Abstract
It is widely accepted that tumor development and progression are due to illegitimate activation of cellular oncogenes by point mutation, retroviral insertion, chromosomal translocation and amplification or deletion of the gene [1–3]. Nonrandom deletions of chromosomal regions 13q14 and 11q13 have been detected in retinoblastoma [1] and Wilm’s tumor [2, 3]. It has been proposed that these rare childhood cancers result from the deletion of dominant-acting genes, permitting the expression of tumorigenic recessive alleles [1], Moreover, restriction fragment length polymorphism (RFLP) analysis has demonstrated loss of H-rasI oncogene allele (chromosome llp15) in primary bladder, breast, ovarian, and lung carcinomas [4–7].
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© 1992 Springer-Verlag Berlin Heidelberg
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Knyazev, P.G. et al. (1992). Molecular Mechanism of Alteration of H-RasI Oncogene in Human Breast Carcinomas: G to T Transversion in 12th Codon of the Undeleted Allele in the Case of the Loss of the Other Gene Allele. In: Neth, R., Frolova, E., Gallo, R.C., Greaves, M.F., Afanasiev, B.V., Elstner, E. (eds) Modern Trends in Human Leukemia IX. Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, vol 35. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76829-3_40
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DOI: https://doi.org/10.1007/978-3-642-76829-3_40
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