ABSTRAK

Jody Hernanto, Ida BagusBudhi Surya Adyana
Digestive Surgery Division of, drMoewardi General Hospital, SebelasMaret University, Solo, Indonesia.
Background
Pancreatic carcinoma is highly invasive and resistant to conventional chemotherapy by producing solid stroma, rich in collagen fibers, extracellular matrix proteins, fibroblasts and inflammatory cells called desmoplastic reactions that form the barrier, so that pancreatic carcinoma becomes the most resistant cancer to chemotherapy.
Objective
In insilico, Brusein D (BD) ligand is highly toxic to pancreatic carcinoma cells compared to Gemcitabine (G). Research needs to be done to prove the ability of BD ligand to inhibit proliferation and induce apoptosis of pancreatic carcinoma cells and suppress mutant p53 protein expression in invitro.
Methods
A cytotoxicity test was performed on PANC-1 pancreatic cancer cells to search for LC50 from BD ligand and G. After LC50 was determined immunohistochemicaltest with concentration of half LC50, LC50 and twice LC50 then mutant p53 expression was shown in percentage of cells.
Results
LC50 of BD ligand is 28,86?l/ml and LC50 G is 1,455,55?g/ml. At the highest concentration of 20?l/ml BD ligand inhibited cancer cell proliferation 25.258%, while G at the highest concentration of 300 ?g/ml was able to inhibit 2.06%. On the kruskalwallis statistic test p = 0,000 (p <0>Conclusions
The potential inhibition of mutant p53 expression of PANC-1 pancreatic cancer cells by invading BD ligand shows a significant difference with G.