ResearcherUniversity of Nebraska–LincolnActive in the last 2 years
Venugopal Gunda
Matched on ORCID iD 0000-0002-9156-2580; OpenAlex author ID A5041700915. Sources: OpenAlex.
Their work
- Papers
- 18 (first author 4, last author 0)
- Trials
- 0
- Grants
- 0
- Labs led
- 0
- Collaborators
- 63
2014: 1 paper · 2015: 2 papers · 2016: none · 2017: 5 papers · 2018: 1 paper · 2019: 3 papers · 2020: 1 paper · 2021: 1 paper · 2022: 2 papers · 2023: none · 2024: none · 2025: 2 papers
Papers 18
- Niclosamide-Loaded Polyanhydride Nanoparticles to Combat Gemcitabine Resistance in Pancreatic Cancer. First author DOI 10.1007/s40883-025-00394-0↗
- Niclosamide nanoparticles enhance pancreatic cancer sensitivity to gemcitabine via HIF-1α inhibition. First author DOI 10.1016/j.isci.2025.114088↗
- CD73 induces GM-CSF/MDSC-mediated suppression of T cells to accelerate pancreatic cancer pathogenesis. Co-author DOI 10.1038/s41388-021-02132-6↗
- Ubiquitous Aberration in Cholesterol Metabolism across Pancreatic Ductal Adenocarcinoma. Co-author DOI 10.3390/metabo12010047↗
- Nuclear factor kappa-B contributes to cigarette smoke tolerance in pancreatic ductal adenocarcinoma through cysteine metabolism. Co-author DOI 10.1016/j.biopha.2021.112312↗
- Author Correction: Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer. Co-author DOI 10.1038/s41591-020-0947-8↗
- Evaluating the Metabolic Alterations in Pancreatic Cancer. Co-author DOI 10.1007/978-1-4939-8879-2_20↗
- Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer. Co-author DOI 10.1038/s41591-019-0368-8↗
- Metabolic Alterations in Pancreatic Cancer Progression. Co-author DOI 10.3390/cancers12010002↗
- Hypoxia-Induced Metabolomic Alterations in Pancreatic Cancer Cells. Co-author DOI 10.1007/978-1-4939-7665-2_9↗
- GOT1-mediated anaplerotic glutamine metabolism regulates chronic acidosis stress in pancreatic cancer cells. First author DOI 10.1016/j.canlet.2017.04.029↗
- 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↗
- Glucose Limitation Alters Glutamine Metabolism in MUC1-Overexpressing Pancreatic Cancer Cells. Co-author DOI 10.1021/acs.jproteome.7b00246↗
- De Novo Lipid Synthesis Facilitates Gemcitabine Resistance through Endoplasmic Reticulum Stress in Pancreatic Cancer. Co-author DOI 10.1158/0008-5472.can-16-3062↗
- MUC1-Mediated Metabolic Alterations Regulate Response to Radiotherapy in Pancreatic Cancer. Co-author DOI 10.1158/1078-0432.ccr-17-1151↗
- MUC16-mediated activation of mTOR and c-Myc reprograms pancreatic cancer metabolism. First author DOI 10.18632/oncotarget.4078↗
- Silibinin-mediated metabolic reprogramming attenuates pancreatic cancer-induced cachexia and tumor growth. Co-author DOI 10.18632/oncotarget.5843↗
- Metabolic reprogramming induced by ketone bodies diminishes pancreatic cancer cachexia. Co-author DOI 10.1186/2049-3002-2-18↗
Closest collaborators
The 25 strongest of 63 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Pankaj Kumar Singh · 14 shared papers, 2014–2022 · strength 1.01
- Paper Evaluating the Metabolic Alterations in Pancreatic Cancer. DOI 10.1007/978-1-4939-8879-2_20↗
- Paper CD73 induces GM-CSF/MDSC-mediated suppression of T cells to accelerate pancreatic cancer pathogenesis. DOI 10.1038/s41388-021-02132-6↗
- Paper Hypoxia-Induced Metabolomic Alterations in Pancreatic Cancer Cells. DOI 10.1007/978-1-4939-7665-2_9↗
- Surinder K. Batra · 5 shared papers, 2015–2025 · strength 0.81
- Paper Niclosamide nanoparticles enhance pancreatic cancer sensitivity to gemcitabine via HIF-1α inhibition. DOI 10.1016/j.isci.2025.114088↗
- Paper Niclosamide-Loaded Polyanhydride Nanoparticles to Combat Gemcitabine Resistance in Pancreatic Cancer. DOI 10.1007/s40883-025-00394-0↗
- Paper Ubiquitous Aberration in Cholesterol Metabolism across Pancreatic Ductal Adenocarcinoma. DOI 10.3390/metabo12010047↗
- Satyanarayana Rachagani · 4 shared papers, 2021–2025 · strength 0.76
- Paper Niclosamide nanoparticles enhance pancreatic cancer sensitivity to gemcitabine via HIF-1α inhibition. DOI 10.1016/j.isci.2025.114088↗
- Paper Niclosamide-Loaded Polyanhydride Nanoparticles to Combat Gemcitabine Resistance in Pancreatic Cancer. DOI 10.1007/s40883-025-00394-0↗
- Paper Ubiquitous Aberration in Cholesterol Metabolism across Pancreatic Ductal Adenocarcinoma. DOI 10.3390/metabo12010047↗
- Surendra Kumar Shukla · 11 shared papers, 2014–2022 · strength 0.75
- Paper Evaluating the Metabolic Alterations in Pancreatic Cancer. DOI 10.1007/978-1-4939-8879-2_20↗
- Paper CD73 induces GM-CSF/MDSC-mediated suppression of T cells to accelerate pancreatic cancer pathogenesis. DOI 10.1038/s41388-021-02132-6↗
- Paper Metabolic Alterations in Pancreatic Cancer Progression. DOI 10.3390/cancers12010002↗
- Nina V. Chaika · 11 shared papers, 2014–2022 · strength 0.70
- Paper CD73 induces GM-CSF/MDSC-mediated suppression of T cells to accelerate pancreatic cancer pathogenesis. DOI 10.1038/s41388-021-02132-6↗
- Paper Metabolic Alterations in Pancreatic Cancer Progression. DOI 10.3390/cancers12010002↗
- Paper Author Correction: Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer. DOI 10.1038/s41591-020-0947-8↗
- Aneesha Dasgupta · 8 shared papers, 2015–2022 · strength 0.66
- Paper Evaluating the Metabolic Alterations in Pancreatic Cancer. DOI 10.1007/978-1-4939-8879-2_20↗
- Paper CD73 induces GM-CSF/MDSC-mediated suppression of T cells to accelerate pancreatic cancer pathogenesis. DOI 10.1038/s41388-021-02132-6↗
- Paper Hypoxia-Induced Metabolomic Alterations in Pancreatic Cancer Cells. DOI 10.1007/978-1-4939-7665-2_9↗
- Nagabhishek Sirpu Natesh · 3 shared papers, 2021–2025 · strength 0.62
- Paper Niclosamide nanoparticles enhance pancreatic cancer sensitivity to gemcitabine via HIF-1α inhibition. DOI 10.1016/j.isci.2025.114088↗
- Paper Niclosamide-Loaded Polyanhydride Nanoparticles to Combat Gemcitabine Resistance in Pancreatic Cancer. DOI 10.1007/s40883-025-00394-0↗
- Paper Nuclear factor kappa-B contributes to cigarette smoke tolerance in pancreatic ductal adenocarcinoma through cysteine me… DOI 10.1016/j.biopha.2021.112312↗
- Jaime Abrego · 8 shared papers, 2015–2022 · strength 0.55
- Paper CD73 induces GM-CSF/MDSC-mediated suppression of T cells to accelerate pancreatic cancer pathogenesis. DOI 10.1038/s41388-021-02132-6↗
- Paper Metabolic Alterations in Pancreatic Cancer Progression. DOI 10.3390/cancers12010002↗
- Paper GOT1-mediated anaplerotic glutamine metabolism regulates chronic acidosis stress in pancreatic cancer cells. DOI 10.1016/j.canlet.2017.04.029↗
- Ryan J. King · 7 shared papers, 2015–2022 · strength 0.52
- Paper Evaluating the Metabolic Alterations in Pancreatic Cancer. DOI 10.1007/978-1-4939-8879-2_20↗
- Paper CD73 induces GM-CSF/MDSC-mediated suppression of T cells to accelerate pancreatic cancer pathogenesis. DOI 10.1038/s41388-021-02132-6↗
- Paper GOT1-mediated anaplerotic glutamine metabolism regulates chronic acidosis stress in pancreatic cancer cells. DOI 10.1016/j.canlet.2017.04.029↗
- Balaji Narasimhan · 2 shared papers, 2025 · strength 0.49
- Brianna M. White · 2 shared papers, 2025 · strength 0.49
- Susheel Kumar Nethi · 2 shared papers, 2025 · strength 0.49
- Enza Vernucci · 7 shared papers, 2015–2022 · strength 0.48
- Paper CD73 induces GM-CSF/MDSC-mediated suppression of T cells to accelerate pancreatic cancer pathogenesis. DOI 10.1038/s41388-021-02132-6↗
- Paper Metabolic Alterations in Pancreatic Cancer Progression. DOI 10.3390/cancers12010002↗
- Paper GOT1-mediated anaplerotic glutamine metabolism regulates chronic acidosis stress in pancreatic cancer cells. DOI 10.1016/j.canlet.2017.04.029↗
- Paul M. Grandgenett · 3 shared papers, 2017–2022 · strength 0.31
- Paper Ubiquitous Aberration in Cholesterol Metabolism across Pancreatic Ductal Adenocarcinoma. DOI 10.3390/metabo12010047↗
- Paper CD73 induces GM-CSF/MDSC-mediated suppression of T cells to accelerate pancreatic cancer pathogenesis. DOI 10.1038/s41388-021-02132-6↗
- 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↗
- Divya Murthy · 3 shared papers, 2017–2022 · strength 0.23
- Paper CD73 induces GM-CSF/MDSC-mediated suppression of T cells to accelerate pancreatic cancer pathogenesis. DOI 10.1038/s41388-021-02132-6↗
- Paper GOT1-mediated anaplerotic glutamine metabolism regulates chronic acidosis stress in pancreatic cancer cells. DOI 10.1016/j.canlet.2017.04.029↗
- 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 · 2 shared papers, 2017–2022 · strength 0.19
- Costas Andreas Lyssiotis · 3 shared papers, 2017–2020 · strength 0.18
- Paper Author Correction: Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer. DOI 10.1038/s41591-020-0947-8↗
- Paper Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer. DOI 10.1038/s41591-019-0368-8↗
- 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↗
- Michael Anthony Hollingsworth · 2 shared papers, 2017–2022 · strength 0.16
- Paper CD73 induces GM-CSF/MDSC-mediated suppression of T cells to accelerate pancreatic cancer pathogenesis. DOI 10.1038/s41388-021-02132-6↗
- 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↗
- Kuldeep Singh Attri · 2 shared papers, 2017–2022 · strength 0.16
- Paper CD73 induces GM-CSF/MDSC-mediated suppression of T cells to accelerate pancreatic cancer pathogenesis. DOI 10.1038/s41388-021-02132-6↗
- 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↗
- Vinee Purohit · 3 shared papers, 2014–2017 · strength 0.15
- Paper Glucose Limitation Alters Glutamine Metabolism in MUC1-Overexpressing Pancreatic Cancer Cells. DOI 10.1021/acs.jproteome.7b00246↗
- 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↗
- Paper Metabolic reprogramming induced by ketone bodies diminishes pancreatic cancer cachexia. DOI 10.1186/2049-3002-2-18↗
- Robert Powers · 3 shared papers, 2014–2017 · strength 0.15
- Paper Glucose Limitation Alters Glutamine Metabolism in MUC1-Overexpressing Pancreatic Cancer Cells. DOI 10.1021/acs.jproteome.7b00246↗
- 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↗
- Paper Metabolic reprogramming induced by ketone bodies diminishes pancreatic cancer cachexia. DOI 10.1186/2049-3002-2-18↗
- Teklab Gebregiworgis · 3 shared papers, 2014–2017 · strength 0.15
- Paper Glucose Limitation Alters Glutamine Metabolism in MUC1-Overexpressing Pancreatic Cancer Cells. DOI 10.1021/acs.jproteome.7b00246↗
- 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↗
- Paper Metabolic reprogramming induced by ketone bodies diminishes pancreatic cancer cachexia. DOI 10.1186/2049-3002-2-18↗
- Joshua J. Souchek · 3 shared papers, 2015–2017 · strength 0.15
- Paper MUC1-Mediated Metabolic Alterations Regulate Response to Radiotherapy in Pancreatic Cancer. DOI 10.1158/1078-0432.ccr-17-1151↗
- Paper MUC16-mediated activation of mTOR and c-Myc reprograms pancreatic cancer metabolism. DOI 10.18632/oncotarget.4078↗
- Paper Silibinin-mediated metabolic reprogramming attenuates pancreatic cancer-induced cachexia and tumor growth. DOI 10.18632/oncotarget.5843↗
- Ramakanth Chirravuri‐Venkata · 1 shared paper, 2022 · strength 0.15
- Jyoti Kaushal · 1 shared paper, 2022 · strength 0.15
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.