ResearcherChiba UniversityActive in the last 2 years
Harold L. Moses
Matched on ORCID iD 0000-0002-0116-0140; OpenAlex author ID A5045030798. Sources: OpenAlex.
Their work
- Papers
- 8 (first author 0, last author 1)
- Trials
- 0
- Grants
- 0
- Labs led
- 0
- Collaborators
- 33
2011: 1 paper · 2012: none · 2013: 2 papers · 2014: none · 2015: 1 paper · 2016: 1 paper · 2017: none · 2018: none · 2019: 1 paper · 2020: 1 paper · 2021: none · 2022: none · 2023: none · 2024: 1 paper
Papers 8
- Author Correction: Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression. Co-author DOI 10.1038/s41591-023-02694-w↗
- Soluble VCAM-1 promotes gemcitabine resistance via macrophage infiltration and predicts therapeutic response in pancreatic cancer. Co-author DOI 10.1038/s41598-020-78320-3↗
- Blocking CXCLs-CXCR2 axis in tumor-stromal interactions contributes to survival in a mouse model of pancreatic ductal adenocarcinoma through reduced cell invas… Co-author DOI 10.1038/s41389-018-0117-8↗
- Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression. Co-author DOI 10.1038/nm.4082↗
- Signal Transducer and Activator of Transcription 3, Mediated Remodeling of the Tumor Microenvironment Results in Enhanced Tumor Drug Delivery in a Mouse Model … Co-author DOI 10.1053/j.gastro.2015.07.058↗
- Therapeutic effect of c-Jun N-terminal kinase inhibition on pancreatic cancer. Co-author DOI 10.1111/cas.12080↗
- Erlotinib prolongs survival in pancreatic cancer by blocking gemcitabine-induced MAPK signals. Co-author DOI 10.1158/0008-5472.can-12-1453↗
- Inhibiting Cxcr2 disrupts tumor-stromal interactions and improves survival in a mouse model of pancreatic ductal adenocarcinoma. Last author DOI 10.1172/jci42754↗
Closest collaborators
The 25 strongest of 33 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Kazuhiko Koike · 5 shared papers, 2011–2020 · strength 0.25
- Paper Soluble VCAM-1 promotes gemcitabine resistance via macrophage infiltration and predicts therapeutic response in pancrea… DOI 10.1038/s41598-020-78320-3↗
- Paper Blocking CXCLs-CXCR2 axis in tumor-stromal interactions contributes to survival in a mouse model of pancreatic ductal a… DOI 10.1038/s41389-018-0117-8↗
- Paper Therapeutic effect of c-Jun N-terminal kinase inhibition on pancreatic cancer. DOI 10.1111/cas.12080↗
- Hideaki Ijichi · 5 shared papers, 2011–2020 · strength 0.25
- Paper Soluble VCAM-1 promotes gemcitabine resistance via macrophage infiltration and predicts therapeutic response in pancrea… DOI 10.1038/s41598-020-78320-3↗
- Paper Blocking CXCLs-CXCR2 axis in tumor-stromal interactions contributes to survival in a mouse model of pancreatic ductal a… DOI 10.1038/s41389-018-0117-8↗
- Paper Therapeutic effect of c-Jun N-terminal kinase inhibition on pancreatic cancer. DOI 10.1111/cas.12080↗
- Koji Miyabayashi · 4 shared papers, 2011–2020 · strength 0.22
- Paper Soluble VCAM-1 promotes gemcitabine resistance via macrophage infiltration and predicts therapeutic response in pancrea… DOI 10.1038/s41598-020-78320-3↗
- Paper Blocking CXCLs-CXCR2 axis in tumor-stromal interactions contributes to survival in a mouse model of pancreatic ductal a… DOI 10.1038/s41389-018-0117-8↗
- Paper Erlotinib prolongs survival in pancreatic cancer by blocking gemcitabine-induced MAPK signals. DOI 10.1158/0008-5472.can-12-1453↗
- Alex Barrett · 2 shared papers, 2016–2024 · strength 0.20
- Paper Author Correction: Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and … DOI 10.1038/s41591-023-02694-w↗
- Paper Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression. DOI 10.1038/nm.4082↗
- Grace Kim · 2 shared papers, 2016–2024 · strength 0.20
- Paper Author Correction: Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and … DOI 10.1038/s41591-023-02694-w↗
- Paper Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression. DOI 10.1038/nm.4082↗
- Hanane Laklai · 2 shared papers, 2016–2024 · strength 0.20
- Paper Author Correction: Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and … DOI 10.1038/s41591-023-02694-w↗
- Paper Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression. DOI 10.1038/nm.4082↗
- Nilotpal Roy · 2 shared papers, 2016–2024 · strength 0.20
- Paper Author Correction: Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and … DOI 10.1038/s41591-023-02694-w↗
- Paper Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression. DOI 10.1038/nm.4082↗
- Matthias Hebrok · 2 shared papers, 2016–2024 · strength 0.20
- Paper Author Correction: Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and … DOI 10.1038/s41591-023-02694-w↗
- Paper Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression. DOI 10.1038/nm.4082↗
- Laura DeLong Wood · 2 shared papers, 2016–2024 · strength 0.20
- Paper Author Correction: Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and … DOI 10.1038/s41591-023-02694-w↗
- Paper Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression. DOI 10.1038/nm.4082↗
- Eric Andrew Collisson · 2 shared papers, 2016–2024 · strength 0.20
- Paper Author Correction: Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and … DOI 10.1038/s41591-023-02694-w↗
- Paper Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression. DOI 10.1038/nm.4082↗
- Raghu Kalluri · 2 shared papers, 2016–2024 · strength 0.20
- Paper Author Correction: Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and … DOI 10.1038/s41591-023-02694-w↗
- Paper Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression. DOI 10.1038/nm.4082↗
- Valerie Marie Weaver · 2 shared papers, 2016–2024 · strength 0.20
- Paper Author Correction: Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and … DOI 10.1038/s41591-023-02694-w↗
- Paper Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression. DOI 10.1038/nm.4082↗
- Julia Sidenius Johansen · 2 shared papers, 2016–2024 · strength 0.20
- Paper Author Correction: Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and … DOI 10.1038/s41591-023-02694-w↗
- Paper Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression. DOI 10.1038/nm.4082↗
- Christine A. Iacobuzio–Donahue · 2 shared papers, 2016–2024 · strength 0.20
- Paper Author Correction: Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and … DOI 10.1038/s41591-023-02694-w↗
- Paper Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression. DOI 10.1038/nm.4082↗
- Kirk Charles Hansen · 2 shared papers, 2016–2024 · strength 0.20
- Paper Author Correction: Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and … DOI 10.1038/s41591-023-02694-w↗
- Paper Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression. DOI 10.1038/nm.4082↗
- Ryota Takahashi · 3 shared papers, 2013–2020 · strength 0.20
- Paper Soluble VCAM-1 promotes gemcitabine resistance via macrophage infiltration and predicts therapeutic response in pancrea… DOI 10.1038/s41598-020-78320-3↗
- Paper Blocking CXCLs-CXCR2 axis in tumor-stromal interactions contributes to survival in a mouse model of pancreatic ductal a… DOI 10.1038/s41389-018-0117-8↗
- Paper Therapeutic effect of c-Jun N-terminal kinase inhibition on pancreatic cancer. DOI 10.1111/cas.12080↗
- Hiroyuki Isayama · 3 shared papers, 2013–2020 · strength 0.20
- Paper Soluble VCAM-1 promotes gemcitabine resistance via macrophage infiltration and predicts therapeutic response in pancrea… DOI 10.1038/s41598-020-78320-3↗
- Paper Blocking CXCLs-CXCR2 axis in tumor-stromal interactions contributes to survival in a mouse model of pancreatic ductal a… DOI 10.1038/s41389-018-0117-8↗
- Paper Erlotinib prolongs survival in pancreatic cancer by blocking gemcitabine-induced MAPK signals. DOI 10.1158/0008-5472.can-12-1453↗
- Makoto Sano · 2 shared papers, 2019–2020 · strength 0.17
- Paper Soluble VCAM-1 promotes gemcitabine resistance via macrophage infiltration and predicts therapeutic response in pancrea… DOI 10.1038/s41598-020-78320-3↗
- Paper Blocking CXCLs-CXCR2 axis in tumor-stromal interactions contributes to survival in a mouse model of pancreatic ductal a… DOI 10.1038/s41389-018-0117-8↗
- Dai Mohri · 3 shared papers, 2011–2020 · strength 0.14
- Paper Soluble VCAM-1 promotes gemcitabine resistance via macrophage infiltration and predicts therapeutic response in pancrea… DOI 10.1038/s41598-020-78320-3↗
- Paper Erlotinib prolongs survival in pancreatic cancer by blocking gemcitabine-induced MAPK signals. DOI 10.1158/0008-5472.can-12-1453↗
- Paper Inhibiting Cxcr2 disrupts tumor-stromal interactions and improves survival in a mouse model of pancreatic ductal adenoc… DOI 10.1172/jci42754↗
- Keisuke Yamamoto · 2 shared papers, 2013–2020 · strength 0.12
- Yousuke Nakai · 2 shared papers, 2013–2020 · strength 0.12
- Gen Kimura · 1 shared paper, 2020 · strength 0.09
- Tomoharu Yamada · 1 shared paper, 2019 · strength 0.08
- Hiroyuki Kato · 1 shared paper, 2019 · strength 0.08
- Shin Maeda · 2 shared papers, 2011–2013 · strength 0.05
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.