ResearcherTaipei Medical UniversityActive in the last 2 years
Yen‐Hao Su
Matched on ORCID iD 0000-0001-8288-3772; OpenAlex author ID A5009800148. Sources: OpenAlex.
Their work
- Papers
- 10 (first author 2, last author 2)
- Trials
- 0
- Grants
- 0
- Labs led
- 1
- Collaborators
- 10
2021: 2 papers · 2022: 2 papers · 2023: none · 2024: 3 papers · 2025: 2 papers · 2026: 1 paper
Papers 10
- Adenylosuccinate lyase in pancreatic ductal adenocarcinoma chemoresistance: from purine metabolism to metabolic vulnerability. Co-author DOI 10.20517/cdr.2026.58↗
- Author Correction: Crosstalk between FTH1 and PYCR1 dysregulates proline metabolism and mediates cell growth in KRAS-mutant pancreatic cancer cells First author DOI 10.1038/s12276-025-01437-w↗
- FOXO3a/miR-4259-driven LDHA expression as a key mechanism of gemcitabine sensitivity in pancreatic ductal adenocarcinoma. Last author DOI 10.1186/s40170-025-00377-3↗
- Nrf2-mediated adenylosuccinate lyase promotes resistance to gemcitabine in pancreatic ductal adenocarcinoma cells through ferroptosis escape. Last author DOI 10.1002/jcp.31416↗
- Crosstalk between FTH1 and PYCR1 dysregulates proline metabolism and mediates cell growth in KRAS-mutant pancreatic cancer cells. First author DOI 10.1038/s12276-024-01300-4↗
- The Role of Dicer Phosphorylation in Gemcitabine Resistance of Pancreatic Cancer. Co-author DOI 10.3390/ijms252111797↗
- Organic cation transporter 2 activation enhances sensitivity to oxaliplatin in human pancreatic ductal adenocarcinoma. Co-author DOI 10.1016/j.biopha.2022.113520↗
- Phosphomimetic Dicer S1016E triggers a switch to glutamine metabolism in gemcitabine-resistant pancreatic cancer. Co-author DOI 10.1016/j.molmet.2022.101576↗
- ERK-mediated transcriptional activation of Dicer is involved in gemcitabine resistance of pancreatic cancer. Co-author DOI 10.1002/jcp.30159↗
- A case-control study in Taiwanese cohort and meta-analysis of serum ferritin in pancreatic cancer. Co-author DOI 10.1038/s41598-021-00650-7↗
Closest collaborators
The 10 strongest of 10 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Ching‐Feng Chiu · 9 shared papers, 2021–2025 · strength 1.63
- Paper The Role of Dicer Phosphorylation in Gemcitabine Resistance of Pancreatic Cancer. DOI 10.3390/ijms252111797↗
- Paper FOXO3a/miR-4259-driven LDHA expression as a key mechanism of gemcitabine sensitivity in pancreatic ductal adenocarcinom… DOI 10.1186/s40170-025-00377-3↗
- Paper Author Correction: Crosstalk between FTH1 and PYCR1 dysregulates proline metabolism and mediates cell growth in KRAS-mu… DOI 10.1038/s12276-025-01437-w↗
- Tung‐Wei Hsu · 5 shared papers, 2021–2026 · strength 1.04
- Paper Adenylosuccinate lyase in pancreatic ductal adenocarcinoma chemoresistance: from purine metabolism to metabolic vulnera… DOI 10.20517/cdr.2026.58↗
- Paper FOXO3a/miR-4259-driven LDHA expression as a key mechanism of gemcitabine sensitivity in pancreatic ductal adenocarcinom… DOI 10.1186/s40170-025-00377-3↗
- Paper Nrf2-mediated adenylosuccinate lyase promotes resistance to gemcitabine in pancreatic ductal adenocarcinoma cells throu… DOI 10.1002/jcp.31416↗
- Ji Min Park · 5 shared papers, 2021–2025 · strength 0.81
- Paper Author Correction: Crosstalk between FTH1 and PYCR1 dysregulates proline metabolism and mediates cell growth in KRAS-mu… DOI 10.1038/s12276-025-01437-w↗
- Paper Crosstalk between FTH1 and PYCR1 dysregulates proline metabolism and mediates cell growth in KRAS-mutant pancreatic can… DOI 10.1038/s12276-024-01300-4↗
- Paper Phosphomimetic Dicer S1016E triggers a switch to glutamine metabolism in gemcitabine-resistant pancreatic cancer. DOI 10.1016/j.molmet.2022.101576↗
- Shih‐Yi Huang · 4 shared papers, 2021–2025 · strength 0.79
- Paper The Role of Dicer Phosphorylation in Gemcitabine Resistance of Pancreatic Cancer. DOI 10.3390/ijms252111797↗
- Paper Author Correction: Crosstalk between FTH1 and PYCR1 dysregulates proline metabolism and mediates cell growth in KRAS-mu… DOI 10.1038/s12276-025-01437-w↗
- Paper Crosstalk between FTH1 and PYCR1 dysregulates proline metabolism and mediates cell growth in KRAS-mutant pancreatic can… DOI 10.1038/s12276-024-01300-4↗
- Tze‐Sing Huang · 2 shared papers, 2024–2025 · strength 0.39
- Paper Author Correction: Crosstalk between FTH1 and PYCR1 dysregulates proline metabolism and mediates cell growth in KRAS-mu… DOI 10.1038/s12276-025-01437-w↗
- Paper Crosstalk between FTH1 and PYCR1 dysregulates proline metabolism and mediates cell growth in KRAS-mutant pancreatic can… DOI 10.1038/s12276-024-01300-4↗
- Chi-Shuan Fan · 2 shared papers, 2024–2025 · strength 0.39
- Paper Author Correction: Crosstalk between FTH1 and PYCR1 dysregulates proline metabolism and mediates cell growth in KRAS-mu… DOI 10.1038/s12276-025-01437-w↗
- Paper Crosstalk between FTH1 and PYCR1 dysregulates proline metabolism and mediates cell growth in KRAS-mutant pancreatic can… DOI 10.1038/s12276-024-01300-4↗
- Wun‐Shaing Wayne Chang · 2 shared papers, 2024–2025 · strength 0.39
- Paper Author Correction: Crosstalk between FTH1 and PYCR1 dysregulates proline metabolism and mediates cell growth in KRAS-mu… DOI 10.1038/s12276-025-01437-w↗
- Paper Crosstalk between FTH1 and PYCR1 dysregulates proline metabolism and mediates cell growth in KRAS-mutant pancreatic can… DOI 10.1038/s12276-024-01300-4↗
- Hsin-An Chen · 1 shared paper, 2026 · strength 0.33
- Yan‐Shen Shan · 1 shared paper, 2022 · strength 0.15
- Chi‐Fen Chang · 1 shared paper, 2022 · 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.