ResearcherNebraska Medical CenterActive in the last 2 years
Kamiya Mehla
Matched on ORCID iD 0000-0001-5875-1868; OpenAlex author ID A5060280196; NIH RePORTER profile ID 12072158. Sources: OpenAlex.
Their work
- Papers
- 23 (first author 2, last author 5)
- Trials
- 0
- Grants
- 2
- Labs led
- 2
- Collaborators
- 69
2012: 3 papers · 2013: none · 2014: 2 papers · 2015: 1 paper · 2016: none · 2017: 1 paper · 2018: 1 paper · 2019: 2 papers · 2020: 3 papers · 2021: 3 papers · 2022: none · 2023: none · 2024: 4 papers · 2025: 1 paper · 2026: 2 papers, 2 grants
Papers 23
- KRAS Signaling Inhibition Induces a Targetable Metabolic Dependency on Lipophagy-Dependent Fatty Acid Oxidation in Pancreatic Cancer. Co-author DOI 10.1158/0008-5472.can-24-1984↗
- Systemic immunosuppression limits NK cell therapy efficacy in pancreatic cancer. Last author DOI 10.1186/s12943-025-02340-8↗
- Tumor-stromal metabolic crosstalk in pancreatic cancer. Co-author DOI 10.1016/j.tcb.2025.04.007↗
- Single-cell RNA-sequencing of human spleens reveals an IDO-1+ tolerogenic dendritic cell subset in pancreatic cancer patients that is absent in normal individu… Co-author DOI 10.1016/j.canlet.2024.217321↗
- Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism via the ACSS2-SP1-SAT1 axis. Co-author DOI 10.1038/s41556-024-01372-4↗
- Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism via the ACSS2-SP1-SAT1 … Co-author DOI 10.1038/s41556-024-01417-8↗
- The MUC1-HIF-1α signaling axis regulates pancreatic cancer pathogenesis through polyamine metabolism remodeling. Co-author DOI 10.1073/pnas.2315509121↗
- Metabolic Rewiring by Loss of Sirt5 Promotes Kras-Induced Pancreatic Cancer Progression. Co-author DOI 10.1053/j.gastro.2021.06.045↗
- IgE-Based Therapeutic Combination Enhances Antitumor Response in Preclinical Models of Pancreatic Cancer. Last author DOI 10.1158/1535-7163.mct-21-0368↗
- Heme Oxygenase-1 Inhibition Potentiates the Effects of Nab-Paclitaxel-Gemcitabine and Modulates the Tumor Microenvironment in Pancreatic Ductal Adenocarcinoma. Co-author DOI 10.3390/cancers13092264↗
- Local and systemic immunosuppression in pancreatic cancer: Targeting the stalwarts in tumor's arsenal. Last author DOI 10.1016/j.bbcan.2020.188387↗
- Macrophages potentiate STAT3 signaling in skeletal muscles and regulate pancreatic cancer cachexia. Last author DOI 10.1016/j.canlet.2020.04.017↗
- Metabolic Subtyping for Novel Personalized Therapies Against Pancreatic Cancer. Co-author DOI 10.1158/1078-0432.ccr-19-2926↗
- Inhibition of geranylgeranyl diphosphate synthase is a novel therapeutic strategy for pancreatic ductal adenocarcinoma. Co-author DOI 10.1038/s41388-019-0794-6↗
- A Polymeric Nanogel-Based Treatment Regimen for Enhanced Efficacy and Sequential Administration of Synergistic Drug Combination in Pancreatic Cancer. Co-author DOI 10.1124/jpet.118.255372↗
- Evaluation of Macrophage Polarization in Pancreatic Cancer Microenvironment Under Hypoxia. First author DOI 10.1007/978-1-4939-7665-2_23↗
- MUC1 and HIF-1alpha Signaling Crosstalk Induces Anabolic Glucose Metabolism to Impart Gemcitabine Resistance to Pancreatic Cancer. Co-author DOI 10.1016/j.ccell.2017.06.004↗
- Silibinin-mediated metabolic reprogramming attenuates pancreatic cancer-induced cachexia and tumor growth. Co-author DOI 10.18632/oncotarget.5843↗
- Structure and function of human DnaJ homologue subfamily a member 1 (DNAJA1) and its relationship to pancreatic cancer. First author DOI 10.1021/bi401329a↗
- Metabolic reprogramming induced by ketone bodies diminishes pancreatic cancer cachexia. Co-author DOI 10.1186/2049-3002-2-18↗
- MicroRNAs in pancreatic cancer metabolism. Last author DOI 10.1038/nrgastro.2012.63↗
- MUC1 mucin stabilizes and activates hypoxia-inducible factor 1 alpha to regulate metabolism in pancreatic cancer. Co-author DOI 10.1073/pnas.1203339109↗
- Differential expression of metabolic genes in tumor and stromal components of primary and metastatic loci in pancreatic adenocarcinoma. Co-author DOI 10.1371/journal.pone.0032996↗
Grants 2
Closest collaborators
The 25 strongest of 69 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Pankaj Kumar Singh · 18 shared papers, 2012–2026 · strength 2.13
- Paper Tumor-stromal metabolic crosstalk in pancreatic cancer. DOI 10.1016/j.tcb.2025.04.007↗
- Paper Metabolic Subtyping for Novel Personalized Therapies Against Pancreatic Cancer. DOI 10.1158/1078-0432.ccr-19-2926↗
- Paper KRAS Signaling Inhibition Induces a Targetable Metabolic Dependency on Lipophagy-Dependent Fatty Acid Oxidation in Panc… DOI 10.1158/0008-5472.can-24-1984↗
- Michael Anthony Hollingsworth · 14 shared papers, 2012–2026 · strength 1.64
- Paper Systemic immunosuppression limits NK cell therapy efficacy in pancreatic cancer. DOI 10.1186/s12943-025-02340-8↗
- Paper Single-cell RNA-sequencing of human spleens reveals an IDO-1+ tolerogenic dendritic cell subset in pancreatic cancer pa… DOI 10.1016/j.canlet.2024.217321↗
- Paper The MUC1-HIF-1α signaling axis regulates pancreatic cancer pathogenesis through polyamine metabolism remodeling. DOI 10.1073/pnas.2315509121↗
- Ravi Kumar Thakur · 7 shared papers, 2021–2026 · strength 1.36
- Paper Tumor-stromal metabolic crosstalk in pancreatic cancer. DOI 10.1016/j.tcb.2025.04.007↗
- Paper KRAS Signaling Inhibition Induces a Targetable Metabolic Dependency on Lipophagy-Dependent Fatty Acid Oxidation in Panc… DOI 10.1158/0008-5472.can-24-1984↗
- Paper Systemic immunosuppression limits NK cell therapy efficacy in pancreatic cancer. DOI 10.1186/s12943-025-02340-8↗
- Surendra Kumar Shukla · 11 shared papers, 2014–2026 · strength 1.32
- Paper KRAS Signaling Inhibition Induces a Targetable Metabolic Dependency on Lipophagy-Dependent Fatty Acid Oxidation in Panc… DOI 10.1158/0008-5472.can-24-1984↗
- Paper Systemic immunosuppression limits NK cell therapy efficacy in pancreatic cancer. DOI 10.1186/s12943-025-02340-8↗
- Paper The MUC1-HIF-1α signaling axis regulates pancreatic cancer pathogenesis through polyamine metabolism remodeling. DOI 10.1073/pnas.2315509121↗
- Kuldeep Singh Attri · 7 shared papers, 2017–2024 · strength 0.83
- Paper The MUC1-HIF-1α signaling axis regulates pancreatic cancer pathogenesis through polyamine metabolism remodeling. DOI 10.1073/pnas.2315509121↗
- Paper Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism vi… DOI 10.1038/s41556-024-01372-4↗
- Paper Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering poly… DOI 10.1038/s41556-024-01417-8↗
- Tuo Hu · 5 shared papers, 2021–2026 · strength 0.81
- Paper KRAS Signaling Inhibition Induces a Targetable Metabolic Dependency on Lipophagy-Dependent Fatty Acid Oxidation in Panc… DOI 10.1158/0008-5472.can-24-1984↗
- Paper Systemic immunosuppression limits NK cell therapy efficacy in pancreatic cancer. DOI 10.1186/s12943-025-02340-8↗
- Paper Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism vi… DOI 10.1038/s41556-024-01372-4↗
- Chunbo He · 5 shared papers, 2021–2026 · strength 0.81
- Paper KRAS Signaling Inhibition Induces a Targetable Metabolic Dependency on Lipophagy-Dependent Fatty Acid Oxidation in Panc… DOI 10.1158/0008-5472.can-24-1984↗
- Paper Systemic immunosuppression limits NK cell therapy efficacy in pancreatic cancer. DOI 10.1186/s12943-025-02340-8↗
- Paper Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism vi… DOI 10.1038/s41556-024-01372-4↗
- Ryan J. King · 7 shared papers, 2015–2026 · strength 0.78
- Paper Systemic immunosuppression limits NK cell therapy efficacy in pancreatic cancer. DOI 10.1186/s12943-025-02340-8↗
- Paper Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism vi… DOI 10.1038/s41556-024-01372-4↗
- Paper Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering poly… DOI 10.1038/s41556-024-01417-8↗
- Nina V. Chaika · 10 shared papers, 2012–2024 · strength 0.77
- Paper The MUC1-HIF-1α signaling axis regulates pancreatic cancer pathogenesis through polyamine metabolism remodeling. DOI 10.1073/pnas.2315509121↗
- Paper Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism vi… DOI 10.1038/s41556-024-01372-4↗
- Paper Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering poly… DOI 10.1038/s41556-024-01417-8↗
- Paul M. Grandgenett · 6 shared papers, 2017–2024 · strength 0.71
- Paper Single-cell RNA-sequencing of human spleens reveals an IDO-1+ tolerogenic dendritic cell subset in pancreatic cancer pa… DOI 10.1016/j.canlet.2024.217321↗
- Paper Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism vi… DOI 10.1038/s41556-024-01372-4↗
- Paper Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering poly… DOI 10.1038/s41556-024-01417-8↗
- Divya Murthy · 5 shared papers, 2017–2024 · strength 0.59
- Paper The MUC1-HIF-1α signaling axis regulates pancreatic cancer pathogenesis through polyamine metabolism remodeling. DOI 10.1073/pnas.2315509121↗
- Paper Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism vi… DOI 10.1038/s41556-024-01372-4↗
- Paper Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering poly… DOI 10.1038/s41556-024-01417-8↗
- Sai Sundeep Kollala · 3 shared papers, 2024–2026 · strength 0.50
- Paper Systemic immunosuppression limits NK cell therapy efficacy in pancreatic cancer. DOI 10.1186/s12943-025-02340-8↗
- Paper Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism vi… DOI 10.1038/s41556-024-01372-4↗
- Paper Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering poly… DOI 10.1038/s41556-024-01417-8↗
- Susanna Varkey Ulahannan · 3 shared papers, 2024–2026 · strength 0.50
- Paper KRAS Signaling Inhibition Induces a Targetable Metabolic Dependency on Lipophagy-Dependent Fatty Acid Oxidation in Panc… DOI 10.1158/0008-5472.can-24-1984↗
- Paper Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism vi… DOI 10.1038/s41556-024-01372-4↗
- Paper Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering poly… DOI 10.1038/s41556-024-01417-8↗
- Aneesha Dasgupta · 5 shared papers, 2015–2024 · strength 0.47
- Paper Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism vi… DOI 10.1038/s41556-024-01372-4↗
- Paper Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering poly… DOI 10.1038/s41556-024-01417-8↗
- Paper Macrophages potentiate STAT3 signaling in skeletal muscles and regulate pancreatic cancer cachexia. DOI 10.1016/j.canlet.2020.04.017↗
- Nicholas James Mullen · 2 shared papers, 2021–2025 · strength 0.45
- Robert Powers · 6 shared papers, 2012–2024 · strength 0.43
- Paper Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism vi… DOI 10.1038/s41556-024-01372-4↗
- Paper Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering poly… DOI 10.1038/s41556-024-01417-8↗
- Paper Structure and function of human DnaJ homologue subfamily a member 1 (DNAJA1) and its relationship to pancreatic cancer. DOI 10.1021/bi401329a↗
- Spas Dimitrov Markov · 3 shared papers, 2020–2026 · strength 0.42
- Paper Systemic immunosuppression limits NK cell therapy efficacy in pancreatic cancer. DOI 10.1186/s12943-025-02340-8↗
- Paper Macrophages potentiate STAT3 signaling in skeletal muscles and regulate pancreatic cancer cachexia. DOI 10.1016/j.canlet.2020.04.017↗
- Paper IgE-Based Therapeutic Combination Enhances Antitumor Response in Preclinical Models of Pancreatic Cancer. DOI 10.1158/1535-7163.mct-21-0368↗
- Voddu Suresh · 2 shared papers, 2024–2026 · strength 0.41
- Paper KRAS Signaling Inhibition Induces a Targetable Metabolic Dependency on Lipophagy-Dependent Fatty Acid Oxidation in Panc… DOI 10.1158/0008-5472.can-24-1984↗
- Paper The MUC1-HIF-1α signaling axis regulates pancreatic cancer pathogenesis through polyamine metabolism remodeling. DOI 10.1073/pnas.2315509121↗
- Teklab Gebregiworgis · 5 shared papers, 2012–2024 · strength 0.38
- Paper Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism vi… DOI 10.1038/s41556-024-01372-4↗
- Paper Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering poly… DOI 10.1038/s41556-024-01417-8↗
- Paper MUC1 and HIF-1alpha Signaling Crosstalk Induces Anabolic Glucose Metabolism to Impart Gemcitabine Resistance to Pancrea… DOI 10.1016/j.ccell.2017.06.004↗
- Scott E. Mulder · 3 shared papers, 2021–2024 · strength 0.36
- Paper Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism vi… DOI 10.1038/s41556-024-01372-4↗
- Paper Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering poly… DOI 10.1038/s41556-024-01417-8↗
- Paper Metabolic Rewiring by Loss of Sirt5 Promotes Kras-Induced Pancreatic Cancer Progression. DOI 10.1053/j.gastro.2021.06.045↗
- Clara S. Mundry · 2 shared papers, 2020–2024 · strength 0.33
- Paper Single-cell RNA-sequencing of human spleens reveals an IDO-1+ tolerogenic dendritic cell subset in pancreatic cancer pa… DOI 10.1016/j.canlet.2024.217321↗
- Paper Local and systemic immunosuppression in pancreatic cancer: Targeting the stalwarts in tumor's arsenal. DOI 10.1016/j.bbcan.2020.188387↗
- Joshua J. Souchek · 3 shared papers, 2015–2024 · strength 0.32
- Paper Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism vi… DOI 10.1038/s41556-024-01372-4↗
- Paper Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering poly… DOI 10.1038/s41556-024-01417-8↗
- Paper Silibinin-mediated metabolic reprogramming attenuates pancreatic cancer-induced cachexia and tumor growth. DOI 10.18632/oncotarget.5843↗
- Enza Vernucci · 4 shared papers, 2015–2021 · strength 0.28
- Paper Macrophages potentiate STAT3 signaling in skeletal muscles and regulate pancreatic cancer cachexia. DOI 10.1016/j.canlet.2020.04.017↗
- Paper Metabolic Rewiring by Loss of Sirt5 Promotes Kras-Induced Pancreatic Cancer Progression. DOI 10.1053/j.gastro.2021.06.045↗
- Paper MUC1 and HIF-1alpha Signaling Crosstalk Induces Anabolic Glucose Metabolism to Impart Gemcitabine Resistance to Pancrea… DOI 10.1016/j.ccell.2017.06.004↗
- Rosa F. Hwang · 2 shared papers, 2024 · strength 0.28
- Paper Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism vi… DOI 10.1038/s41556-024-01372-4↗
- Paper Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering poly… DOI 10.1038/s41556-024-01417-8↗
- Ajay Jain · 2 shared papers, 2024 · strength 0.28
- Paper Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism vi… DOI 10.1038/s41556-024-01372-4↗
- Paper Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering poly… DOI 10.1038/s41556-024-01417-8↗
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.