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Cell and Molecular Biology Graduate Group


Ben Stanger, MD, PhD
Assistant Professor of Medicine
Assistant Investigator, Abramson Family Cancer Research Institute

Cancer Biology Program


Address

512 Biomedical Rsch Bldg II/III (Office)
527 Biomedical Rsch Bldg II/III (Lab)
421 Curie Boulevard
Philadelphia, PA 19104-6160

Office tel.: 215-746-5560
E-mail: bstanger@mail.med.upenn.edu

Link(s)

Abramson Family Cancer Research Institute
Division of Gastroenterology
Penn Digestive Disease Center

Education

MIT: SB (Life Sciences), 1988.

Harvard Medical School: PhD (Genetics), 1997.

Harvard Medical School: MD (Medicine), 1997.

University of California, San Francisco (Internal Medicine Residency), 1997-1999.

Massachusetts General Hospital/Harvard University (GI Fellowship), 1999-2003.

Research Interests

  • Organogenesis
  • Stem Cells
  • Pancreatic Cancer
  • Regulation of Organ Size

Key words: Cancer cell of origin, Notch, stem cells, development

PubMed Search
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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.

Recent Publications

Stanger, B.Z., Datar, R., Murtaugh, L.C., and Melton, D.A. (2005). Direct regulation of intestinal fate by Notch. Proc. Natl. Acad. Sci. USA. 102, 12443-12448.

Stanger, B.Z., Stiles, B., Lauwers, G.Y., Bardeesy, N., Mendoza, M., Wang, Y., Greenwood, A., McLaughlin, M., Brown, D., DePinho, R.A., Wu, H., Melton, D.A., and Dor, Y. (2005). Pten constrains centroacinar cell expansion and malignant transformation in the pancreas. Cancer Cell. 8, 185-195.

Hezel, A.F., Kimmelman, A.C., Stanger, B.Z., Bardeesy, N., and DePinho, R.A. (2006). Genetics and biology of pancreatic ductal adenocarcinoma. Genes and Dev. 20, 1218-49.

Xu, Y., Wang, S., Zhang, J., Zhao, A., Stanger, B.Z., and Gu, G. (2006). The fringe molecules induce endocrine differentiation in embryonic endoderm by activating cMyt1/cMyt3. Dev. Biol. 297, 340-349.

Stanger, B.Z., Tanaka, A.J., and Melton, D.A. (2007). Organ size is limited by the number of embryonic progenitor cells in the pancreas but not the liver. Nature. 445, 886-91.

LAB

Rotation Projects

  • Determinants of organ size in the developing and regenerating pancreas and liver

  • Role of Notch signaling in the development of endoderm-derived organs

  • Lab Personnel

    Ben Stanger, Principal Investigator
    Tao Gao, Postdoctoral Fellow
    Anica Law, Medical Student
    Matthew LeBoeuf, Combined Degree Student
    Archana Panikkar, Lab Manager
    Andrew Rhim, Postdoctoral Fellow
    Xiaoyi Sheng, Research Specialist
    Yiwei Zong, Graduate Student

     
    last updated 7/2007
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