What is it about?
Epithelial-mesenchymal transition (EMT) is a process associated with cancer metastasis. EMT can be induced by a soluble factor called TGF-beta, and we found that TGF-beta can also induce the expression of a molecule known as PD-L1 in lung cancer cells. PD-L1 can protect tumor cells from killing by antitumor T cells, thereby blocking successful anti-cancer immune responses. Then, we used a new drug called M7824 that targets both PD-L1 and TGF-beta and found that it can reverse the process of EMT in lung cancer cells.
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Why is it important?
This work suggests that upregulation of tumor cell PD-L1 is a novel mechanism of TGF-beta-induced immunosuppression in lung cancer, and that tumor cell EMT driven by TGF-beta can be effectively antagonized using M7824. These findings provide supporting rationale for the development of M7824 for patients with lung cancer, and potentially other cancers.
Perspectives
My hope is that this study deepens our scientific understanding of the complex interplay between tumor cells and immune cells, and provides insights into overcoming tumor resistance to immunotherapy. I also hope that this article helps to guide the successful clinical development and use of the M7824 drug for patients with cancer.
Justin David
Precision Biologics, Inc.
Read the Original
This page is a summary of: A novel bifunctional anti-PD-L1/TGF-β Trap fusion protein (M7824) efficiently reverts mesenchymalization of human lung cancer cells, OncoImmunology, July 2017, Taylor & Francis,
DOI: 10.1080/2162402x.2017.1349589.
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