Reference List

Notes: Three human pancreatic cancer cell lines, designated as KP-1N, KP-2 and KP-3 have been established in both tissue cultures and in nude mice. The KP-1N and KP-3 tumors were obtained from liver metastases of pancreatic tumors and the KP-2 tumors was of primary pancreatic origin. The patients' tumors from which KP-1N and KP-2 were derived showed characteristics of adenocarcinoma, and the KP-3 tumor had adenosquamous carcinoma characteristics. Inoculations of samples from surgical specimens into athymic nude mice resulted in tumor formation, with the tumors histologically closely resembling the original neoplasms. Subcutaneous injections of the established cell lines also induced tumor formation and the tumors histologically resembled the original lesion in the cases of KP-2 and KP-3 tumors, but the KP-1N tumors in the mice were histologically different from the surgical specimen. The KP-1N, KP-2 and KP-3 cell lines have been cultured continuously in a medium supplemented with 10% fetal calf serum for more than 20, 21 and 17 months, respectively. The KP-2 and KP-3 cell lines produced and released carbohydrate antigen 19-9 into the spent medium but the KP-1N cell line did not. KP-1N and KP-3, produced liver metastases after intrasplenic injection into nude mice, whereas KP-2 produced few liver colonies. Cell lines highly metastatic to the liver, KP-1NLs and KP-3Ls, were isolated from the liver colonies of KP-1N and KP-3, respectively. PMID: 2172194
Reference ID: 5090

Notes: Alterations of the p53 and Ki-ras genes were examined in 12 human pancreatic cancer-derived cell lines with different metastatic potential. Point mutations of the Ki-ras gene at codon 12 were found in 10 out of 12 cell lines (83%), while abnormalities of the p53 gene were identified in 8 out of 12 cell lines (67%) which included point mutations (n=7) and one base deletein (n=1). The comparison between alterations of the Ki-ras gene or p53 gene were noted among the cell lines with increased metastatic potential and their parental cell lines. These findings suggest that alterations of the p53 gene, like the Ki-ras gene is a frequent event in pancreatic cancer, and could contribute cooperatively in the onco genic steps of pancreatic cancer. It is also suggested that the genetic changes of the p53 and Ki-ras genes are not substantially associated with the metastatic potential in pancratic cancer.
Reference ID: 5092

Notes: Various genetic changes are involved in progression of various cancers. We examined alterations (deletion, sequence abnormalities, methylation) of the CDKN2A gene in cell lines and tumor tissues of pancreatic cancers. Some alterations of this gene were found in all the 12 cell lines examined. In the primary lesions of pancreatic cancers, homozygous or hemizygous deletion were found in 8 of 24 ductal carcinoma and 4 of 9 other types of carcinomas. It appears that there is an association between the alteration of this gene and tumor size, regional lymph node metastasis and hematogenous distant metastasis in the ductal carcinoma, but not in the other types of carcinomas. All the 5 liver metastatic lesions of the ductal carcinoma examined revealed homozygous or hemizygous deletion and 3 bp deletion. These results suggest that inactivation of the CDKN2A gene occurs more frequently in cell lines than in pancreatic cancer tissues. Such genetic events on the CDKN2A gene may play an important role possibly at a later step in the progression of pancreatic ductal carcinoma. PMID: 9735394
Reference ID: 5091