Five primary human pancreatic adenocarcinoma cell lines established by the outgrowth method

F Rückert, D Aust, I Böhme, K Werner, A Brandt… - Journal of Surgical …, 2012 - Elsevier
F Rückert, D Aust, I Böhme, K Werner, A Brandt, EP Diamandis, C Krautz, S Hering…
Journal of Surgical Research, 2012Elsevier
BACKGROUND: Pancreatic ductal adenocarcinoma is an aggressive tumor; treatment
remains a challenge because of the lack of effective therapeutic strategies. Basic research in
this field is dependent on the availability of model systems. New pancreatic cancer cell lines
are therefore important for the study of its biology. In the present study, we report the
establishment and characterization of five new pancreatic cancer cell lines (PaCaDD-43,-60,-
119,-135,-137). MATERIAL AND METHODS: All cell lines were derived from pancreatic …
BACKGROUND
Pancreatic ductal adenocarcinoma is an aggressive tumor; treatment remains a challenge because of the lack of effective therapeutic strategies. Basic research in this field is dependent on the availability of model systems. New pancreatic cancer cell lines are therefore important for the study of its biology. In the present study, we report the establishment and characterization of five new pancreatic cancer cell lines (PaCaDD-43, -60, -119, -135, -137).
MATERIAL AND METHODS
All cell lines were derived from pancreatic ductal adenocarcinomas by the Dresden outgrowth protocol. The five cell lines originated from primary pancreatic tumors, lymph node metastases, or malignant pleural effusions. We characterized the cell lines by examining their morphology and their cytostructural and functional profiles.
RESULTS
All cell lines grew as adherent monolayers and were cultured in optimized Dresden-medium. The doubling time ranged from 22 to 47 h. v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations were detected in four of the five cell lines. KRAS mutations were identical between each primary tumor and the cell line derived from it. Immunohistochemical staining showed cytoplasmic expression of CK8/18, mostly membrane and partially cytoplasmic expression of E-cadherin and strong expression of ezrin in all cell lines. Three cell lines showed nuclear p53 accumulation and heterogeneous expression of vimentin. SMAD4 was heterogeneously expressed in four of the cell lines.
CONCLUSIONS
We were able to establish five new primary pancreatic carcinoma cell lines. As applicable tools for basic research, these cell lines might contribute to a better understanding and treatment of this aggressive tumor.
Elsevier