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)

Description

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.

Applications

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Stage of Development

Validated in mice xenograft models.

Relevant Publications

Inventors

Geeta Upadhyay