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Preferential Loss of Heterozygosity of Chromosome 7 Loci in Simian Virus 40 t/T Antigen-Induced Mouse Hepatocellular Carcinomas Does Not Involve H-ras Muatations

Published online by Cambridge University Press:  01 August 2014

S. Casola
Affiliation:
Center of Experimental Endocrinology and Oncology, CNR, Department of Molecular Cellular Biology and Pathology, University of Naples, Naples, Italy
M. Vernucci
Affiliation:
Center of Experimental Endocrinology and Oncology, CNR, Department of Molecular Cellular Biology and Pathology, University of Naples, Naples, Italy
P. Ungaro
Affiliation:
Center of Experimental Endocrinology and Oncology, CNR, Department of Molecular Cellular Biology and Pathology, University of Naples, Naples, Italy
C.B. Bruni
Affiliation:
Center of Experimental Endocrinology and Oncology, CNR, Department of Molecular Cellular Biology and Pathology, University of Naples, Naples, Italy
A. Riccio*
Affiliation:
Center of Experimental Endocrinology and Oncology, CNR, Department of Molecular Cellular Biology and Pathology, University of Naples, Naples, Italy
*
Centro di Endocrinologia ed Oncologia Sperimentale, CNR; Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli “Federico II”, via Pansini 5, 80131, Naples, Italy

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Genetic complementation experiments have indicated that both a maternal and a paternal copy of the distal region of mouse chromosome 7 are essential for normal development [1]. This suggested the presence of genes whose expression is dependent on the gamete of origin in this chromosomal region. Two such imprinted genes, namely insulin-like growth factor II (Igf2) and H19, have been identified so far [2, 3]. The first encodes a peptide with mitotic activity towards several cell types, that contributes significantly to prenatal growth of mammals, whereas the second has, as yet, no defined role and seems not to encode any protein, but works as RNA. (Igf2) and H19 are located 90 kb apart, have similar expression patterns during development and are reciprocally imprinted, since the maternal Igf2 and the paternal H19 alleles are inactive in most fetal tissues [4, 5].

Type
Research Article
Copyright
Copyright © The International Society for Twin Studies 1996

References

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