© 1985 Oxford University Press
research-article |
Mouse cell clones for improved quantitation of carcinogen-induced altered differentiation
1Grace Cancer Drug Center, Roswell Park Memorial Institute Buffalo, NY 14263
3Department of Genetics and Endocrinology, Roswell Park Memorial Institute Buffalo, NY 14263
4In Vitro Carcinogenesis Section, Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute Bethesda, MD 2025, USA
2To whom reprint requests should be sent
Two new mouse epidermal cell lines have been isolated and characterized as target cells for three chemical carcinogens. The ability to grow these cells at low density ( 
5 clonogenic cells/cm2) has permitted more precise quantitation of chemical carcinogen-induced changes in epidermal differentiation. The cell lines, designated 291 and 271c, retain the property previously observed in primary cultures of mouse epidermal cells, that is the regulation of terminal differentiation by extracellular Ca2+ ion. Altered response to extracellular Ca2+ after carcinogen treatment of these cells is the basis of the assay endpoint. Other normal properties demonstrated by these cells are keratin immunofluorescence patterns, ability to form cornified envelopes in response to Ca2+ and a lack of tumorigenicity. Both of the lines have high cloning efficiencies (up to 20%) and characteristic epidermal morphology. Their chromosome number, however, is near tetraploid. Dose response studies indicated an increase in colonies with altered response to Ca2+ proportional to the dose of three chemical carcinogens: DMBA 0.001 – 0.5 µg/ml x 24 h, MCA 0.01 – 5 µg/ml x 24 h and MNNG 0.01 – 0.2 µg/ml x 1 h. The optimized assay protocol has provided a reproducible means of quantitating carcinogen-altered epidermal cells relative to carcinogen dose, and of isolating cell clones for studies of altered differentiation in carcinogenesis and chemotherapy.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  E. J. Horn, A. Albor, Y. Liu, S. El-Hizawi, G. E. Vanderbeek, M. Babcock, G. T. Bowden, H. Hennings, G. Lozano, W. C. Weinberg, et al. RING protein Trim32 associated with skin carcinogenesis has anti-apoptotic and E3-ubiquitin ligase properties Carcinogenesis, February 1, 2004; 25(2): 157 - 167. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. D. Knights, Y. Liu, E. Appella, and M. Kulesz-Martin Defective p53 Post-translational Modification Required for Wild Type p53 Inactivation in Malignant Epithelial Cells with mdm2 Gene Amplification J. Biol. Chem., December 26, 2003; 278(52): 52890 - 52900. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Liu, H. Asch, and M. F. Kulesz-Martin Functional Quantification of DNA-binding Proteins p53 and Estrogen Receptor in Cells and Tumor Tissues by DNA Affinity Immunoblotting Cancer Res., July 1, 2001; 61(14): 5402 - 5406. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. M. Witkowski, G.T. Bowden, R. B. Nagle, and A. E. Cress Altered surface expression and increased turnover of the {alpha}6{beta}4 integrin in an undifferentiated carcinoma Carcinogenesis, February 1, 2000; 21(2): 325 - 330. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. L. Cmarik, H. Min, G. Hegamyer, S. Zhan, M. Kulesz-Martin, H. Yoshinaga, S. Matsuhashi, and N. H. Colburn Differentially expressed protein Pdcd4 inhibits tumor promoter-induced neoplastic transformation PNAS, November 23, 1999; 96(24): 14037 - 14042. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Wu, H. Huang, Z. Miner, and M. Kulesz-Martin Activities and response to DNA damage of latent and active sequence-specific DNA binding forms of mouse p53 PNAS, August 19, 1997; 94(17): 8982 - 8987. [Abstract] [Full Text] [PDF]
|
|