Michael Karin

I have spent my entire academic career investigating stress and inflammation signaling covering the entire
gamut of research approaches from basic biochemistry through molecular cell biology to animal pathophysiology.
After discovering how environmental stress caused by either infection, inflammation or exposure to toxic
substances leads to activation of AP-1, NF-κB and other transcription factors, we begun to examine the role of
the key signaling pathways controlling these transcription factors in the pathogenesis of cancer, degenerative
and metabolic diseases. My group has identified some of the fundamental mechanisms through which
inflammation and obesity promote tumor development and progression and contribute to type II diabetes and
insulin resistance. We were also among the first to highlight the role of inflammation in metabolic disease. We
had established the mechanisms through which members of the IL-6 cytokine family contribute to the
development of colorectal and liver cancer through activation of STAT3 and other transcription factors. We had
established the complex and cell type specific mechanisms through which NF-κB activation via IkB kinases (IKK)
controls development and progression of colon, liver and prostate cancers. We were amongst the first to
demonstrate that not only innate immune cells, especially macrophages, but also adaptive immune cells,
including T regulatory cells and B lymphocytes, contribute to tumorigenesis and its progression. Through this
work, I have contributed to the founding of the Inflammation and Cancer field. More recently, my laboratory
demonstrated the existence of immunosuppressive plasma cells and their role in negative regulation of
immunogenic chemotherapy based on the combination of checkpoint inhibitors with certain chemotherapeutic