Biography and Research Information
OverviewAI-generated summary
Nadine Hempel's research investigates the molecular mechanisms underlying cancer progression and metastasis, with a particular focus on cellular signaling pathways and metabolic adaptations.
Her work has explored the role of mitochondrial calcium uniporters in driving metastasis and conferring dependencies in pancreatic cancer. She has also examined the complex interplay of STIM, Orai, and IP3Rs in mammalian calcium signaling, and the reciprocal regulation of SOX2 by SMAD1-SMAD3 in promoting anoikis resistance and metastasis in cancer. Hempel's research further investigates how mesenchymal stem cells contribute to ovarian cancer heterogeneity and metastasis through mitochondrial transfer, and the metabolic relationships between growth factors in the ovarian cancer ascites environment. Additionally, her studies have addressed the adaptation to anchorage-independence through HuR-dependent SOD2 protein synthesis and the metabolic effects of diet-induced obesity in mice through antisense oligonucleotide-mediated knockdown of Mpzl3.
Hempel holds a faculty position as an Associate Professor at the University of Arkansas for Medical Sciences. Her scholarly output includes 269 publications and 4,959 citations, with an h-index of 39. She has collaborated with Karthikeyan Mythreye on 17 shared publications.
Metrics
- h-index: 39
- Publications: 269
- Citations: 4,959
Positions
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Associate Professor 2021–presentUniversity of Pittsburgh School of Medicine UPMC Hillman Cancer Center ORCID
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Associate ProfessorUniversity of Arkansas for Medical Sciences ORCID
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Associate Professor 2015–2021Penn State Milton S. Hershey Medical Center Department of Pharmacology ORCID
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Assistant Professor 2011–2015SUNY Albany / SUNY Polytechnic Institute College of Nanoscale Science and Engineering ORCID
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Post-Doc 2007–2011Albany Medical College Center for Immunology and Microbial Diseases ORCID
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Post-Doc 2004–2007Duke University Medical Center Department of Pharmacology and Cancer Biology ORCID
Selected Publications
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αKG-mediated carnitine synthesis drives DNA repair via histone acetylation (2026)
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The chemotherapy-induced senescence-associated secretome promotes cell detachment and metastatic dissemination through metabolic reprogramming (2026)
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Loss of STIM2, but not of STIM1, drives colorectal cancer metastasis through metabolic reprogramming and the ATF4 ER stress pathway (2025)
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ATR promotes mTORC1 activity via de novo cholesterol synthesis (2025)
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Data from Aged and BRCA-Mutated Stromal Cells Drive Epithelial Cell Transformation (2025)
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Crosstalk between calcium and reactive oxygen species signaling in cancer revisited (2025)
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Aged and BRCA -Mutated Stromal Cells Drive Epithelial Cell Transformation (2025)
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Zinc availability in the tumor microenvironment dictates anti-PD1 response in CDKN2A Low tumors via increased macrophage phagocytosis (2025)
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Loss of the predicted cell adhesion molecule MPZL3 promotes EMT and chemoresistance in ovarian cancer (2024)
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Stress response regulation of mRNA translation: Implications for antioxidant enzyme expression in cancer (2024)
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Hypomorphic NOTCH1 Expression Alters Cardiomyocyte Cellular Architecture in Hypoplastic Left Heart Syndrome (2024)
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Acetate drives ovarian cancer quiescence via ACSS2-mediated acetyl-CoA production (2024)
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Drp1 splice variants regulate ovarian cancer mitochondrial dynamics and tumor progression (2024)
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Carcinoma-associated mesenchymal stem cells promote ovarian cancer heterogeneity and metastasis through mitochondrial transfer (2024)
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Acetate drives ovarian cancer quiescence via ACSS2-mediated acetyl-CoA production (2024)
Collaboration Network
Top Collaborators
- Insights into the Dichotomous Regulation of SOD2 in Cancer
- GPx3 supports ovarian cancer progression by manipulating the extracellular redox environment
- Context-dependent activation of SIRT3 is necessary for anchorage-independent survival and metastasis of ovarian cancer cells
- TAK1 activation of alpha-TAT1 and microtubule hyperacetylation control AKT signaling and cell growth
- Reciprocal SOX2 regulation by SMAD1-SMAD3 is critical for anoikis resistance and metastasis in cancer
Showing 5 of 51 shared publications
- Crosstalk between calcium and reactive oxygen species signaling in cancer
- The native ORAI channel trio underlies the diversity of Ca2+ signaling events
- Negative Regulation of TRPC3 Channels by Protein Kinase C-Mediated Phosphorylation of Serine 712
- Mitochondrial Calcium Regulation of Redox Signaling in Cancer
- Mitochondria control store‐operated Ca2+ entry through Na+ and redox signals
Showing 5 of 44 shared publications
- GPx3 supports ovarian cancer progression by manipulating the extracellular redox environment
- Context-dependent activation of SIRT3 is necessary for anchorage-independent survival and metastasis of ovarian cancer cells
- TAK1 activation of alpha-TAT1 and microtubule hyperacetylation control AKT signaling and cell growth
- Reciprocal SOX2 regulation by SMAD1-SMAD3 is critical for anoikis resistance and metastasis in cancer
- The type III TGF-β receptor suppresses breast cancer progression through GIPC-mediated inhibition of TGF-β signaling
Showing 5 of 34 shared publications
- Extracellular Glutathione Peroxidase GPx3 and Its Role in Cancer
- Insights into the Dichotomous Regulation of SOD2 in Cancer
- GPx3 supports ovarian cancer progression by manipulating the extracellular redox environment
- Context-dependent activation of SIRT3 is necessary for anchorage-independent survival and metastasis of ovarian cancer cells
- Reciprocal SOX2 regulation by SMAD1-SMAD3 is critical for anoikis resistance and metastasis in cancer
Showing 5 of 26 shared publications
- Emerging perspectives on growth factor metabolic relationships in the ovarian cancer ascites environment
- HuR-dependent SOD2 protein synthesis is an early adaptation to anchorage-independence
- Drp1 splice variants regulate ovarian cancer mitochondrial dynamics and tumor progression
- GPX3 supports ovarian cancer tumor progression in vivo and promotes expression of GDF15
- Aged and BRCA -Mutated Stromal Cells Drive Epithelial Cell Transformation
Showing 5 of 23 shared publications
- Insights into the Dichotomous Regulation of SOD2 in Cancer
- GPx3 supports ovarian cancer progression by manipulating the extracellular redox environment
- Context-dependent activation of SIRT3 is necessary for anchorage-independent survival and metastasis of ovarian cancer cells
- HuR-dependent SOD2 protein synthesis is an early adaptation to anchorage-independence
- Drp1 splice variants regulate ovarian cancer mitochondrial dynamics and tumor progression
Showing 5 of 21 shared publications
- Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Glycosaminoglycan modifications of betaglycan regulate ectodomain shedding to fine-tune TGF-β signaling responses in ovarian cancer
- Figure S3 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Table S1 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Figure S4 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
Showing 5 of 21 shared publications
- Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Hypoxia-induced inhibin promotes tumor growth and vascular permeability in ovarian cancers
- Hypoxia Regulated Inhibin Promotes Tumor Growth and Vascular Permeability By ACVRL1 and CD105 Dependent VE-Cadherin Internalization
- Figure S3 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Table S1 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
Showing 5 of 21 shared publications
- Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Hypoxia-induced inhibin promotes tumor growth and vascular permeability in ovarian cancers
- Hypoxia Regulated Inhibin Promotes Tumor Growth and Vascular Permeability By ACVRL1 and CD105 Dependent VE-Cadherin Internalization
- Figure S3 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Table S1 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
Showing 5 of 21 shared publications
- Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Anoikis resistance and metastasis of ovarian cancer can be overcome by CDK8/19 Mediator kinase inhibition
- Figure S3 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Table S1 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Figure S4 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
Showing 5 of 21 shared publications
- Carcinoma-associated mesenchymal stem cells promote ovarian cancer heterogeneity and metastasis through mitochondrial transfer
- Emerging perspectives on growth factor metabolic relationships in the ovarian cancer ascites environment
- HuR-dependent SOD2 protein synthesis is an early adaptation to anchorage-independence
- Drp1 splice variants regulate ovarian cancer mitochondrial dynamics and tumor progression
- GPX3 supports ovarian cancer tumor progression in vivo and promotes expression of GDF15
Showing 5 of 21 shared publications
- Bioenergetic Analysis of Ovarian Cancer Cell Lines: Profiling of Histological Subtypes and Identification of a Mitochondria-Defective Cell Line
- Mitochondrial Superoxide Dismutase Has a Protumorigenic Role in Ovarian Clear Cell Carcinoma
- Context-dependent activation of SIRT3 is necessary for anchorage-independent survival and metastasis of ovarian cancer cells
- Increased expression and activity of Sod2 promotes transcoelomic metastasis in ovarian cancer
- Superoxide Dismutase 2 is Necessary for Key Steps in the Transcoelomic Route of Ovarian Cancer Metastasis
Showing 5 of 20 shared publications
- Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Figure S3 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Table S1 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Figure S4 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Figure S1 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
Showing 5 of 19 shared publications
- Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Figure S3 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Table S1 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Figure S4 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Figure S1 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
Showing 5 of 19 shared publications
- Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Figure S3 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Table S1 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Figure S4 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Figure S1 from Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
Showing 5 of 19 shared publications
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