ResearcherAmsterdam University Medical CentersActive in the last 2 years
C. Arnold Spek
Matched on ORCID iD 0000-0002-2149-4068; OpenAlex author ID A5034585119. Sources: OpenAlex.
Their work
- Papers
- 22 (first author 1, last author 18)
- Trials
- 0
- Grants
- 0
- Labs led
- 3
- Collaborators
- 20
2011: 1 paper · 2012: none · 2013: 1 paper · 2014: 2 papers · 2015: 1 paper · 2016: none · 2017: 2 papers · 2018: 1 paper · 2019: none · 2020: 4 papers · 2021: 2 papers · 2022: 3 papers · 2023: 2 papers · 2024: 3 papers
Papers 22
- CAPN2-responsive mesoporous silica nanoparticles: A promising nanocarrier for targeted therapy of pancreatic cancer. Last author DOI 10.1016/j.canlet.2024.216845↗
- Identification of pancreatic cancer-specific protease substrates for protease-dependent targeted delivery. Last author DOI 10.1038/s41389-024-00542-1↗
- Hypoxia Abrogates Tumor-Suppressive Activities of C/EBPδ in Pancreatic Cancer. Last author DOI 10.3390/ijms25179449↗
- C/EBP-Family Redundancy Determines Patient Survival and Lymph Node Involvement in PDAC. Last author DOI 10.3390/ijms24021537↗
- Preclinical Assessment of ADAM9-Responsive Mesoporous Silica Nanoparticles for the Treatment of Pancreatic Cancer. Last author DOI 10.3390/ijms241310704↗
- Macrophage C/EBPδ Drives Gemcitabine, but Not 5-FU or Paclitaxel, Resistance of Pancreatic Cancer Cells in a Deoxycytidine-Dependent Manner. Co-author DOI 10.3390/biomedicines10020219↗
- C/EBPδ Suppresses Motility-Associated Gene Signatures and Reduces PDAC Cell Migration. Last author DOI 10.3390/cells11213334↗
- Mesoporous Silica Nanoparticle-Based Drug Delivery Systems for the Treatment of Pancreatic Cancer: A Systematic Literature Overview. Last author DOI 10.3390/pharmaceutics14020390↗
- Non-Tumor CCAAT/Enhancer-Binding Protein Delta Potentiates Tumor Cell Extravasation and Pancreatic Cancer Metastasis Formation. Last author DOI 10.3390/biom11081079↗
- ADAM9-Responsive Mesoporous Silica Nanoparticles for Targeted Drug Delivery in Pancreatic Cancer. Last author DOI 10.3390/cancers13133321↗
- Macrophage-secreted MMP9 induces mesenchymal transition in pancreatic cancer cells via PAR1 activation. Last author DOI 10.1007/s13402-020-00549-x↗
- Early macrophage infiltrates impair pancreatic cancer cell growth by TNF-α secretion. Last author DOI 10.1186/s12885-020-07697-1↗
- Matrix Metalloproteases in Pancreatic Ductal Adenocarcinoma: Key Drivers of Disease Progression? Last author DOI 10.3390/biology9040080↗
- CCAAT/Enhancer-Binding Protein Delta (C/EBPδ): A Previously Unrecognized Tumor Suppressor that Limits the Oncogenic Potential of Pancreatic Ductal Adenocarcino… Last author DOI 10.3390/cancers12092546↗
- PAR1 signaling on tumor cells limits tumor growth by maintaining a mesenchymal phenotype in pancreatic cancer. Last author DOI 10.18632/oncotarget.25880↗
- Association between protein C levels and mortality in patients with advanced prostate, lung and pancreatic cancer. Co-author DOI 10.1016/j.thromres.2017.03.001↗
- Dabigatran potentiates gemcitabine-induced growth inhibition of pancreatic cancer in mice. Last author DOI 10.2119/molmed.2016.00214↗
- Authors' reply-Re: Shi et al. Protease-activated receptor 2 suppresses lymphangiogenesis and subsequent lymph node metastasis in a murine pancreatic cancer mod… First author DOI 10.1002/path.4499↗
- Protease-activated receptor-1 drives pancreatic cancer progression and chemoresistance. Last author DOI 10.1002/ijc.28726↗
- Protease-activated receptor 2 suppresses lymphangiogenesis and subsequent lymph node metastasis in a murine pancreatic cancer model. Last author DOI 10.1002/path.4411↗
- Protease-activated receptor-2 induces migration of pancreatic cancer cells in an extracellular ATP-dependent manner. Last author DOI 10.1111/jth.12361↗
- mTOR inhibitor treatment of pancreatic cancer in a patient With Peutz-Jeghers syndrome. Co-author DOI 10.1200/jco.2010.32.7825↗
Closest collaborators
The 20 strongest of 20 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Maarten F. Bijlsma · 14 shared papers, 2018–2024 · strength 2.53
- Paper Identification of pancreatic cancer-specific protease substrates for protease-dependent targeted delivery. DOI 10.1038/s41389-024-00542-1↗
- Paper CAPN2-responsive mesoporous silica nanoparticles: A promising nanocarrier for targeted therapy of pancreatic cancer. DOI 10.1016/j.canlet.2024.216845↗
- Paper Hypoxia Abrogates Tumor-Suppressive Activities of C/EBPδ in Pancreatic Cancer. DOI 10.3390/ijms25179449↗
- JanWillem Duitman · 8 shared papers, 2014–2024 · strength 1.33
- Paper Macrophage C/EBPδ Drives Gemcitabine, but Not 5-FU or Paclitaxel, Resistance of Pancreatic Cancer Cells in a Deoxycytid… DOI 10.3390/biomedicines10020219↗
- Paper Hypoxia Abrogates Tumor-Suppressive Activities of C/EBPδ in Pancreatic Cancer. DOI 10.3390/ijms25179449↗
- Paper C/EBP-Family Redundancy Determines Patient Survival and Lymph Node Involvement in PDAC. DOI 10.3390/ijms24021537↗
- Etienne J. Slapak · 6 shared papers, 2020–2024 · strength 1.27
- Paper Identification of pancreatic cancer-specific protease substrates for protease-dependent targeted delivery. DOI 10.1038/s41389-024-00542-1↗
- Paper CAPN2-responsive mesoporous silica nanoparticles: A promising nanocarrier for targeted therapy of pancreatic cancer. DOI 10.1016/j.canlet.2024.216845↗
- Paper Mesoporous Silica Nanoparticle-Based Drug Delivery Systems for the Treatment of Pancreatic Cancer: A Systematic Literat… DOI 10.3390/pharmaceutics14020390↗
- Leonie Hartl · 5 shared papers, 2020–2024 · strength 0.88
- Paper Hypoxia Abrogates Tumor-Suppressive Activities of C/EBPδ in Pancreatic Cancer. DOI 10.3390/ijms25179449↗
- Paper C/EBP-Family Redundancy Determines Patient Survival and Lymph Node Involvement in PDAC. DOI 10.3390/ijms24021537↗
- Paper Non-Tumor CCAAT/Enhancer-Binding Protein Delta Potentiates Tumor Cell Extravasation and Pancreatic Cancer Metastasis Fo… DOI 10.3390/biom11081079↗
- Cansu Tekin · 4 shared papers, 2018–2020 · strength 0.52
- Paper Early macrophage infiltrates impair pancreatic cancer cell growth by TNF-α secretion. DOI 10.1186/s12885-020-07697-1↗
- Paper Matrix Metalloproteases in Pancreatic Ductal Adenocarcinoma: Key Drivers of Disease Progression? DOI 10.3390/biology9040080↗
- Paper Macrophage-secreted MMP9 induces mesenchymal transition in pancreatic cancer cells via PAR1 activation. DOI 10.1007/s13402-020-00549-x↗
- Frederike Dijk · 3 shared papers, 2020–2023 · strength 0.43
- Paper C/EBP-Family Redundancy Determines Patient Survival and Lymph Node Involvement in PDAC. DOI 10.3390/ijms24021537↗
- Paper Macrophage-secreted MMP9 induces mesenchymal transition in pancreatic cancer cells via PAR1 activation. DOI 10.1007/s13402-020-00549-x↗
- Paper CCAAT/Enhancer-Binding Protein Delta (C/EBPδ): A Previously Unrecognized Tumor Suppressor that Limits the Oncogenic Pot… DOI 10.3390/cancers12092546↗
- Kun Shi · 6 shared papers, 2013–2018 · strength 0.43
- Paper Authors' reply-Re: Shi et al. Protease-activated receptor 2 suppresses lymphangiogenesis and subsequent lymph node meta… DOI 10.1002/path.4499↗
- Paper PAR1 signaling on tumor cells limits tumor growth by maintaining a mesenchymal phenotype in pancreatic cancer. DOI 10.18632/oncotarget.25880↗
- Paper Dabigatran potentiates gemcitabine-induced growth inhibition of pancreatic cancer in mice. DOI 10.2119/molmed.2016.00214↗
- Dick J. Richel · 5 shared papers, 2011–2017 · strength 0.25
- Paper Dabigatran potentiates gemcitabine-induced growth inhibition of pancreatic cancer in mice. DOI 10.2119/molmed.2016.00214↗
- Paper Protease-activated receptor 2 suppresses lymphangiogenesis and subsequent lymph node metastasis in a murine pancreatic … DOI 10.1002/path.4411↗
- Paper Protease-activated receptor-2 induces migration of pancreatic cancer cells in an extracellular ATP-dependent manner. DOI 10.1111/jth.12361↗
- Karla C. S. Queiroz · 4 shared papers, 2011–2014 · strength 0.17
- Paper Protease-activated receptor 2 suppresses lymphangiogenesis and subsequent lymph node metastasis in a murine pancreatic … DOI 10.1002/path.4411↗
- Paper Protease-activated receptor-2 induces migration of pancreatic cancer cells in an extracellular ATP-dependent manner. DOI 10.1111/jth.12361↗
- Paper Protease-activated receptor-1 drives pancreatic cancer progression and chemoresistance. DOI 10.1002/ijc.28726↗
- Mark P.G. Dings · 1 shared paper, 2020 · strength 0.09
- Maikel Petrus Peppelenbosch · 1 shared paper, 2020 · strength 0.09
- Marc G. Besselink · 1 shared paper, 2020 · strength 0.09
- I.T. Wilts · 1 shared paper, 2017 · strength 0.08
- Pieter Willem Kamphuisen · 1 shared paper, 2017 · strength 0.08
- Harry Roger Buller · 1 shared paper, 2017 · strength 0.08
- Helene Damhofer · 1 shared paper, 2017 · strength 0.08
- Johanna W. Wilmink · 1 shared paper, 2014 · strength 0.04
- Heinz‐Josef Klümpen · 1 shared paper, 2011 · strength 0.02
- G. Johan A. Offerhaus · 1 shared paper, 2011 · strength 0.02
- Roeland F. de Wilde · 1 shared paper, 2011 · strength 0.02
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.