Pancreatic Cancer Research

ResearcherUniversity of Nebraska–LincolnActive in the last 2 years

Nina V. Chaika

ORCID-verified (high confidence, 0.95), identity_conf@1As of 8 November 2026

Matched on ORCID iD 0000-0002-2429-3851; OpenAlex author ID A5079624314. Sources: OpenAlex.

Their work

Papers
22 (first author 1, last author 0)
Trials
0
Grants
0
Labs led
0
Collaborators
76
Papers, trials and grants by year

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

Papers 22

  1. Mitochondrial-Localized Keratin 17 Promotes Chemoresistance in Basal-like Pancreatic Cancer. Co-author DOI 10.1158/0008-5472.can-25-4534↗
  2. Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism via the ACSS2-SP1-SAT1 axis. Co-author DOI 10.1038/s41556-024-01372-4↗
  3. Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism via the ACSS2-SP1-SAT1 … Co-author DOI 10.1038/s41556-024-01417-8↗
  4. The MUC1-HIF-1α signaling axis regulates pancreatic cancer pathogenesis through polyamine metabolism remodeling. Co-author DOI 10.1073/pnas.2315509121↗
  5. ENT1 blockade by CNX-774 overcomes resistance to DHODH inhibition in pancreatic cancer. Co-author DOI 10.1016/j.canlet.2022.215981↗
  6. CD73 induces GM-CSF/MDSC-mediated suppression of T cells to accelerate pancreatic cancer pathogenesis. Co-author DOI 10.1038/s41388-021-02132-6↗
  7. Targeting keratin 17-mediated reprogramming of de novo pyrimidine biosynthesis to overcome chemoresistance in pancreatic cancer First author DOI 10.1101/2022.08.24.504873↗
  8. Metabolic Rewiring by Loss of Sirt5 Promotes Kras-Induced Pancreatic Cancer Progression. Co-author DOI 10.1053/j.gastro.2021.06.045↗
  9. Author Correction: Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer. Co-author DOI 10.1038/s41591-020-0947-8↗
  10. Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer. Co-author DOI 10.1038/s41591-019-0368-8↗
  11. Metabolic Alterations in Pancreatic Cancer Progression. Co-author DOI 10.3390/cancers12010002↗
  12. MUC1 and HIF-1alpha Signaling Crosstalk Induces Anabolic Glucose Metabolism to Impart Gemcitabine Resistance to Pancreatic Cancer. Co-author DOI 10.1016/j.ccell.2017.06.004↗
  13. Glucose Limitation Alters Glutamine Metabolism in MUC1-Overexpressing Pancreatic Cancer Cells. Co-author DOI 10.1021/acs.jproteome.7b00246↗
  14. De Novo Lipid Synthesis Facilitates Gemcitabine Resistance through Endoplasmic Reticulum Stress in Pancreatic Cancer. Co-author DOI 10.1158/0008-5472.can-16-3062↗
  15. MUC1-Mediated Metabolic Alterations Regulate Response to Radiotherapy in Pancreatic Cancer. Co-author DOI 10.1158/1078-0432.ccr-17-1151↗
  16. Up-regulation of N-cadherin by Collagen I-activated Discoidin Domain Receptor 1 in Pancreatic Cancer Requires the Adaptor Molecule Shc1. Co-author DOI 10.1074/jbc.m116.740605↗
  17. MUC16-mediated activation of mTOR and c-Myc reprograms pancreatic cancer metabolism. Co-author DOI 10.18632/oncotarget.4078↗
  18. Silibinin-mediated metabolic reprogramming attenuates pancreatic cancer-induced cachexia and tumor growth. Co-author DOI 10.18632/oncotarget.5843↗
  19. Structure and function of human DnaJ homologue subfamily a member 1 (DNAJA1) and its relationship to pancreatic cancer. Co-author DOI 10.1021/bi401329a↗
  20. Metabolic reprogramming induced by ketone bodies diminishes pancreatic cancer cachexia. Co-author DOI 10.1186/2049-3002-2-18↗
  21. MUC1 mucin stabilizes and activates hypoxia-inducible factor 1 alpha to regulate metabolism in pancreatic cancer. Co-author DOI 10.1073/pnas.1203339109↗
  22. Differential expression of metabolic genes in tumor and stromal components of primary and metastatic loci in pancreatic adenocarcinoma. Co-author DOI 10.1371/journal.pone.0032996↗

Closest collaborators

The 25 strongest of 76 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.

  1. Pankaj Kumar Singh · 21 shared papers, 2012–2026 · strength 1.86
  2. Surendra Kumar Shukla · 14 shared papers, 2014–2024 · strength 1.28
  3. Ravi Kumar Thakur · 6 shared papers, 2021–2024 · strength 0.84
  4. Kamiya Mehla · 10 shared papers, 2012–2024 · strength 0.77
  5. Scott E. Mulder · 6 shared papers, 2017–2024 · strength 0.72
  6. Divya Murthy · 6 shared papers, 2017–2024 · strength 0.71
  7. Kuldeep Singh Attri · 6 shared papers, 2017–2024 · strength 0.71
  8. Venugopal Gunda · 11 shared papers, 2014–2022 · strength 0.70
  9. Ryan J. King · 8 shared papers, 2015–2024 · strength 0.69
  10. Michael Anthony Hollingsworth · 7 shared papers, 2012–2024 · strength 0.68
  11. Chunbo He · 5 shared papers, 2021–2024 · strength 0.65
  12. Aneesha Dasgupta · 7 shared papers, 2015–2024 · strength 0.63
  13. Enza Vernucci · 7 shared papers, 2015–2022 · strength 0.50
  14. Robert Powers · 7 shared papers, 2012–2024 · strength 0.50
  15. Jaime Abrego · 7 shared papers, 2015–2022 · strength 0.48
  16. Teklab Gebregiworgis · 6 shared papers, 2012–2024 · strength 0.45
  17. Sai Sundeep Kollala · 3 shared papers, 2023–2024 · strength 0.44
  18. Paul M. Grandgenett · 4 shared papers, 2017–2024 · strength 0.44
  19. Joshua J. Souchek · 5 shared papers, 2015–2024 · strength 0.42
  20. Tuo Hu · 3 shared papers, 2021–2024 · strength 0.36
  21. Vikrant Rai · 3 shared papers, 2019–2024 · strength 0.36
  22. Chun‐Hao Pan · 2 shared papers, 2022–2026 · strength 0.34
  23. Lucia Roa‐Peña · 2 shared papers, 2022–2026 · strength 0.34
  24. Luisa F. Escobar‐Hoyos · 2 shared papers, 2022–2026 · strength 0.34
  25. Kenneth Reed Shroyer · 2 shared papers, 2022–2026 · strength 0.34

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.