ResearcherUniversity of MichiganNo recent work listed
Yaqing Zhang
Matched on ORCID iD 0009-0000-6019-0844; OpenAlex author ID A5115593514. Sources: OpenAlex.
Their work
- Papers
- 21 (first author 2, last author 1)
- Trials
- 0
- Grants
- 0
- Labs led
- 0
- Collaborators
- 69
2012: 2 papers · 2013: 1 paper · 2014: 2 papers · 2015: 2 papers · 2016: none · 2017: 1 paper · 2018: none · 2019: 2 papers · 2020: 1 paper · 2021: 5 papers · 2022: 3 papers · 2023: 2 papers
Papers 21
- Tyrosine Sulfation: A New Player and Potential Target in Pancreatic Cancer. Co-author DOI 10.1016/j.jcmgh.2023.06.007↗
- Arginase 1 is a key driver of immune suppression in pancreatic cancer. Co-author DOI 10.7554/elife.80721↗
- Combinatorial Gli activity directs immune infiltration and tumor growth in pancreatic cancer. Co-author DOI 10.1371/journal.pgen.1010315↗
- Metabolic requirement for GOT2 in pancreatic cancer depends on environmental context. Co-author DOI 10.7554/elife.73245↗
- Multiomic characterization of pancreatic cancer-associated macrophage polarization reveals deregulated metabolic programs driven by the GM-CSF-PI3K pathway. Co-author DOI 10.7554/elife.73796↗
- The Gustatory Sensory G-Protein GNAT3 Suppresses Pancreatic Cancer Progression in Mice. Co-author DOI 10.1016/j.jcmgh.2020.08.011↗
- Apolipoprotein E Promotes Immune Suppression in Pancreatic Cancer through NF-κB-Mediated Production of CXCL1. Co-author DOI 10.1158/0008-5472.can-20-3929↗
- Inhibition of Hedgehog Signaling Alters Fibroblast Composition in Pancreatic Cancer. Co-author DOI 10.1158/1078-0432.ccr-20-3715↗
- Pancreatic cancer is marked by complement-high blood monocytes and tumor-associated macrophages. Co-author DOI 10.26508/lsa.202000935↗
- Therapeutic Potential of Targeting Stromal Crosstalk-Mediated Immune Suppression in Pancreatic Cancer. Last author DOI 10.3389/fonc.2021.682217↗
- Discoidin Domain Receptor 1 (DDR1) Is Necessary for Tissue Homeostasis in Pancreatic Injury and Pathogenesis of Pancreatic Ductal Adenocarcinoma. Co-author DOI 10.1016/j.ajpath.2020.03.020↗
- Macrophage-Released Pyrimidines Inhibit Gemcitabine Therapy in Pancreatic Cancer. Co-author DOI 10.1016/j.cmet.2019.02.001↗
- Epithelial-Stromal Interactions in Pancreatic Cancer. Co-author DOI 10.1146/annurev-physiol-020518-114515↗
- Myeloid cells are required for PD-1/PD-L1 checkpoint activation and the establishment of an immunosuppressive environment in pancreatic cancer. Co-author DOI 10.1136/gutjnl-2016-312078↗
- Bmi1 is required for the initiation of pancreatic cancer through an Ink4a-independent mechanism. Co-author DOI 10.1093/carcin/bgv058↗
- CD44 regulates pancreatic cancer invasion through MT1-MMP. First author DOI 10.1158/1541-7786.mcr-14-0076↗
- Dosage-dependent regulation of pancreatic cancer growth and angiogenesis by hedgehog signaling. First author DOI 10.1016/j.celrep.2014.09.010↗
- Immune cells in pancreatic cancer: Joining the dark side. Co-author DOI 10.4161/onci.29125↗
- Interleukin-6 is required for pancreatic cancer progression by promoting MAPK signaling activation and oxidative stress resistance. Co-author DOI 10.1158/0008-5472.can-13-1558-t↗
- Oncogenic Kras is required for both the initiation and maintenance of pancreatic cancer in mice. Co-author DOI 10.1172/jci59227↗
- Metastatic pancreatic cancer is dependent on oncogenic Kras in mice. Co-author DOI 10.1371/journal.pone.0049707↗
Closest collaborators
The 25 strongest of 69 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Marina Pasca di Magliano · 21 shared papers, 2012–2023 · strength 2.23
- Paper Tyrosine Sulfation: A New Player and Potential Target in Pancreatic Cancer. DOI 10.1016/j.jcmgh.2023.06.007↗
- Paper Therapeutic Potential of Targeting Stromal Crosstalk-Mediated Immune Suppression in Pancreatic Cancer. DOI 10.3389/fonc.2021.682217↗
- Paper Epithelial-Stromal Interactions in Pancreatic Cancer. DOI 10.1146/annurev-physiol-020518-114515↗
- Howard C. Crawford · 10 shared papers, 2019–2023 · strength 1.11
- Paper Epithelial-Stromal Interactions in Pancreatic Cancer. DOI 10.1146/annurev-physiol-020518-114515↗
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Paper Combinatorial Gli activity directs immune infiltration and tumor growth in pancreatic cancer. DOI 10.1371/journal.pgen.1010315↗
- Nina G. Steele · 7 shared papers, 2021–2022 · strength 0.76
- Paper Multiomic characterization of pancreatic cancer-associated macrophage polarization reveals deregulated metabolic progra… DOI 10.7554/elife.73796↗
- Paper Combinatorial Gli activity directs immune infiltration and tumor growth in pancreatic cancer. DOI 10.1371/journal.pgen.1010315↗
- Paper The Gustatory Sensory G-Protein GNAT3 Suppresses Pancreatic Cancer Progression in Mice. DOI 10.1016/j.jcmgh.2020.08.011↗
- Costas Andreas Lyssiotis · 7 shared papers, 2019–2023 · strength 0.73
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Paper Multiomic characterization of pancreatic cancer-associated macrophage polarization reveals deregulated metabolic progra… DOI 10.7554/elife.73796↗
- Paper Apolipoprotein E Promotes Immune Suppression in Pancreatic Cancer through NF-κB-Mediated Production of CXCL1. DOI 10.1158/0008-5472.can-20-3929↗
- Filip Bednar · 9 shared papers, 2012–2023 · strength 0.69
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Paper Combinatorial Gli activity directs immune infiltration and tumor growth in pancreatic cancer. DOI 10.1371/journal.pgen.1010315↗
- Paper The Gustatory Sensory G-Protein GNAT3 Suppresses Pancreatic Cancer Progression in Mice. DOI 10.1016/j.jcmgh.2020.08.011↗
- Zeribe C. Nwosu · 6 shared papers, 2021–2023 · strength 0.65
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Paper Combinatorial Gli activity directs immune infiltration and tumor growth in pancreatic cancer. DOI 10.1371/journal.pgen.1010315↗
- Paper Apolipoprotein E Promotes Immune Suppression in Pancreatic Cancer through NF-κB-Mediated Production of CXCL1. DOI 10.1158/0008-5472.can-20-3929↗
- Samantha B. Kemp · 6 shared papers, 2019–2022 · strength 0.57
- Paper The Gustatory Sensory G-Protein GNAT3 Suppresses Pancreatic Cancer Progression in Mice. DOI 10.1016/j.jcmgh.2020.08.011↗
- Paper Apolipoprotein E Promotes Immune Suppression in Pancreatic Cancer through NF-κB-Mediated Production of CXCL1. DOI 10.1158/0008-5472.can-20-3929↗
- Paper Metabolic requirement for GOT2 in pancreatic cancer depends on environmental context. DOI 10.7554/elife.73245↗
- Christopher J. Halbrook · 5 shared papers, 2019–2023 · strength 0.53
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Paper Multiomic characterization of pancreatic cancer-associated macrophage polarization reveals deregulated metabolic progra… DOI 10.7554/elife.73796↗
- Paper Metabolic requirement for GOT2 in pancreatic cancer depends on environmental context. DOI 10.7554/elife.73245↗
- Eileen S. Carpenter · 4 shared papers, 2021–2023 · strength 0.42
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Paper Apolipoprotein E Promotes Immune Suppression in Pancreatic Cancer through NF-κB-Mediated Production of CXCL1. DOI 10.1158/0008-5472.can-20-3929↗
- Paper Pancreatic cancer is marked by complement-high blood monocytes and tumor-associated macrophages. DOI 10.26508/lsa.202000935↗
- Daniel James Salas-Escabillas · 3 shared papers, 2021–2023 · strength 0.38
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Paper Combinatorial Gli activity directs immune infiltration and tumor growth in pancreatic cancer. DOI 10.1371/journal.pgen.1010315↗
- Paper The Gustatory Sensory G-Protein GNAT3 Suppresses Pancreatic Cancer Progression in Mice. DOI 10.1016/j.jcmgh.2020.08.011↗
- Rosa Elena Menjivar · 3 shared papers, 2021–2023 · strength 0.37
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Paper Combinatorial Gli activity directs immune infiltration and tumor growth in pancreatic cancer. DOI 10.1371/journal.pgen.1010315↗
- Paper Apolipoprotein E Promotes Immune Suppression in Pancreatic Cancer through NF-κB-Mediated Production of CXCL1. DOI 10.1158/0008-5472.can-20-3929↗
- Wenting Du · 2 shared papers, 2021–2023 · strength 0.36
- Katelyn L. Donahue · 3 shared papers, 2021–2023 · strength 0.34
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Paper Apolipoprotein E Promotes Immune Suppression in Pancreatic Cancer through NF-κB-Mediated Production of CXCL1. DOI 10.1158/0008-5472.can-20-3929↗
- Paper Pancreatic cancer is marked by complement-high blood monocytes and tumor-associated macrophages. DOI 10.26508/lsa.202000935↗
- Li Zhang · 3 shared papers, 2019–2022 · strength 0.31
- Paper Multiomic characterization of pancreatic cancer-associated macrophage polarization reveals deregulated metabolic progra… DOI 10.7554/elife.73796↗
- Paper Metabolic requirement for GOT2 in pancreatic cancer depends on environmental context. DOI 10.7554/elife.73245↗
- Paper Macrophage-Released Pyrimidines Inhibit Gemcitabine Therapy in Pancreatic Cancer. DOI 10.1016/j.cmet.2019.02.001↗
- Megan T. Hoffman · 3 shared papers, 2021–2022 · strength 0.30
- Paper The Gustatory Sensory G-Protein GNAT3 Suppresses Pancreatic Cancer Progression in Mice. DOI 10.1016/j.jcmgh.2020.08.011↗
- Paper Metabolic requirement for GOT2 in pancreatic cancer depends on environmental context. DOI 10.7554/elife.73245↗
- Paper Inhibition of Hedgehog Signaling Alters Fibroblast Composition in Pancreatic Cancer. DOI 10.1158/1078-0432.ccr-20-3715↗
- Benjamin Allen · 3 shared papers, 2014–2022 · strength 0.26
- Paper Combinatorial Gli activity directs immune infiltration and tumor growth in pancreatic cancer. DOI 10.1371/journal.pgen.1010315↗
- Paper Inhibition of Hedgehog Signaling Alters Fibroblast Composition in Pancreatic Cancer. DOI 10.1158/1078-0432.ccr-20-3715↗
- Paper Dosage-dependent regulation of pancreatic cancer growth and angiogenesis by hedgehog signaling. DOI 10.1016/j.celrep.2014.09.010↗
- Timothy L. Frankel · 3 shared papers, 2019–2021 · strength 0.25
- Paper Pancreatic cancer is marked by complement-high blood monocytes and tumor-associated macrophages. DOI 10.26508/lsa.202000935↗
- Paper Inhibition of Hedgehog Signaling Alters Fibroblast Composition in Pancreatic Cancer. DOI 10.1158/1078-0432.ccr-20-3715↗
- Paper Macrophage-Released Pyrimidines Inhibit Gemcitabine Therapy in Pancreatic Cancer. DOI 10.1016/j.cmet.2019.02.001↗
- Meredith A. Collins · 5 shared papers, 2012–2015 · strength 0.19
- Paper CD44 regulates pancreatic cancer invasion through MT1-MMP. DOI 10.1158/1541-7786.mcr-14-0076↗
- Paper Bmi1 is required for the initiation of pancreatic cancer through an Ink4a-independent mechanism. DOI 10.1093/carcin/bgv058↗
- Paper Interleukin-6 is required for pancreatic cancer progression by promoting MAPK signaling activation and oxidative stress… DOI 10.1158/0008-5472.can-13-1558-t↗
- Kenneth P. Olive · 2 shared papers, 2015–2022 · strength 0.16
- Diane M. Simeone · 3 shared papers, 2015–2017 · strength 0.16
- Paper Myeloid cells are required for PD-1/PD-L1 checkpoint activation and the establishment of an immunosuppressive environme… DOI 10.1136/gutjnl-2016-312078↗
- Paper CD44 regulates pancreatic cancer invasion through MT1-MMP. DOI 10.1158/1541-7786.mcr-14-0076↗
- Paper Bmi1 is required for the initiation of pancreatic cancer through an Ink4a-independent mechanism. DOI 10.1093/carcin/bgv058↗
- Padma Kadiyala · 1 shared paper, 2023 · strength 0.14
- Allison Bischoff · 1 shared paper, 2023 · strength 0.14
- Seth Boyer · 1 shared paper, 2022 · strength 0.13
- Matthew H. Ward · 1 shared paper, 2022 · strength 0.13
- Rima Singh · 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.