| Differences in molecular biological, biological and growth characteristics between the immortal and malignant hamster pancreatic cells. | |
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MedLine Citation:
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PMID: 7728976 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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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Authors:
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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:
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Type: Comparative Study; Journal Article |
Journal Detail:
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Title: Carcinogenesis Volume: 16 ISSN: 0143-3334 ISO Abbreviation: Carcinogenesis Publication Date: 1995 Apr |
Date Detail:
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Created Date: 1995-05-30 Completed Date: 1995-05-30 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8008055 Medline TA: Carcinogenesis Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 931-9 Citation Subset: IM |
Affiliation:
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Eppley Institute for Research in Cancer, University of Nebraska Medical Center, Omaha, USA. |
| Data Bank Information | |
Bank Name/Acc. No.:
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GENBANK/S77068; S77069 |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenocarcinoma
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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:
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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:
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Carcinogenesis 1995 May;16(5):1257 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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