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The basis of the tumorigenicity of BHK 21 cells
Author(s) -
Jarrett Oswald,
Macpherson Ian
Publication year - 1968
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910030514
Subject(s) - polyoma virus , in vitro , biology , virus , cloning (programming) , cell culture , cell , baby hamster kidney cell , phenotype , tumor cells , virology , microbiology and biotechnology , cancer research , genetics , gene , computer science , programming language
BHK 21/13 cells, 50 generations from cloning, are transplantable owing to the presence of a small proportion (about 0.001%) of highly tumorigenic variant cells. Non‐tumorigenic cells can easily be isolated from these stocks by recloning. With passage in vitro the proportion of tumorigenic variants can increase to over 90%. This may be due to any or all of three situations: 1) the appearance of many different new tumorigenic variants, 2) the selection of the initially observed variant cells because of their greater capacity for growth in culture, or 3) the presence of a replicating agent transmitted from a variant to other cells. Means by which the increase in the proportion of variants might be minimized are discussed. In contrast to BHK 21/13 cells in early passage, their polyoma‐transformed derivatives are highly tumorigenic. Polyoma virus does not selectively transform existing tumorigenic variant cells; thus, the tumorigenicity of the transformed cells is a consequence of the virus‐cell interaction.