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Oncogenic mutations of -Gi2 protein are not determinant for human adrenocortical tumourigenesis

Gicquel C, Dib A, Bertagna X, Amselem S, Le Bouc Y. Oncogenic mutations of -Gi2 protein are not determinant for human adrenocortical tumourigenesis. Eur J Endocrinol 1995:133:166–72. ISSN 0804–4643

Activating mutations of G proteins, which are membrane signal transducers, have been associated recently with the development of various endocrine neoplasms. Mutations of two highly conserved codons, Arg²⁰¹ and Gin²²⁷, in the -subunit of the Gs protein, the adenylyl cyclase-stimulating protein, were first described in growth hormone-producing pituitary tumours. They resulted in constitutive activation of the s-subunit by decreasing intrinsic GTPase activity. A similar mutation, affecting codon Arg¹⁷⁹ (exon 5) in the -subunit of the Gi2 protein, the adenylyl cyclase-inhibiting protein, has been described by a single group in ovarian and adrenocortical tumours. We evaluated the frequency of activating mutations in the -subunit of the Gi2 protein in 18 human adrenocortical tumours. We screened exons 5 (codon Arg¹⁷⁹) and 6 (codon Gln²⁰⁵) for mutations by denaturing gradient gel electrophoresis analysis of leucocyte and tumoural DNA. No abnormal migration pattern was found in either exon. The absence of mutation in exon 5, which includes the Arg¹⁷⁹ codon, was confirmed in all tumoural DNA by direct sequencing. In conclusion, we did not find any oncogenic mutations in the GTPase domain of the -subunit of the Gi2 protein in adrenocortical tumours. Thus, the previously oncogenic gip2 mutations do not appear to be determinant for adrenocortical tumourigenesis.

Christine Gicquel, Laboratoire d'Explorations Fonctionnelles Endocriniennes, Hôpital Trousseau, 26 Avenue Arnold Netter, 75012 Paris, France

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