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Date: 20-11-2020
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Ehrlich Cells
1. Origin
Ehrlich cells, more properly known as Ehrlich–Lettre ascites carcinoma, were originally established as an ascites tumor of mice (1) from Ehrlich's “Strain 7” transplantable mouse carcinoma (2), which was probably of mammary origin. Several successful attempts at tissue culture have been performed, the earliest being hanging drop preparations that were passaged for 12 years (3). Subsequently, several other laboratories have cultured Ehrlich's cells (4-9), but the cell line that has been used most frequently, and which is lodged in the American Type Culture Collection (ATCC) repository as ATCC CCL-77, is the Strain E of Ehrlich–Lettre ascites (10). These cells were established as a monolayer from a 7-day-old tumor in NCTC 109 culture medium with 10% calf serum, and subcultured by scraping. The culture lodged with ATCC has been maintained in a later modification of NCTC 109, NCTC 135 supplemented with fetal calf serum.
2. Properties
Strain E has a short population doubling time in vitro: 20–24 h in Strain E and 14–16 h in Strain E (4) . Strain E(4) was derived from alternate in vitro and in vivo passage, adapts rapidly to culture following in vivo passage, and is, presumably, the strain that was submitted to ATCC. The cells tend to have a fusiform morphology in vitro, suggesting an undifferentiated phenotype, and have a hyperdiploid karyotype (modal number 44, 2C = 40) with distinctive A chromosome, metacentric, and minute markers.
3. Usage
The Ehrlich ascites became popular because it could be expanded manyfold by in vivo passage, making it useful for biochemical studies involving large amounts of tissue, while it could still be maintained in vitro for more physiologically controlled studies. With the advent of large-scale cell culture techniques that can yield 109–1012 cells, ascites passage is less attractive, due to the contamination of the tumor with a variety of host inflammatory cells and the development of legislation limiting the use of ascites tumors.
References
1. H. Lowenthal and G. Jahn (1932) Z. Krebsforsh. 37, 439–447.
2. P. Ehrlich and H. Apolant (1905) Berl. Klin. Wehr. 42, 871–874.
3. A. Fisher and F. Davidsohn (1939) Nature (Lond.) 143, 436–437.
4. G. E. Foley, B. P. Drolet, R. E. McCarthy, K. A. Goulet, J. M. Dokos, and D. A. Filler (1960( Cancer Res. 20, 930–939.
5.M. M. Guerin and J. F. Morgan (1961) Cancer Res. 21, 378–382.
6. J. O. Ely and J. H. Gray (1960) Cancer Res. 20, 918–922.
7. R. Cailleau and F. Costa (1961) J. Natl. Cancer Inst. 26, 271–282.
8. P. W. Jackson, N. Giuffre, and D. Perlman (1960) Can. J. Biochem. Physiol. 38, 1377–1378.
9. J. A. DiPaolo (1962) Proc. Soc. Exp. Biol. Med. 109, 616–618.
10. C. Boone, M. Sasaki, and R. W. McKee (1965) Characterization of an in vitro strain of EhrlichLettre ascites carcinoma subjected to many periodic mouse passages. J. Natl. Cancer Inst. 34, 725–730. References
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