ResearcherGarvan Institute of Medical ResearchActive in the last 2 years
Jennifer P. Morton
Matched on ORCID iD 0000-0001-5766-9141; OpenAlex author ID A5004126873. Sources: OpenAlex.
Their work
- Papers
- 71 (first author 8, last author 5)
- Trials
- 0
- Grants
- 0
- Labs led
- 1
- Collaborators
- 257
2011: 3 papers · 2012: 1 paper · 2013: 3 papers · 2014: 2 papers · 2015: 2 papers · 2016: 4 papers · 2017: 8 papers · 2018: 6 papers · 2019: 6 papers · 2020: 4 papers · 2021: 5 papers · 2022: 5 papers · 2023: 3 papers · 2024: 7 papers · 2025: 5 papers · 2026: 7 papers
Papers 50 of 71
- Engineered cyclic peptide targeting ITGA5 disrupts tumor-stroma interaction to overcome desmoplasia and resistance in pancreatic ductal adenocarcinoma. Co-author DOI 10.1016/j.apsb.2025.10.022↗
- Comparative Analysis of Primary and Liver Fibroblasts Reveals MET as a Potent Target in Pancreatic Cancer Metastasis. Co-author DOI 10.1016/j.jcmgh.2026.101872↗
- HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. Co-author DOI 10.1038/s41388-026-03865-y↗
- βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. Co-author DOI 10.1038/s41419-026-08657-6↗
- Activation of PP2A-B56a leads to aberrant EGFR signaling and proliferative phenotypes in PDAC. Co-author DOI 10.1158/1535-7163.mct-25-0970↗
- Pulsed priming with the FAK inhibitor narmafotinib enhances both gemcitabine/Abraxane and FOLFIRINOX chemotherapy response in pancreatic cancer Co-author DOI 10.64898/2026.07.23.740234↗
- Pharmacological arginine deprivation renders pancreatic cancer cells susceptible to senolysis and inhibition of the integrated stress response Co-author DOI 10.64898/2026.08.03.740778↗
- Targeting PIKfyve-driven lipid metabolism in pancreatic cancer. Co-author DOI 10.1038/s41586-025-08917-z↗
- Tumour genotype shapes blood biomarker expression for use in pancreatic cancer detection and diagnosis Co-author DOI 10.1101/2025.08.15.670486↗
- Targeting the NPY/NPY1R signaling axis in mutant p53-dependent pancreatic cancer impairs metastasis. Co-author DOI 10.1126/sciadv.adq4416↗
- Induction of macrophage efferocytosis in pancreatic cancer via PI3Kγ inhibition and radiotherapy promotes tumour control. Co-author DOI 10.1136/gutjnl-2024-333492↗
- KRAS Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition. Co-author DOI 10.1158/0008-5472.can-23-2709↗
- Macrophage-fibroblast JAK/STAT dependent crosstalk promotes liver metastatic outgrowth in pancreatic cancer. Co-author DOI 10.1038/s41467-024-47949-3↗
- Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. Co-author DOI 10.1038/s43018-024-00731-2↗
- Author Correction: Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. Co-author DOI 10.1038/s43018-024-00751-y↗
- Temporally resolved proteomics identifies nidogen-2 as a cotarget in pancreatic cancer that modulates fibrosis and therapy response. Co-author DOI 10.1126/sciadv.adl1197↗
- Targeted irradiation in an autochthonous mouse model of pancreatic cancer. Last author DOI 10.1242/dmm.050463↗
- The preclinical gap in pancreatic cancer and radiotherapy. First author DOI 10.1242/dmm.050703↗
- Tissue-resident natural killer cells support survival in pancreatic cancer through promotion of cDC1-CD8 T activity. Co-author DOI 10.7554/elife.92672↗
- NUAK1 governs centrosome replication in pancreatic cancer via MYPT1/PP1β and GSK3β-dependent regulation of PLK4. Co-author DOI 10.1002/1878-0261.13425↗
- USP9X mediates an acute adaptive response to MAPK suppression in pancreatic cancer but creates multiple actionable therapeutic vulnerabilities. Co-author DOI 10.1016/j.xcrm.2023.101007↗
- Defining the spatial distribution of extracellular adenosine revealed a myeloid-dependent immunosuppressive microenvironment in pancreatic ductal adenocarcinom… Co-author DOI 10.1136/jitc-2022-006457↗
- A microenvironment-inspired synthetic three-dimensional model for pancreatic ductal adenocarcinoma organoids. Co-author DOI 10.1038/s41563-021-01085-1↗
- Differential integrated stress response and asparagine production drive symbiosis and therapy resistance of pancreatic adenocarcinoma cells. Co-author DOI 10.1038/s43018-022-00463-1↗
- βIII-Tubulin is a Brake on Extrinsic Cell-Death in Pancreatic Cancer Co-author DOI 10.1101/2022.09.29.510034↗
- Chemotherapy-induced infiltration of neutrophils promotes pancreatic cancer metastasis via Gas6/AXL signalling axis. Co-author DOI 10.1136/gutjnl-2021-325272↗
- Prognostic implications of microRNA-21 overexpression in pancreatic ductal adenocarcinoma: an international multicenter study of 686 patients. Co-author PMID 36628279↗
- Suppression of tumor-associated neutrophils by lorlatinib attenuates pancreatic cancer growth and improves treatment with immune checkpoint blockade. Co-author DOI 10.1038/s41467-021-23731-7↗
- New Insights Into Pancreatic Cancer: Notes from a Virtual Meeting. Co-author DOI 10.1053/j.gastro.2021.04.082↗
- Intravital imaging technology guides FAK-mediated priming in pancreatic cancer precision medicine according to Merlin status. Co-author DOI 10.1126/sciadv.abh0363↗
- Cancer-Associated Fibroblasts in Pancreatic Ductal Adenocarcinoma Determine Response to SLC7A11 Inhibition. Co-author DOI 10.1158/0008-5472.can-20-2496↗
- Heterogeneity in Pancreatic Cancer Fibroblasts-TGFβ as a Master Regulator? First author DOI 10.3390/cancers13194984↗
- Pancreatic Cancer: From Genome Discovery to PRECISION-Panc. Co-author DOI 10.1016/j.clon.2019.08.007↗
- Asymmetrically Substituted Quadruplex-Binding Naphthalene Diimide Showing Potent Activity in Pancreatic Cancer Models. Co-author DOI 10.1021/acsmedchemlett.0c00317↗
- Repression of the Type I Interferon Pathway Underlies MYC- and KRAS-Dependent Evasion of NK and B Cells in Pancreatic Ductal Adenocarcinoma. Co-author DOI 10.1158/2159-8290.cd-19-0620↗
- Environment Influences Tumor Progression and Transcriptional Subtype in a New Model of Pancreatic Cancer. First author DOI 10.1158/2159-8290.cd-20-1090↗
- The integrin αvβ6 drives pancreatic cancer through diverse mechanisms and represents an effective target for therapy. Co-author DOI 10.1002/path.5320↗
- Glutamine Anabolism Plays a Critical Role in Pancreatic Cancer by Coupling Carbon and Nitrogen Metabolism. Co-author DOI 10.1016/j.celrep.2019.09.056↗
- Macrophage-Released Pyrimidines Inhibit Gemcitabine Therapy in Pancreatic Cancer. Co-author DOI 10.1016/j.cmet.2019.02.001↗
- CAF Subpopulations: A New Reservoir of Stromal Targets in Pancreatic Cancer. Co-author DOI 10.1016/j.trecan.2019.09.010↗
- Combating pancreatic cancer with PI3K pathway inhibitors in the era of personalised medicine. Co-author DOI 10.1136/gutjnl-2018-316822↗
- Activation of PP2A and Inhibition of mTOR Synergistically Reduce MYC Signaling and Decrease Tumor Growth in Pancreatic Ductal Adenocarcinoma. Co-author DOI 10.1158/0008-5472.can-18-0717↗
- Intravital Imaging to Monitor Therapeutic Response in Moving Hypoxic Regions Resistant to PI3K Pathway Targeting in Pancreatic Cancer. Co-author DOI 10.1016/j.celrep.2018.05.038↗
- Targeting Multiple Effector Pathways in Pancreatic Ductal Adenocarcinoma with a G-Quadruplex-Binding Small Molecule. Co-author DOI 10.1021/acs.jmedchem.7b01781↗
- MiR-142-3p is downregulated in aggressive p53 mutant mouse models of pancreatic ductal adenocarcinoma by hypermethylation of its locus. First author DOI 10.1038/s41419-018-0628-4↗
- Reshaping the Tumor Stroma for Treatment of Pancreatic Cancer. Co-author DOI 10.1053/j.gastro.2017.11.280↗
- Tailored first-line and second-line CDK4-targeting treatment combinations in mouse models of pancreatic cancer. Co-author DOI 10.1136/gutjnl-2017-315144↗
- Mutant p53R270H drives altered metabolism and increased invasion in pancreatic ductal adenocarcinoma. Co-author DOI 10.1172/jci.insight.97422↗
- PTEN deficiency permits the formation of pancreatic cancer in the absence of autophagy. Co-author DOI 10.1038/cdd.2016.120↗
- SerpinB2 regulates stromal remodelling and local invasion in pancreatic cancer. Co-author DOI 10.1038/onc.2017.63↗
Closest collaborators
The 25 strongest of 257 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Owen James Sansom · 29 shared papers, 2011–2025 · strength 2.29
- Paper Targeted irradiation in an autochthonous mouse model of pancreatic cancer. DOI 10.1242/dmm.050463↗
- Paper KRAS Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic… DOI 10.1158/0008-5472.can-23-2709↗
- Paper CXCR2 inhibition in pancreatic cancer: opportunities for immunotherapy? DOI 10.2217/imt-2016-0115↗
- Paul Timpson · 12 shared papers, 2011–2026 · strength 0.94
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper Combating pancreatic cancer with PI3K pathway inhibitors in the era of personalised medicine. DOI 10.1136/gutjnl-2018-316822↗
- Paper CAF Subpopulations: A New Reservoir of Stromal Targets in Pancreatic Cancer. DOI 10.1016/j.trecan.2019.09.010↗
- Mathias Tesson · 3 shared papers, 2024–2025 · strength 0.89
- Paper The preclinical gap in pancreatic cancer and radiotherapy. DOI 10.1242/dmm.050703↗
- Paper Induction of macrophage efferocytosis in pancreatic cancer via PI3Kγ inhibition and radiotherapy promotes tumour contro… DOI 10.1136/gutjnl-2024-333492↗
- Paper Targeted irradiation in an autochthonous mouse model of pancreatic cancer. DOI 10.1242/dmm.050463↗
- Anthony James Gill · 7 shared papers, 2018–2026 · strength 0.85
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper Prognostic implications of microRNA-21 overexpression in pancreatic ductal adenocarcinoma: an international multicenter… PMID 36628279↗
- Andrew Victor Biankin · 11 shared papers, 2014–2022 · strength 0.78
- Paper Pancreatic Cancer: From Genome Discovery to PRECISION-Panc. DOI 10.1016/j.clon.2019.08.007↗
- Paper Prognostic implications of microRNA-21 overexpression in pancreatic ductal adenocarcinoma: an international multicenter… PMID 36628279↗
- Paper Repression of the Type I Interferon Pathway Underlies MYC- and KRAS-Dependent Evasion of NK and B Cells in Pancreatic D… DOI 10.1158/2159-8290.cd-19-0620↗
- David Kuang-Fu Chang · 9 shared papers, 2014–2025 · strength 0.77
- Paper KRAS Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic… DOI 10.1158/0008-5472.can-23-2709↗
- Paper Pancreatic Cancer: From Genome Discovery to PRECISION-Panc. DOI 10.1016/j.clon.2019.08.007↗
- Paper Prognostic implications of microRNA-21 overexpression in pancreatic ductal adenocarcinoma: an international multicenter… PMID 36628279↗
- Marina Pajic · 8 shared papers, 2017–2026 · strength 0.73
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper βIII-Tubulin is a Brake on Extrinsic Cell-Death in Pancreatic Cancer DOI 10.1101/2022.09.29.510034↗
- Paper Reshaping the Tumor Stroma for Treatment of Pancreatic Cancer. DOI 10.1053/j.gastro.2017.11.280↗
- Amber L. Johns · 6 shared papers, 2018–2026 · strength 0.72
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper βIII-Tubulin is a Brake on Extrinsic Cell-Death in Pancreatic Cancer DOI 10.1101/2022.09.29.510034↗
- Valeria Quaranta · 4 shared papers, 2022–2024 · strength 0.64
- Paper Macrophage-fibroblast JAK/STAT dependent crosstalk promotes liver metastatic outgrowth in pancreatic cancer. DOI 10.1038/s41467-024-47949-3↗
- Paper Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00731-2↗
- Paper Author Correction: Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00751-y↗
- Yuliana Astuti · 4 shared papers, 2022–2024 · strength 0.64
- Paper Macrophage-fibroblast JAK/STAT dependent crosstalk promotes liver metastatic outgrowth in pancreatic cancer. DOI 10.1038/s41467-024-47949-3↗
- Paper Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00731-2↗
- Paper Author Correction: Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00751-y↗
- Paula Ghaneh · 4 shared papers, 2022–2024 · strength 0.64
- Paper Macrophage-fibroblast JAK/STAT dependent crosstalk promotes liver metastatic outgrowth in pancreatic cancer. DOI 10.1038/s41467-024-47949-3↗
- Paper Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00731-2↗
- Paper Author Correction: Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00751-y↗
- Michael C. Schmid · 4 shared papers, 2022–2024 · strength 0.64
- Paper Macrophage-fibroblast JAK/STAT dependent crosstalk promotes liver metastatic outgrowth in pancreatic cancer. DOI 10.1038/s41467-024-47949-3↗
- Paper Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00731-2↗
- Paper Author Correction: Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00751-y↗
- Ainhoa Mielgo · 4 shared papers, 2022–2024 · strength 0.64
- Paper Macrophage-fibroblast JAK/STAT dependent crosstalk promotes liver metastatic outgrowth in pancreatic cancer. DOI 10.1038/s41467-024-47949-3↗
- Paper Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00731-2↗
- Paper Author Correction: Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00751-y↗
- Daniel H. Palmer · 4 shared papers, 2022–2024 · strength 0.64
- Paper Macrophage-fibroblast JAK/STAT dependent crosstalk promotes liver metastatic outgrowth in pancreatic cancer. DOI 10.1038/s41467-024-47949-3↗
- Paper Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00731-2↗
- Paper Author Correction: Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00751-y↗
- Meirion Raymant · 4 shared papers, 2022–2024 · strength 0.64
- Paper Macrophage-fibroblast JAK/STAT dependent crosstalk promotes liver metastatic outgrowth in pancreatic cancer. DOI 10.1038/s41467-024-47949-3↗
- Paper Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00731-2↗
- Paper Author Correction: Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00751-y↗
- Gaia Bellomo · 4 shared papers, 2022–2024 · strength 0.64
- Paper Macrophage-fibroblast JAK/STAT dependent crosstalk promotes liver metastatic outgrowth in pancreatic cancer. DOI 10.1038/s41467-024-47949-3↗
- Paper Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00731-2↗
- Paper Author Correction: Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00751-y↗
- Christopher Michael Halloran · 4 shared papers, 2022–2024 · strength 0.64
- Paper Macrophage-fibroblast JAK/STAT dependent crosstalk promotes liver metastatic outgrowth in pancreatic cancer. DOI 10.1038/s41467-024-47949-3↗
- Paper Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00731-2↗
- Paper Author Correction: Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis. DOI 10.1038/s43018-024-00751-y↗
- Keaton Ian Jones · 3 shared papers, 2024–2025 · strength 0.62
- Paper Induction of macrophage efferocytosis in pancreatic cancer via PI3Kγ inhibition and radiotherapy promotes tumour contro… DOI 10.1136/gutjnl-2024-333492↗
- Paper Targeted irradiation in an autochthonous mouse model of pancreatic cancer. DOI 10.1242/dmm.050463↗
- Paper Tissue-resident natural killer cells support survival in pancreatic cancer through promotion of cDC1-CD8 T activity. DOI 10.7554/elife.92672↗
- David Goldstein · 4 shared papers, 2021–2026 · strength 0.59
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper βIII-Tubulin is a Brake on Extrinsic Cell-Death in Pancreatic Cancer DOI 10.1101/2022.09.29.510034↗
- Val Gebski · 4 shared papers, 2021–2026 · strength 0.59
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper βIII-Tubulin is a Brake on Extrinsic Cell-Death in Pancreatic Cancer DOI 10.1101/2022.09.29.510034↗
- Joshua A. McCarroll · 4 shared papers, 2021–2026 · strength 0.59
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper βIII-Tubulin is a Brake on Extrinsic Cell-Death in Pancreatic Cancer DOI 10.1101/2022.09.29.510034↗
- Mert Erkan · 4 shared papers, 2021–2026 · strength 0.59
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper βIII-Tubulin is a Brake on Extrinsic Cell-Death in Pancreatic Cancer DOI 10.1101/2022.09.29.510034↗
- Koroush Shahsavar Haghighi · 4 shared papers, 2021–2026 · strength 0.59
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper βIII-Tubulin is a Brake on Extrinsic Cell-Death in Pancreatic Cancer DOI 10.1101/2022.09.29.510034↗
- Phoebe A. Phillips · 4 shared papers, 2021–2026 · strength 0.59
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper βIII-Tubulin is a Brake on Extrinsic Cell-Death in Pancreatic Cancer DOI 10.1101/2022.09.29.510034↗
- George Sharbeen · 4 shared papers, 2021–2026 · strength 0.59
- Paper HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer. DOI 10.1038/s41388-026-03865-y↗
- Paper βIII-tubulin can act as a brake on extrinsic apoptosis in pancreatic cancer. DOI 10.1038/s41419-026-08657-6↗
- Paper βIII-Tubulin is a Brake on Extrinsic Cell-Death in Pancreatic Cancer DOI 10.1101/2022.09.29.510034↗
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.