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Research

Primary Areas of Interests

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Non-classical mechanisms driving therapeutic resistance

Cell death-induced compensatory proliferation and immunosuppression: Most cancer therapies designate cancer cell death as the therapeutic end goal. Intriguingly, our study reveals that cell death-associated release of PGE2 functions as a mitogen, which recruits quiescent cancer stem cells (CSCs) to repopulate residual tumors [Nature 517, 209–213 (2015)]. PGE2 also acts as an inhibitory DAMP to dampen dendritic cell activation, and thus T cell priming [Nature Communications 11, 6299 (2020)]. Studies are underway to further characterize how CSCs interact with the immune microenvironment to modulate resistance to chemo- and immune checkpoint blockade therapy.

 

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Cedars-Sinai Medical Center
127 S San Vicente Bl A9200.8
Los Angeles, CA, 90048

424-315-2517

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