Education & Training
- B.Sc., Molecular Biology, University of Umea, Sweden, 1994
- Ph.D., Developmental Biology, University of Goteborg, Sweden, 2000
- Postdoctoral Fellow, Johns Hopkins University, Baltimore, MD, 2001-2005
- Instructor, Johns Hopkins University, Baltimore, MD, 2005-2006
- Assistant Professor, University of Pittsburgh, Pittsburgh, PA, 2006-2015
- Associate Professor, University of Pittsburgh, Pittsburgh, PA, 2015-Present
Research Interest Summary
My lab studies pancreatic regeneration and cancer. Both tissue regeneration and cancer rely on complexinteractions between cells that provide necessary signals for each process, and cells that are receptive tothose signals. We have shown that the influx of macrophages during pancreatic regeneration not onlyserves to debride the site of injury, but it is also critical for creating microenvironments for cell-specificdifferentiation.
In my lab, we also study a population of progenitor-like cells, which is highly abundant in the regeneratingmouse pancreas. More importantly, we have identified similar population in the adult human pancreas,which expand significantly in both chronic pancreatitis and Type 1 diabetic patients. Our lineage tracingstudies show that while these cells under certain conditions can give rise to acinar- and β-cells, upononcogenic Kras activation, transform to premalignant lesions to pancreatic invasive ductaladenocarcinoma.
Pancreatic ductal adenocarcinoma is an almost uniformly fatal disease. Recent studies have suggestedthat it takes about 17 years from the time of tumor initiation to the time of patient’s death. This timelineoffers opportunities for early detection and intervention. Our goal is to better understand thetransformation of noninvasive precursor lesions to invasive ductal adenocarcinomas.
Eisses J.F., Criscimanna A., Orabi A.I., Javed TA., Sarwar S., Dionise Z.R., Davis AW., Burak Tosun A.,Ozolek J.A., Lowe M.E., Monga S.P.S., Rohde G.K., Esni F.*, Husain S.Z* (2015).Valporic acid limitspancreatic recovery following pancreatitis by inhibiting HDACs and preventing acinar redifferentiationprograms. Am J Pathol. 185(12):3304-15. *Shared senior authorship.
Criscimanna A., Coudriet G.M., Gittes, G.K., Piganelli J.D., and Esni F (2014). Activated macrophagescreate lineage-specific microenvironments for pancreatic acinar- and β-cell regeneration in mice. Gastroenterology, 147:1106-1118.
Criscimann A., Duan L.J., Rhodes J.A., Fendrich V., Wickline E., Hartman D.J., Monga P.S., Lotze M.T.,Gittes G.K., Fong G.H., and Esni F. (2013). PanIN-specific regulation of Wnt signaling by HIF2α duringearly pancreatic tumorigenesis. Cancer Research, 73 (15): 4781-90.
Rhodes J.A., Criscimanna A., and Esni F. (2012). Induction of mouse pancreatic ductal differentiation,an in vitro assay. In Vitro Cell & Dev. Bio.-Animal, 48 (10): 641-649.
Criscimanna A., Speicher J.A., Houshmand G., Shiota C., Prasadan K., Baoan Ji, Logsdon C., Gittes G.K.,and Esni F. (2011). Duct cells contribute to regeneration of endocrine and acinar cells followingpancreatic damage in adult mice. Gastroenterology 141:1451-1462.
Chen H., Houshmand H., Mishra S., Fong G.H, Gittes G.K., and Esni F. (2010). Impaired pancreaticdevelopment in Hif2-alpha deficient mice. BBRC, 399:440-445.
Habbe N., Shi G., Meguid R.A, Fendrich V., Esni F., Chen H., Feldmann G., Konieczny S.F., Leach S.D.,and Maitra A. (2008). Spontaneous induction of murine pancreatic intraepithelial neoplasia (mPanIN)by acinar targeting of oncogenic Kras in adult mice. PNAS, 105 (48):18913-8.
Esni F.*, Fendrich V.*, Garay M., Feldman G., Nygard Jensen J., Dor Y., Stoffers D., Jensen J., LeachS. D., and Maitra A. (2008). Hedgehog signaling is required for effective regeneration of exocrinepancreas. Gastroenterology 135: 621-631.
Esni F., Ghosh B., Biankin A.V., Lin J.W., Albert M.A., Yu X., MacDonald R.J., Civin C.I., Real F.X., BallD.W., and Leach S.D. (2004). Notch inhibits PTF1 function and acinar cell differentiation in developingmouse and zebrafish pancreas. Development 131: 4213-4224.
Esni F., Stoffers D.A., Takeuchi T., and Leach S.D. (2004). Origin of exocrine pancreatic cells fromnestin-positive precursors in developing mouse pancreas. Mech Dev. 121: 15-25.