Dually Targeting the PI3K/Akt and MAP Kinase Pathways in Poorly Differentiated and Undifferentiated Thyroid Cancer Cells has High Therapeutic Promise

Abstract (Set) JHU scientists have discovered an innovative method of targeting aggressive thyroid cancers that are resistant to conventional treatment. Poorly differentiated anaplastic thyroid cancer cells do not respond to radioiodine treatment due to abnormal silencing of iodide-metabolizing genes. Recent studies suggest that two signal transduction pathways have critical roles in expression and activity of the iodide-metabolizing genes. JHU scientists found that modulation of both the PI3K/Akt and MAP kinase pathway has strong anti-cancer cell effects and can beneficially induce gene expression. Modulation of the PI3K/Akt and MAP kinase pathway can be done using specific inhibitor molecules or siRNA molecules. Modulation of both pathways was significantly better than modulation of a single pathway as shown by multiple measurements of anti-cancer effects in cell culture tests. Remarkably, dual alteration of the two pathways synergistically and robustly induced expression of thyroid genes that restored the ability of cells to take up radioiodine. Description (Set) Specific PI3K/Akt and MAP kinase pathway inhibitors or introduction of siRNA into thyroid cancer cells has strong anti-thyroid cancer cell effects and can particularly induce gene expression. This may prove to be an effective therapeutic strategy for poorly differentiated and undifferentiated thyroid cancers. Proposed Use (Set) Restoration of thyroid iodine-metabolizing gene expression in anaplastic thyroid cancer cells would render them susceptible to conventional therapy. This technology could be commercialized as a combination therapeutic strategy to target poorly differentiated anaplastic thyroid cancers.

Inventor(s): Xing, Michael

Type of Offer: Licensing

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