Pancreatic cancer is the fourth commonest cause of cancer death in North America and has one of the worst prognoses.1 Greater than 90% of these tumors arise from the pancreatic duct epithelium. These tumors are highly metastatic and only 20% of the patients are treated by surgical resection.2 Even when the primary tumor is small and localized, the prognosis remains poor and chemotherapy or radiotherapy has demonstrated limited effectiveness.3,4 Therefore, it seems that a significant improvement in pancreatic cancer mortality depends on the development of better treatment and preventive strategies, which require knowledge on the molecular biology and pathogenesis of this disease. Recent definitions of genetic changes that occur commonly in pancreatic cancer represent important first steps toward such a goal. 5Nevertheless, the availability of dynamic models remains crucial to the study and understanding of the biological significance of these genetic changes, especially in the context of pancreatic duct epithelial cell carcinogenesis.Our laboratory has previously reported the establishment of primary and immortal epithelial cell lines from normal human pancreatic ducts. 6 We also reported that in comparison with the pancreatic cancer cell lines, the human pancreatic duct epithelial (HPDE) cells demonstrated a gene expression pattern that more consistently resembled the phenotype of normal cells rather than cancerous duct cells in vivo.7 These similarities included relatively low expression levels of various tyrosine kinase receptors, a wild-type Ki-ras genotype, and the retention and expression of p16INK4A gene. We have subsequently isolated several clones of these cell lines. We report here the phenotypic and genotypic characteristics of two of these cell lines that demonstrate anchoragedependent growth requirement and that are nontumorigenic in immune-deficient mice.

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In this small study, a combinatorial analysis using SKY, CGH, and microarray provides a model linking the changes in gene expression to changes in chromosomal dosage and structure. This approach has identified a subset of genetic changes that provide new opportunities for investigating the genetic basis of tumorigenesis in HNSCC.