Characterization of FAMPAC, a newly identified human pancreatic carcinoma cell line with a hereditary background

✍ Scribed by Sven Eisold; Eduard Ryschich; Michael Linnebacher; Thomas Giese; Dirk Nauheimer; Anja Wild; Detlef K. Bartsch; Markus W. Büchler; Jan Schmidt

• Publisher: John Wiley and Sons
• Year: 2004
• Tongue: English
• Weight: 743 KB
• Volume: 100
• Category: Article
• ISSN: 0008-543X
• DOI: 10.1002/cncr.20193

✦ Synopsis

Abstract

BACKGROUND

A novel pancreatic carcinoma cell line, FAMPAC, was identified from investigation of poorly differentiated pancreatic adenocarcinoma cells found in a patient with a familial predisposition to pancreatic carcinoma. A gene responsible for familial pancreatic carcinoma has not been identified to date.

METHODS

The FAMPAC cell line was characterized by its morphology, growth rate, tumorigenicity, and chromosomal analysis. Three known tumor suppressor genes, p16/CDKN2, BRCA2, and p53, all of which are important in the development of pancreatic carcinoma and frequently are involved in a variety of cancer syndromes, were analyzed.

RESULTS

FAMPAC cells grew as an adhering monolayer in culture medium supplemented with 10% fetal bovine serum and formed tumors rapidly in nude mice. The doubling time ranged from 24 to 48 hours. Karyotype analysis demonstrated the complexity of chromosomal deletions and rearrangements. The cells were negative for ductal differentiation markers such as cytokeratin 7 and MUC1, indicating poor differentiation. Analysis of FAMPAC cells revealed overexpression of the mutated p53 gene (exon 5, codon 175: CGC → CAC), the presence of a homozygous deletion in the p16 gene, and the presence of wild‐type BRCA2 in the tested hot spots.

CONCLUSIONS

To the authors' knowledge, FAMPAC is the first established human pancreatic carcinoma cell line associated with a familial background. FAMPAC is a tumorigenic cell line with a complex molecular pattern of mutations. These findings may be useful in understanding the mechanisms responsible for the development of sporadic or hereditary forms of pancreatic carcinoma. Cancer 2004. © 2004 American Cancer Society.