Literature DB >> 7728976

Differences in molecular biological, biological and growth characteristics between the immortal and malignant hamster pancreatic cells.

T Takahashi1, M P Moyer, M Cano, Q J Wang, C P Mountjoy, W Sanger, T E Adrian, H Sugiura, H Katoh, P M Pour.   

Abstract

We compared morphological, biological and molecular biological patterns of a newly established, spontaneously immortalized pancreatic ductal cell line, TAKA-1, with a hamster pancreatic ductal adenocarcinoma cell line, PC-1. PC-1 cells grew in a monolayer on plastic tissue culture flasks, whereas TAKA-1 cells required type I collagen gel matrix to propagate. The growth rate and argyrophilic nuclear organizer region (Ag-NOR) counts were greater in PC-1 cells than in TAKA-1 cells. More TAKA-1 cells were in G0/G1 and less were in the S cell cycle phase than PC-1 cells. Karyotypically, the consistent change in TAKA-1 cells was an abnormal no. 3 chromosome, whereas additional chromosomal abnormalities were found in PC-1 cells. Ultrastructurally, TAKA-1 cells formed ductal structures and were composed of two types of cells, as in the normal hamster pancreatic ducts, whereas PC-1 cells were pleomorphic, showed evidence for loss of differentiation and contained intracytoplasmic lumens. Unlike the PC-1, TAKA-1 cells did not show a point mutation at codon 12 in the c-Ki-ras oncogene and did not grow in soft agar. Receptor binding assay showed specific epidermal growth factor binding to both cell lines, but secretin binding only to TAKA-1 cells. Both cells produced and released transforming growth factor-alpha in serum-free medium. Both cell lines expressed blood group A antigen, carbonic anhydrase, coexpressed cytokeratin and vimentin, and reacted with tomato and Phaseolus vulgaris leucoagglutinin (L-PHA) lectins. The results demonstrate that chromosomal abnormalities, cell cycle patterns, expression of cytokeratin 18, lectin bindings and the c-Ki-ras mutation are the features that distinguish the benign from the malignant pancreatic ductal cells in Syrian hamster.

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Year:  1995        PMID: 7728976     DOI: 10.1093/carcin/16.4.931

Source DB:  PubMed          Journal:  Carcinogenesis        ISSN: 0143-3334            Impact factor:   4.944


  6 in total

1.  Culture of human main pancreatic duct epithelial cells.

Authors:  D Oda; C E Savard; T D Nguyen; E R Swenson; S P Lee
Journal:  In Vitro Cell Dev Biol Anim       Date:  1998-03       Impact factor: 2.416

2.  Experimental evidence for the origin of ductal-type adenocarcinoma from the islets of Langerhans.

Authors:  P M Pour; L Weide; G Liu; K Kazakoff; M Scheetz; I Toshkov; Y Ikematsu; M A Fienhold; W Sanger
Journal:  Am J Pathol       Date:  1997-06       Impact factor: 4.307

3.  In vitro induction of giant cell tumors from cultured hamster islets treated with N-Nitrosobis(2-Oxopropyl)amine.

Authors:  H Matsuzaki; B M Schmied; A Ulrich; S K Batra; P M Pour
Journal:  Am J Pathol       Date:  2000-02       Impact factor: 4.307

4.  Localization of galectin-3 in normal and diseased pancreatic tissue.

Authors:  C Schaffert; P M Pour; W G Chaney
Journal:  Int J Pancreatol       Date:  1998-02

5.  The role of pancreatic islets in experimental pancreatic carcinogenicity.

Authors:  O Ishikawa; H Ohigashi; S Imaoka; I Nakai; M Mitsuo; L Weide; P M Pour
Journal:  Am J Pathol       Date:  1995-11       Impact factor: 4.307

Review 6.  What is the origin of pancreatic adenocarcinoma?

Authors:  Parviz M Pour; Krishan K Pandey; Surinder K Batra
Journal:  Mol Cancer       Date:  2003-01-22       Impact factor: 27.401

  6 in total

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