PDAC Stroma by Targeting Coagulation in the Tumor Microenvironment U01CA274304↗
- Grant Targeting the Plasminogen Activation System to Limit Pancreatic Cancer Progression and Associated Thrombosis U01HL143403↗
- Matthew J. Flick · 3 shared papers, 2 shared grants, 2022–2026 · strength 2.10
- Grant Reprogramming PDAC Stroma by Targeting Coagulation in the Tumor Microenvironment U01CA274304↗
- Grant Targeting the Plasminogen Activation System to Limit Pancreatic Cancer Progression and Associated Thrombosis U01HL143403↗
- Paper Extravascular coagulation stabilizes pro-fibrotic stromal states via tumor-intrinsic PAR1 signaling in pancreatic ducta… DOI 10.64898/2026.06.25.734662↗
- Silpa Gampala · 8 shared papers, 2021–2026 · strength 1.66
- Paper Integrated Post-Translational Modification (PTM) Proteomics Reveals Early Redox and Mitochondrial Remodeling Following … DOI 10.2139/ssrn.7345898↗
- Paper Beyond Cys65: Redox Effector Factor-1 CRISPR-Engineered Cys93 and Cys99 Mutants Reveal Cooperative and Secondary Roles … DOI 10.1177/15230864261489484↗
- Paper Targeting APE1 endonuclease activity impairs metastasis and enhances genotoxic therapy response in pancreatic cancer. DOI 10.1186/s13046-026-03705-7↗
- Mahmut Mijit · 5 shared papers, 2022–2026 · strength 1.04
- Paper Beyond Cys65: Redox Effector Factor-1 CRISPR-Engineered Cys93 and Cys99 Mutants Reveal Cooperative and Secondary Roles … DOI 10.1177/15230864261489484↗
- Paper Targeting APE1 endonuclease activity impairs metastasis and enhances genotoxic therapy response in pancreatic cancer. DOI 10.1186/s13046-026-03705-7↗
- Paper In vitro and In vivo evidence demonstrating chronic absence of Ref-1 Cysteine 65 impacts Ref-1 folding configuration, r… DOI 10.1016/j.redox.2023.102977↗
- Qingji Huo · 4 shared papers, 2023–2026 · strength 0.90
- Paper Correction: Cui et al. Anticancer Peptides Derived from Aldolase A and Induced Tumor-Suppressing Cells Inhibit Pancreat… DOI 10.3390/pharmaceutics18070808↗
- Paper Anticancer Peptides Derived from Aldolase A and Induced Tumor-Suppressing Cells Inhibit Pancreatic Ductal Adenocarcinom… DOI 10.3390/pharmaceutics15102447↗
- Paper Exploring the Tumor-Suppressing Potential of PSCA in Pancreatic Ductal Adenocarcinoma. DOI 10.3390/cancers15204917↗
- Kexin Li · 4 shared papers, 2023–2026 · strength 0.90
- Paper Correction: Cui et al. Anticancer Peptides Derived from Aldolase A and Induced Tumor-Suppressing Cells Inhibit Pancreat… DOI 10.3390/pharmaceutics18070808↗
- Paper Anticancer Peptides Derived from Aldolase A and Induced Tumor-Suppressing Cells Inhibit Pancreatic Ductal Adenocarcinom… DOI 10.3390/pharmaceutics15102447↗
- Paper Exploring the Tumor-Suppressing Potential of PSCA in Pancreatic Ductal Adenocarcinoma. DOI 10.3390/cancers15204917↗
- Hiroki Yokota · 4 shared papers, 2023–2026 · strength 0.90
- Paper Correction: Cui et al. Anticancer Peptides Derived from Aldolase A and Induced Tumor-Suppressing Cells Inhibit Pancreat… DOI 10.3390/pharmaceutics18070808↗
- Paper Anticancer Peptides Derived from Aldolase A and Induced Tumor-Suppressing Cells Inhibit Pancreatic Ductal Adenocarcinom… DOI 10.3390/pharmaceutics15102447↗
- Paper Exploring the Tumor-Suppressing Potential of PSCA in Pancreatic Ductal Adenocarcinoma. DOI 10.3390/cancers15204917↗
- Eyram K. Kpenu · 4 shared papers, 2023–2026 · strength 0.89
- Paper Beyond Cys65: Redox Effector Factor-1 CRISPR-Engineered Cys93 and Cys99 Mutants Reveal Cooperative and Secondary Roles … DOI 10.1177/15230864261489484↗
- Paper Targeting APE1 endonuclease activity impairs metastasis and enhances genotoxic therapy response in pancreatic cancer. DOI 10.1186/s13046-026-03705-7↗
- Paper In vitro and In vivo evidence demonstrating chronic absence of Ref-1 Cysteine 65 impacts Ref-1 folding configuration, r… DOI 10.1016/j.redox.2023.102977↗
- Alisa S. Wolberg · 2 shared papers, 1 shared grant, 2022–2026 · strength 0.85
- Grant Targeting the Plasminogen Activation System to Limit Pancreatic Cancer Progression and Associated Thrombosis U01HL143403↗
- Paper Depletion of Fibrinogen Suppresses Growth of Primary Tumors and Metastasis of Pancreatic Ductal Adenocarcinoma. DOI 10.1053/j.gastro.2025.09.024↗
- Paper Plasminogen deficiency suppresses pancreatic ductal adenocarcinoma disease progression. DOI 10.1002/1878-0261.13552↗
- Nayela N. Chowdhury · 4 shared papers, 2023–2026 · strength 0.77
- Paper Depletion of Fibrinogen Suppresses Growth of Primary Tumors and Metastasis of Pancreatic Ductal Adenocarcinoma. DOI 10.1053/j.gastro.2025.09.024↗
- Paper In vitro and In vivo evidence demonstrating chronic absence of Ref-1 Cysteine 65 impacts Ref-1 folding configuration, r… DOI 10.1016/j.redox.2023.102977↗
- Paper Plasminogen deficiency suppresses pancreatic ductal adenocarcinoma disease progression. DOI 10.1002/1878-0261.13552↗
- Sanya Haiaty · 3 shared papers, 2025–2026 · strength 0.74
- Paper Beyond Cys65: Redox Effector Factor-1 CRISPR-Engineered Cys93 and Cys99 Mutants Reveal Cooperative and Secondary Roles … DOI 10.1177/15230864261489484↗
- Paper Targeting APE1 endonuclease activity impairs metastasis and enhances genotoxic therapy response in pancreatic cancer. DOI 10.1186/s13046-026-03705-7↗
- Paper The absence of Peroxiredoxin-1 in human pancreatic ductal adenocarcinoma (PDAC) markedly reduces cell survival and tumo… DOI 10.1016/j.redox.2025.103848↗
- Rajesh Sardar · 3 shared papers, 2023–2026 · strength 0.68
- Paper Beyond Cys65: Redox Effector Factor-1 CRISPR-Engineered Cys93 and Cys99 Mutants Reveal Cooperative and Secondary Roles … DOI 10.1177/15230864261489484↗
- Paper Targeting APE1 endonuclease activity impairs metastasis and enhances genotoxic therapy response in pancreatic cancer. DOI 10.1186/s13046-026-03705-7↗
- Paper Amplification-Free, High-Throughput Nanoplasmonic Quantification of Circulating MicroRNAs in Unprocessed Plasma Microsa… DOI 10.1021/acssensors.2c02105↗
- Chang-peng Cui · 2 shared papers, 2023–2026 · strength 0.54
- Paper Correction: Cui et al. Anticancer Peptides Derived from Aldolase A and Induced Tumor-Suppressing Cells Inhibit Pancreat… DOI 10.3390/pharmaceutics18070808↗
- Paper Anticancer Peptides Derived from Aldolase A and Induced Tumor-Suppressing Cells Inhibit Pancreatic Ductal Adenocarcinom… DOI 10.3390/pharmaceutics15102447↗
- Fenil Shah · 5 shared papers, 2017–2024 · strength 0.53
- Paper Plasminogen deficiency suppresses pancreatic ductal adenocarcinoma disease progression. DOI 10.1002/1878-0261.13552↗
- Paper Ref-1 redox activity alters cancer cell metabolism in pancreatic cancer: exploiting this novel finding as a potential t… DOI 10.1186/s13046-021-02046-x↗
- Paper APE1/Ref-1 knockdown in pancreatic ductal adenocarcinoma - characterizing gene expression changes and identifying novel… DOI 10.1002/1878-0261.12138↗
- Chien‐Chi Lin · 2 shared papers, 2023–2025 · strength 0.50
- Han D. Nguyen · 2 shared papers, 2023–2025 · strength 0.50
- Sae Rome Choi · 2 shared papers, 2026 · strength 0.47
- Paper Extravascular coagulation stabilizes pro-fibrotic stromal states via tumor-intrinsic PAR1 signaling in pancreatic ducta… DOI 10.64898/2026.06.25.734662↗
- Paper Depletion of Fibrinogen Suppresses Growth of Primary Tumors and Metastasis of Pancreatic Ductal Adenocarcinoma. DOI 10.1053/j.gastro.2025.09.024↗
- Kazuhiko Ogawa · 2 shared papers, 2023 · strength 0.36
- Hye‐ran Moon · 2 shared papers, 2021–2026 · strength 0.36
- Paper Extravascular coagulation stabilizes pro-fibrotic stromal states via tumor-intrinsic PAR1 signaling in pancreatic ducta… DOI 10.64898/2026.06.25.734662↗
- Paper Ref-1 redox activity alters cancer cell metabolism in pancreatic cancer: exploiting this novel finding as a potential t… DOI 10.1186/s13046-021-02046-x↗
- Loan Duong · 1 shared paper, 2026 · strength 0.32
- Xin Lü · 1 shared paper, 2026 · strength 0.32
- Reginald Hill · 3 shared papers, 2017–2018 · strength 0.29
- Paper PTEN-Dependent Stabilization of MTSS1 Inhibits Metastatic Phenotype in Pancreatic Ductal Adenocarcinoma. DOI 10.1016/j.neo.2017.10.004↗
- Paper Loss of MTSS1 results in increased metastatic potential in pancreatic cancer. DOI 10.18632/oncotarget.14869↗
- Paper Cancer-associated fibroblast exosomes regulate survival and proliferation of pancreatic cancer cells. DOI 10.1038/onc.2016.353↗
- Ann E. Zeleniak · 3 shared papers, 2017–2018 · strength 0.29
- Paper PTEN-Dependent Stabilization of MTSS1 Inhibits Metastatic Phenotype in Pancreatic Ductal Adenocarcinoma. DOI 10.1016/j.neo.2017.10.004↗
- Paper Loss of MTSS1 results in increased metastatic potential in pancreatic cancer. DOI 10.18632/oncotarget.14869↗
- Paper Cancer-associated fibroblast exosomes regulate survival and proliferation of pancreatic cancer cells. DOI 10.1038/onc.2016.353↗
- Claudius H. Conrad · 1 shared paper, 2026 · strength 0.25
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.