Biography and Research Information
OverviewAI-generated summary
Karthikeyan Mythreye investigates the molecular mechanisms underlying cancer progression, with a particular focus on ovarian cancer. His research explores the roles of signal transduction pathways, such as transforming growth factor beta (TGFβ) signaling, and specific molecules like SOX2, SMAD1, and SMAD3 in promoting cancer cell resistance to anoikis and facilitating metastasis. Mythreye's work also examines the influence of the tumor microenvironment, including the ascites environment in ovarian cancer, on cellular metabolism and growth factor relationships. He has published research on the stress-responsive lncRNA PVT1 and its role in driving ovarian cancer metastasis and chemoresistance, as well as the impact of hypoxia-induced inhibin on tumor growth and vascular permeability.
His scholarship extends to bioinformatic analyses, identifying prognostic markers like the inhibin-betaglycan-endoglin/CD105 network in various solid tumors. Mythreye also studies cellular adaptations to anchorage independence, such as HuR-dependent SOD2 protein synthesis. His research network includes collaborators like Nadine Hempel and Analiz Rodriguez. Mythreye's work contributes to understanding disease mechanisms and identifying potential therapeutic targets in cancer.
Metrics
- h-index: 29
- Publications: 223
- Citations: 3,043
Positions
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Associate Professor 2019–presentUAB Comprehensive Cancer Center Pathology/Molecular Cellular ORCID
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Associate ProfessorUniversity of Arkansas for Medical Sciences ORCID
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Assistant Professor 2013–2019University of South Carolina Chemistry and Biochemistry ORCID
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Post Doctoral_ Research Assistant Professor 2006–2013Duke University Medical Oncology ORCID
Selected Publications
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Figure 2 from Loss of Predicted Cell Adhesion Molecule MPZL3 Promotes EMT in Ovarian Cancer (2025)
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Loss of Predicted Cell Adhesion Molecule MPZL3 Promotes EMT in Ovarian Cancer (2025)
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Abstract 2264 Role of atypical Mitogen-Activated Protein Kinase 15 (MAPK15) in ovarian cancer cell survival and metastasis (2025)
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Targeting Mediator Kinase Cyclin-Dependent Kinases 8/19 Potentiates Chemotherapeutic Responses, Reverses Tumor Growth, and Prolongs Survival from Ovarian Clear Cell Carcinoma (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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Targeting Mediator kinases CDK8/19 potentiates chemotherapeutic responses, reverses tumor growth, and prolongs survival from ovarian clear cell carcinoma (2024)
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Table S2 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)
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Table S1 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)
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Table S3 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)
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Data from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)
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Fig S1 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)
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Fig S3 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)
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Fig S4 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)
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Fig S2 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)
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Table S2 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (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 54 shared publications
- TGFβ signaling networks in ovarian cancer progression and plasticity
- 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 53 shared publications
- HCK Promotes High-Grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Anoikis resistance and metastasis of ovarian cancer can be overcome by CDK8/19 Mediator kinase inhibition
- Table S1 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Fig S2 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Table S1 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
Showing 5 of 50 shared publications
- Mediator kinase CDK8/CDK19 drives YAP1-dependent BMP4-induced EMT in cancer
- TβRIII/β-arrestin2 regulates integrin α5β1 trafficking, function, and localization in epithelial cells
- HCK Promotes High-Grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Table S1 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Fig S2 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
Showing 5 of 49 shared publications
- HCK Promotes High-Grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Table S1 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Fig S2 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Table S1 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Data from HCK Promotes High-Grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
Showing 5 of 47 shared publications
- HCK Promotes High-Grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Table S1 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Fig S2 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Table S1 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Data from HCK Promotes High-Grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
Showing 5 of 47 shared publications
- CDK8 Selectively Promotes the Growth of Colon Cancer Metastases in the Liver by Regulating Gene Expression of TIMP3 and Matrix Metalloproteinases
- Mediator kinase CDK8/CDK19 drives YAP1-dependent BMP4-induced EMT in cancer
- Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- Depletion of COPI in cancer cells: the role of reactive oxygen species in the induction of lipid accumulation, noncanonical lipophagy and apoptosis
- Abstract 4896: Role of CDK8 in colon cancer hepatic metastasis
Showing 5 of 43 shared publications
- HCK Promotes High-Grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Table S1 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Fig S2 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Table S1 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
- Fig S4 from HCK Promotes High-grade Serous Ovarian Cancer Tumorigenesis through CD44 and NOTCH3 Signaling
Showing 5 of 31 shared publications
- Mechanical Stiffness Grades Metastatic Potential in Patient Tumor Cells and in Cancer Cell Lines
- The type III TGF-β receptor regulates epithelial and cancer cell migration through β-arrestin2-mediated activation of Cdc42
- Proteoglycan signaling co-receptors: Roles in cell adhesion, migration and invasion
- Endoglin mediates fibronectin/α5β1 integrin and TGF‐β pathway crosstalk in endothelial cells
- The type III transforming growth factor-β receptor inhibits proliferation, migration, and adhesion in human myeloma cells
Showing 5 of 30 shared publications
- Mediator kinase CDK8/CDK19 drives YAP1-dependent BMP4-induced EMT in cancer
- Dually modified transmembrane proteoglycans in development and disease
- Altering the Proteoglycan State of Transforming Growth Factor β Type III Receptor (TβRIII)/Betaglycan Modulates Canonical Wnt/β-Catenin Signaling
- Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- TGF-β triggers rapid fibrillogenesis via a novel TβRII-dependent fibronectin-trafficking mechanism
Showing 5 of 29 shared publications
- Mediator kinase CDK8/CDK19 drives YAP1-dependent BMP4-induced EMT in cancer
- Dually modified transmembrane proteoglycans in development and disease
- Inhibin Is a Novel Paracrine Factor for Tumor Angiogenesis and Metastasis
- A bioinformatic analysis of the inhibin-betaglycan-endoglin/CD105 network reveals prognostic value in multiple solid tumors
- Hypoxia-induced inhibin promotes tumor growth and vascular permeability in ovarian cancers
Showing 5 of 27 shared publications
- Mechanical Stiffness Grades Metastatic Potential in Patient Tumor Cells and in Cancer Cell Lines
- Reciprocal SOX2 regulation by SMAD1-SMAD3 is critical for anoikis resistance and metastasis in cancer
- Hypoxia-induced inhibin promotes tumor growth and vascular permeability in ovarian cancers
- Reciprocal epigenetic Sox2 regulation by SMAD1-SMAD3 is critical for anoikis resistance and metastasis in cancer
- Hypoxia Regulated Inhibin Promotes Tumor Growth and Vascular Permeability By ACVRL1 and CD105 Dependent VE-Cadherin Internalization
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
- A bioinformatic analysis of the inhibin-betaglycan-endoglin/CD105 network reveals prognostic value in multiple solid tumors
- A meta-analysis of the inhibin network reveals prognostic value in multiple solid tumors
- 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
- Mechanical Stiffness Grades Metastatic Potential in Patient Tumor Cells and in Cancer Cell Lines
- TGF-β regulates LARG and GEF-H1 during EMT to affect stiffening response to force and cell invasion
- TβRIII Restores Normal Cytoskeleton Mechanics In Ovarian Cancer Cells
- Mechanical Stiffness Grades Metastatic Potential in Patient Tumor Cells and in Cancer Cell Lines
- TGF- regulates LARG and GEF-H1 during EMT to affect stiffening response to force and cell invasion
Showing 5 of 19 shared publications
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