EpigenetiC MECHANISMS IN Inflammation & CANCER
The Chandwani laboratory focuses on the chromatin-based mechanisms that drive the cell fate alterations required for inflammation and tumor initiation and maintenance, largely using the pancreas as a model system. We leverage our expertise in mouse modeling, chromatin biology, lineage-tracing, and the application of robust low-input epigenomic tools to interrogate epithelial cells in vivo.
To date, our efforts have been applied to understand chromatin landscapes and drivers of epigenetic plasticity central to lineage specification in the exocrine pancreas, the mechanisms of acinar cell fate destabilization in the progression to neoplasia, and the key transcription factors crucial to maintenance of identity.
Currently our laboratory (1) characterizes the epigenetic dysregulation that occurs in tumor initiation, using pancreatic cancer as a model; (2) employs chromatin-based analyses to identify novel molecular mechanisms central to inflammation, tumor development, and malignant progression ; and (3) utilizes our unique interaction with patients to comprehensively interrogate human specimens as a means to inform and enhance our ongoing investigations. These efforts are rooted in the notion that genetic determinants do not fully explain malignant phenotypes, and that in chromatin lies the key to targeting critical determinants of tumorigenicity and malignant progression.
