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Showing papers by "Saraswati Sukumar published in 1986"


Journal ArticleDOI
TL;DR: Results indicated that the mutation activation of Harvey ras-1 oncogenes was specific to dimethylbenzanthracene treatment in the mouse mammary tumor system.
Abstract: Genomic DNAs from dimethylbenzanthracene-induced BALB/c mouse mammary tumors arising from the transplantable hyperplastic outgrowth (HPO) line designated DI/UCD transformed NIH 3T3 cells upon transfection. Transforming activity was attributed to the presence of activated Harvey ras-1 oncogenes containing an A----T transversion at the middle adenosine nucleotide in codon 61. DNAs from untreated DI/UCD HPO cells and radiation-induced and spontaneous mammary tumors from the DI/UCD HPO line failed to transform NIH 3T3 cells. The results indicated that the mutation activation of Harvey ras-1 oncogenes was specific to dimethylbenzanthracene treatment in the mouse mammary tumor system.

113 citations


Book ChapterDOI
TL;DR: Observations of ras oncogenes known to efficiently induce tumors in animals upon incorporation into retrovial vectors cannot be considered as sufficient evidence to establish a causal relationship between oncogene activation and the onset of human malignancies.
Abstract: Accumulating evidence indicates that oncogene activation is intimately associated with the development of at least certain human cancers. Genes capable of inducing malignant transformation of normal, non-tumorigenic cells in culture have been identified in a significant fraction of human tumors (for a review, see Ref. 1). Most of these transforming genes are members of the ras gene family,2–5 which are known to acquire their neoplastic properties by single point mutations within their coding sequences.6–8 Recent studies have demonstrated that these critical mutations are somatic events associated with tumor development.9 Furthermore, ras oncogenes are known to efficiently induce tumors in animals upon incorporation into retrovial vectors.10–15 Yet these observations cannot be considered as sufficient evidence to establish a causal relationship between oncogene activation and the onset of human malignancies.

9 citations