ResearcherHouston MethodistActive in the last 2 years
Bülent Özpolat
Matched on ORCID iD 0000-0001-8602-7463; OpenAlex author ID A5040193650; NIH RePORTER profile ID 9150330. Sources: OpenAlex.
Their work
- Papers
- 9 (first author 1, last author 7)
- Trials
- 0
- Grants
- 1
- Labs led
- 1
- Collaborators
- 16
2014: 4 papers · 2015: none · 2016: 1 grant · 2017: 1 paper · 2018: 1 paper · 2019: 1 paper · 2020: 1 paper · 2021: none · 2022: none · 2023: none · 2024: none · 2025: 1 paper
Papers 9
- eEF2K is a poor prognostic factor and novel molecular target in pancreatic cancer: regulating tumor growth and progression via the tumor microenvironment. Last author DOI 10.1038/s41419-025-07803-w↗
- Delivery of Small Molecule EF2 Kinase Inhibitor for Breast and Pancreatic Cancer Cells Using Hyaluronic Acid Based Nanogels. Last author DOI 10.1007/s11095-020-2774-5↗
- MicroRNA-based Targeted Therapeutics in Pancreatic Cancer. First author DOI 10.21873/anticanres.13144↗
- Targeted Therapies for Pancreatic Cancer and Hurdles Ahead. Last author DOI 10.21873/anticanres.13026↗
- Pancreatic Cancer Stem Cells and Therapeutic Approaches. Last author DOI 10.21873/anticanres.11628↗
- Targeting elongation factor-2 kinase (eEF-2K) induces apoptosis in human pancreatic cancer cells. Last author DOI 10.1007/s10495-013-0927-2↗
- Elongation factor-2 kinase regulates TG2/β1 integrin/Src/uPAR pathway and epithelial-mesenchymal transition mediating pancreatic cancer cells invasion. Last author DOI 10.1111/jcmm.12361↗
- Bisphosphonates inhibit stellate cell activity and enhance antitumor effects of nanoparticle albumin-bound paclitaxel in pancreatic ductal adenocarcinoma. Co-author DOI 10.1158/1535-7163.mct-14-0028↗
- Down-regulation of 5-HT1B and 5-HT1D receptors inhibits proliferation, clonogenicity and invasion of human pancreatic cancer cells. Last author DOI 10.1371/journal.pone.0105245↗
Grants 1
Closest collaborators
The 16 strongest of 16 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Ahmed Amine Ashour · 4 shared papers, 2014–2025 · strength 0.40
- Paper eEF2K is a poor prognostic factor and novel molecular target in pancreatic cancer: regulating tumor growth and progress… DOI 10.1038/s41419-025-07803-w↗
- Paper Down-regulation of 5-HT1B and 5-HT1D receptors inhibits proliferation, clonogenicity and invasion of human pancreatic c… DOI 10.1371/journal.pone.0105245↗
- Paper Targeting elongation factor-2 kinase (eEF-2K) induces apoptosis in human pancreatic cancer cells. DOI 10.1007/s10495-013-0927-2↗
- Nilgün Gürbüz · 3 shared papers, 2014–2019 · strength 0.31
- Paper MicroRNA-based Targeted Therapeutics in Pancreatic Cancer. DOI 10.21873/anticanres.13144↗
- Paper Down-regulation of 5-HT1B and 5-HT1D receptors inhibits proliferation, clonogenicity and invasion of human pancreatic c… DOI 10.1371/journal.pone.0105245↗
- Paper Elongation factor-2 kinase regulates TG2/β1 integrin/Src/uPAR pathway and epithelial-mesenchymal transition mediating p… DOI 10.1111/jcmm.12361↗
- Didem Karakaş · 1 shared paper, 2025 · strength 0.24
- Engı̇n Ulukaya · 1 shared paper, 2025 · strength 0.24
- Gabriel Lopez-Berestein · 1 shared paper, 1 shared grant, 2014–2016 · strength 0.23
- Anirban Maitra · 1 shared grant, 2016 · strength 0.20
- Ferah Cömert Önder · 1 shared paper, 2020 · strength 0.15
- Minela Aslan · 1 shared paper, 2018 · strength 0.12
- Gülinnaz Ercan · 1 shared paper, 2017 · strength 0.12
- Rosa F. Hwang · 1 shared paper, 2014 · strength 0.03
- Thiruvengadam Arumugam · 1 shared paper, 2014 · strength 0.03
- Bincy Philip · 1 shared paper, 2014 · strength 0.03
- Huamin Wang · 1 shared paper, 2014 · strength 0.03
- Vianey González-Villasana · 1 shared paper, 2014 · strength 0.03
- Zobeida Cruz‐Monserrate · 1 shared paper, 2014 · strength 0.03
- Craig D. Logsdon · 1 shared paper, 2014 · strength 0.03
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.