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Journal of Cell Science, Vol 16, 189-198, Copyright © 1974 by Company of Biologists
Submitted on February 25, 1974
1 Department of Tumour Biology, Karolinska Institutet, 104 01 Stockholm 60, Sweden
2 Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, England
Previous studies with a variety of transplantable mouse tumours showed that in hybrids between malignant and non-malignant cells, malignancy behaved as a recessive character: the hybrid cells, so long as they retained something close to the complete parental chromosome sets, had little or no ability to grow progressively in vivo. In the experiments we now describe the heritable lesions determining the malignant phenotype were further explored by complementation analysis in which the various tumour cells were fused with each other. Forty-two clonal populations derived from twelve crosses between different kinds of tumour cells were examined. Only one cross generated hybrid cells with reduced tumorigenicity: in all other cases the hybrid cells formed were highly malignant. It thus appears that, in a wide range of different tumours, the lesions determining the malignant phenotype, although recessive, fail to complement each other.
Submitted on February 25, 1974
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