Ben Z. Stanger, M.D., Ph.D.
Assistant Professor of Medicine
Division of Gastroenterology
Division of Gastroenterology
Department: Medicine
Graduate Group Affiliations
Contact information
Abramson Family Cancer Research Institute
Department of Cancer Biology
University of Pennsylvania School of Medicine
512 Biomedical Rsch Bldg II/III (Office)
527 Biomedical Rsch Bldg II/III (Lab)
421 Curie Boulevard
Philadelphia, PA 19104
Department of Cancer Biology
University of Pennsylvania School of Medicine
512 Biomedical Rsch Bldg II/III (Office)
527 Biomedical Rsch Bldg II/III (Lab)
421 Curie Boulevard
Philadelphia, PA 19104
Office: 215-746-5560
Fax: 215-573-2486
Fax: 215-573-2486
Email:
bstanger@mail.med.upenn.edu
bstanger@mail.med.upenn.edu
Publications
Education
SB (Life Sciences)
MIT, 1988.
MD (Medicine)
Harvard Medical School, 1997.
PhD (Genetics)
Harvard Medical School, 1997.
SB (Life Sciences)
MIT, 1988.
MD (Medicine)
Harvard Medical School, 1997.
PhD (Genetics)
Harvard Medical School, 1997.
Post-Graduate Training
Research and Clinical Fellow in Gastroenterology, Massachusetts General Hospital, 1999-2003.
Resident in Internal Medicine, UCSF, 1997-1999.
Research Fellow in Molecular and Cellular Biology, Harvard University, 2000-2006.
Permanent linkResearch and Clinical Fellow in Gastroenterology, Massachusetts General Hospital, 1999-2003.
Resident in Internal Medicine, UCSF, 1997-1999.
Research Fellow in Molecular and Cellular Biology, Harvard University, 2000-2006.
Description of Research Expertise
Research InterestsOrganogenesis
Stem Cells
Pancreatic Cancer
Regulation of Organ Size
Key words: Cancer cell of origin, Notch, stem cells, development
Description of Research
Stem/Progenitor Cells in Development and Disease
How do internal organs achieve their remarkable structures? What determines the size of organs? How are stem cells regulated in adult solid organs? What cells give rise to cancer? During mammalian organogenesis, stem/progenitor cells and their derivatives undergo carefully controlled division, differentiation, and morphogenesis to generate complex functioning three-dimensional structures. Our laboratory uses the tools of developmental biology to address problems relevant to development, regenerative medicine and cancer. We use the mouse as a model system to genetically tag specific cellular lineages, or to alter the function of important signaling pathways. The focus is on stem cells and progenitor cells in the vertebrate liver and pancreas, essential organs with great clinical importance and a rich history in developmental biology.
Many of the mechanisms used during organ formation are also important in carcinogenesis and tissue regeneration. One hypothesis that links development and cancer is the idea that cancers originate from cells with stem-like properties. We have previously shown that Notch signaling is a key embryonic regulator of pancreatic progenitor cells, the cells that give rise to all of the mature cell types of the pancreas. Our more recent studies in a mouse model of pancreatic cancer have pointed to the potential importance of pancreatic centroacinar cells – a cell type that maintains active Notch signaling in the adult – in the pathogenesis of pancreatic cancer. Current studies are aimed at further exploring cellular lineage relationships in pancreatic cancer and regeneration and understanding the biology of the centroacinar cell, a candidate stem cell in the adult pancreas. Another area of major interest is the control of organ size. We have developed tools to determine the extent to which size is regulated versus intrinsically determined during pancreas development. Studies employing the same tools and techniques are being applied and contrasted to the developing liver. Our goal is to understand in detail how these different cell types behave during development, organ regeneration, and carcinogenesis. We hope to exploit insights gained from these studies to develop new approaches to cancer therapy and bioengineering.
Rotation Projects for 2006-2007
Several rotation projects in the areas of are available based upon applicant interests. Please contact Dr. Stanger directly to discuss potential projects.
Lab personnel:
Ben Stanger, Principle Investigator
Archana Panikkar, Research Specialist
Selected Publications
Stanger BZ: Organ size determination and the limits of regulation. Cell Cycle 7: 543-46, 2008.Dor Y, and Stanger BZ: Regeneration in liver and pancreas: Time to cut the umbilical cord? Science STKE Page: pe66, 2007.
Stanger, BZ, Tanaka, AJ, and Melton, DA: Organ size is limited by the number of embryonic progenitor cells in the pancreas but not the liver. Nature (DOI 10.1038/nature05537), 2007 Notes: Advanced online publication.
Stanger, BZ, Dor, Y: Dissecting the cellular origins of pancreatic cancer. Cell Cycle 5: 43-46, 2006.
Xu, Y, Wang, S, Zhang, J, Zhao, A, Stanger, BZ, and Gu, G: The fringe molecules induce endocrine differentiation in embryonic endoderm by activating cMyt1/cMyt3. Dev. Biol 2006.
Hezel, AF, Kimmelman, AC, Stanger, BZ, Bardeesy, N., and DePinho, RA.: Genetics and biology of pancreatic ductal adenocarcinoma. Genes and Development 20: 1218-49, 2006.
Stanger, BZ, Datar, R, Murtaugh, LC, and Melton, DA: Direct regulation of intestinal fate by Notch. Proc Natl Acad Sci USA 102: 12443-12448, 2005.
Stanger, BZ, Stiles, B, Lauwers, GY, Bardeesy, N, Mendoza, M, Wang, Y, Greenwood, A, McLaughlin, M, Brown, D, DePinho, RA, Wu, H, Melton, DA, and Dor, Y: Pten constrains centroacinar cell expansion and malignant transformation in the pancreas. Cancer Cell 8: 185-195, 2005.
Stanger BZ, and Melton DA: Development of the endodermal derivatives in lung, liver, pancreas, and gut. Epstein CJ, Erickson RP, Wynshaw-Boris A, eds. Inborn Errors of Development, Oxford University Press 2003.
Murtaugh, LC, Stanger, BZ, Kwan, KM, and Melton, DA.: Notch signaling controls multiple steps of pancreatic differentiation. Proc Natl Acad Sci USA 100: 14920-14925, 2003.
