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A potential motor neurone-specific monoclonal antibody (MN-1)

Rogers, A.T., Harrison, R., Blaydes, J., Barnes, J. and Lunt, G.G. (1991) A potential motor neurone-specific monoclonal antibody (MN-1) Oncogene, 19, (3), pp. 49-59.

Record type: Article


Using the thyroid as a model of multistep epithelial tumorigenesis, we have used representative cell lines to correlate the degree of malignant transformation with the functional status of p53 and the integrity of cell-cycle check-points. Three distinct phenotypes were observed: Type I lines, derived from poorly-differentiated human thyroid cancers, expressed high levels of mutant p53 protein; Type II, also poorly-differentiated but derived from rat, showed over-expression of wild-type (wt) p53 with marked cell-cell heterogeneity: Type III, from well-differentiated human cancers, contained uniformly low levels of wt p53. All cell lines containing wt p53 retained a near-normal induction of p53 by DNA damage. However, the ability to undergo growth arrest differed strikingly. Whereas Type I and II lines had lost both G2/M and G1/S check points, Type III cells retained both. In Type III cells, as in diploid human fibroblasts, mutant p53 expression specifically abrogated G1/S check-point function with no other change in phenotype. These data demonstrate 3 mechanisms for evasion of p53 growth control: (i) direct mutation (ii) indirect inactivation, or (iii) 'avoidance' of activation, most probably due to failure to reach a critical threshold of DNA damage.

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Published date: August 1991


Local EPrints ID: 150595
ISSN: 0950-9232
PURE UUID: 0b88cd31-a643-45bb-a8b7-e0075cb71ca7

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Date deposited: 20 Jul 2010 15:45
Last modified: 18 Jul 2017 12:57

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Author: A.T. Rogers
Author: R. Harrison
Author: J. Blaydes
Author: J. Barnes
Author: G.G. Lunt

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