Active areas of investigation in my laboratory are focused on uncovering molecular mechanisms of inflammation and their link to cancer. Specifically, we are studying the role of the transcription factor STAT2 in bacterial-induced inflammation and colorectal cancer. STAT2 is a ubiquitous protein that plays a pivotal role in the signal transduction pathway initiated by type I and type III interferons, a family of cytokines shown to exert antitumor and antiviral activity and protect the intestinal tract. Work from my lab has collected evidence to support STAT2 as a critical component in mediating the antitumor and apoptotic actions of type I IFN. However, our recent studies have revealed that STAT2 displays pro-inflammatory and tumor promoting activity in animal models of colorectal cancer thus indicating that it plays a dual role in cancer by an unknown mechanism. Understanding at the molecular level what drives STAT2 to deliver a tumor promoting signal as opposed to an antitumor trigger will have clinical implications.
Current projects include:
Identification of STAT2 dependent signaling pathways promoting colorectal carcinogenesis: The goal is to elucidate the molecular mechanisms by which STAT2 promotes inflammation, tumor promotion, disease progression and ultimately metastasis. Of major interest to the lab is to identify biomarkers of disease progression, STAT2-dependent target genes and transcriptional signatures associated with STAT2 linked to disease prognosis.
The role of STAT2 in bacterial-induced colorectal carcinogenesis. Recent studies show the intestinal microbiome can influence the development of colorectal cancer. Colonic commensals have been identified with oncogenic activity and are found enriched in colorectal tissues from cancer patients and inflammatory bowel disease patients. We are investigating the role of STAT2 as an axis in linking bacterial infection to colorectal neoplasia.
Screens for drugs that target STAT2. Based on our recent findings, we are interested in identifying small molecules that can directly target STAT2 or affect STAT2-dependent signaling pathways to attenuate inflammation and prevent cancer.
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