Inhibition of Ly6K and Ly6E enhances anti PDL1/PDL2 Therapy Response

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Categories:  “Cancer Therapeutics

Reference #: 2015-030

OTC Contact: Ruchika Nijhara, Ph.D., MBA, CLP (Directory Information | Send a Message)


Targeted immunotherapy for the treatment of triple negative breast cancer (TNBC) that uses Ly6K and Ly6E
inhibition for anti-TGFβ and for inhibition of PD-L1 expression.

Recent discoveries in triple negative breast cancer suggest that the immune checkpoint protein PD-L1 is increased in TNBC and that its increased expression contributes to tumor immune escape. TGFβ signaling represents another key hub in cancer that activates both immune and non-immune associated pathways of tumor progression. The widespread expression and essential function of TGFβ signaling and PD-L1 in many normal tissues make them problematic targets for therapeutic intervention.

Georgetown researchers identified the cell surface protein Ly6K as a potent activator of TGFβ signaling and epithelial to mesenchymal transition required for in vivo tumor growth. Ly6K is also required for IFNg induced overexpression of PD-L1 in cancer cells. The researchers found that the knockdown or pharmacological inhibition of Ly6K inhibits PD-L1 expression in TNBC cells and have identified small molecule binders of Ly6K potentially leading to this outcome. Importantly, an antibody targeted approach would also be suitable to target Ly6K.



Stage of Development

Validated in mice xenograft models.

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Geeta Upadhyay