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Presence Current · Arkansas
Last published 2026
Sources OpenAlex · ORCID
Refreshed 2026-10-05

Karthikeyan Mythreye

Associate Professor

29 h-index 223 pubs 3,043 cited

  • Humans
  • Ovarian Neoplasms
  • Animals
  • Mice
  • Female
  • Signal Transduction
  • Cell Line, Tumor
  • Receptors, Transforming Growth Factor beta
  • Cell Movement
  • Proteoglycans
  • Gene Expression Regulation, Neoplastic
  • Transforming Growth Factor beta
  • Neoplasms
  • Cell Adhesion
  • Cell Proliferation

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

  • Associate Professor 2019–present
    UAB Comprehensive Cancer Center Pathology/Molecular Cellular ORCID
  • Associate Professor
    University of Arkansas for Medical Sciences ORCID
  • Assistant Professor 2013–2019
    University of South Carolina Chemistry and Biochemistry ORCID
  • Post Doctoral_ Research Assistant Professor 2006–2013
    Duke University Medical Oncology ORCID

Selected Publications

  • Figure 2 from Loss of Predicted Cell Adhesion Molecule MPZL3 Promotes EMT in Ovarian Cancer (2025)
  • Loss of Predicted Cell Adhesion Molecule MPZL3 Promotes EMT in Ovarian Cancer (2025)
    Cancer Research Communications DOI OpenAlex
  • Abstract 2264 Role of atypical Mitogen-Activated Protein Kinase 15 (MAPK15) in ovarian cancer cell survival and metastasis (2025)
    Journal of Biological Chemistry DOI OpenAlex
  • Targeting Mediator Kinase Cyclin-Dependent Kinases 8/19 Potentiates Chemotherapeutic Responses, Reverses Tumor Growth, and Prolongs Survival from Ovarian Clear Cell Carcinoma (2025)
    Cancers 1 citation DOI OpenAlex
  • Loss of the predicted cell adhesion molecule MPZL3 promotes EMT and chemoresistance in ovarian cancer (2024)
    bioRxiv (Cold Spring Harbor Laboratory) 1 citation DOI OpenAlex
  • Targeting Mediator kinases CDK8/19 potentiates chemotherapeutic responses, reverses tumor growth, and prolongs survival from ovarian clear cell carcinoma (2024)
    Gynecologic Oncology DOI OpenAlex
  • Table S2 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)
  • Table S1 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)
  • Table S3 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)
  • Data from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)
  • Fig S1 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)
  • Fig S3 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)
  • Fig S4 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)
  • Fig S2 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)
  • Table S2 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling (2024)

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Collaboration Network

295 Collaborators 83 Institutions 13 Countries

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