[2] He then completed postdoctoral fellowships with Beatrice Mintz at the Fox Chase Cancer Center, and subsequently with John Baxter at the University of California, San Francisco.
That work has led to identification and molecular cloning of the IκB kinase (IKK) complex, which has turned out to be one of the major activators of the inflammatory response and innate immunity.
Within two years of making this proposal they obtained strong experimental evidence that NF-κB activation does provide a major mechanism through which inflammation and infection promote cancer development, especially in the gastrointestinal track.
NASH to HCC progression depends on suppression of CD8 T cell-mediated immunosurveillance, caused by accumulation of immunosuppressive IgA producing plasma cells.
These pathogenic mechanisms were shown to be clinically relevant, thus providing an explanation to the surprising efficacy of PD-1 checkpoint inhibitory drugs in human non-viral HCC.