Document Detail


Differences in molecular biological, biological and growth characteristics between the immortal and malignant hamster pancreatic cells.
MedLine Citation:
PMID:  7728976     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
T Takahashi; M P Moyer; M Cano; Q J Wang; C P Mountjoy; W Sanger; T E Adrian; H Sugiura; H Katoh; P M Pour
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Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  Carcinogenesis     Volume:  16     ISSN:  0143-3334     ISO Abbreviation:  Carcinogenesis     Publication Date:  1995 Apr 
Date Detail:
Created Date:  1995-05-30     Completed Date:  1995-05-30     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8008055     Medline TA:  Carcinogenesis     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  931-9     Citation Subset:  IM    
Affiliation:
Eppley Institute for Research in Cancer, University of Nebraska Medical Center, Omaha, USA.
Data Bank Information
Bank Name/Acc. No.:
GENBANK/S77068;  S77069
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MeSH Terms
Descriptor/Qualifier:
Adenocarcinoma / genetics,  metabolism,  pathology*
Animals
Base Sequence
Cell Adhesion / physiology
Cell Cycle / physiology
Cell Division / drug effects,  physiology
Cell Line
Cholecystokinin / metabolism
Cricetinae
Epidermal Growth Factor / pharmacology
Flow Cytometry
Gastrin-Releasing Peptide
Genes, ras
Immunohistochemistry
Karyotyping
Kinetics
Light
Mesocricetus
Microscopy
Microscopy, Electron
Molecular Sequence Data
Pancreas / cytology*,  drug effects,  physiology
Pancreatic Ducts / cytology*,  pathology
Pancreatic Neoplasms / genetics,  metabolism,  pathology*
Peptides / metabolism
Point Mutation
Secretin / metabolism
Tumor Cells, Cultured / drug effects
Chemical
Reg. No./Substance:
0/Peptides; 1393-25-5/Secretin; 62229-50-9/Epidermal Growth Factor; 80043-53-4/Gastrin-Releasing Peptide; 9011-97-6/Cholecystokinin
Comments/Corrections
Erratum In:
Carcinogenesis 1995 May;16(5):1257

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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