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Identification of a Putative Tumor Suppressor Gene Rap1GAP in Pancreatic Cancer

Departments of ¹ Surgery, ² Internal Medicine, ³ Pathology, ⁴ Oral Medicine, and ⁵ Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan; Departments of ⁶ Cancer Biology and ⁷ Medical Oncology, University of Texas M.D. Anderson Cancer Center, Houston, Texas

Requests for reprints: Diane M. Simeone, University of Michigan Medical Center, TC 2922D, Box 0331, 1500 East Medical Center Drive, Ann Arbor, MI 48109. Phone: 734-615-1600; Fax: 734-936-5830; E-mail: simeone{at}umich.edu.

Human chromosome 1p35-p36 has long been suspected to harbor a tumor suppressor gene in pancreatic cancer and other tumors. We found that expression of rap1GAP, a gene located in this chromosomal region, is significantly down-regulated in pancreatic cancer. Only a small percentage of preneoplastic pancreatic intraductal neoplasia lesions lost rap1GAP expression, whereas loss of rap1GAP expression occurred in 60% of invasive pancreatic cancers, suggesting that rap1GAP contributes to pancreatic cancer progression. In vitro and in vivo studies showed that loss of rap1GAP promotes pancreatic cancer growth, survival, and invasion, and may function through modulation of integrin activity. Furthermore, we showed a high frequency of loss of heterozygosity of rap1GAP in pancreatic cancer. Collectively, our data identify rap1GAP as a putative tumor suppressor gene in pancreatic cancer. (Cancer Res 2006; 66(2): 898-906)

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