Dual evolutionary origin for the rat genetic sequences of Harvey murine sarcoma virus

Ellis, Ronald W.; DeFeo, D; Maryak, Jean; Young, Howard A.; Shih, Thomas Y.; Chang, Esther H.; Lowy, Douglas R.; Scolnick, Edward M.

doi:10.1128/jvi.36.2.408-420.1980

Cited by 347 publications

(75 citation statements)

References 43 publications

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“…To facilitate transfer to nitrocellulose in certain instances, gels were depurinated by being soaked 15 min in 0.25 N HCI 1161. As a probe for the Xbal polymorphism indicating c-Ha61 -fa5 gene activation and v-Hams gene integration, the v-Ha-ras gene purified from the BS9 plasmid [18] was radiolabeled by random priming to a specific activity of 2 x lo8 cpmipg DNA. Filters were washedtoafinalstringencyof 1 x SSCor0.5 x SSC-0.1% SDS at 68°C prior to autoradiography using Kodak X-Omat film and an intensifying screen at -70°C.…”

Section: Dna Analysismentioning

confidence: 99%

Spontaneous Ha‐ras Gene Activation in Cultured Primary Murine Keratinocytes: Consequences of Ha‐ras Gene Activation in Malignant Conversion and Malignant Progression

Greenhalgh

Welty

Strickland

et al. 1989

Molecular Carcinogenesis

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The activation of the c-Ha-ras gene and its contribution to the tumorigenic phenotype were examined in cultured mouse keratinocytes and squamous tumors using transfection into NIH 3T3 cells and nucleic acid hybridization. When normal keratinocytes were cultured in medium with 0.05 mM Ca2+ (low Ca2+ medium), many cells died within 2-3 wk, while others formed rapidly growing foci that could be subcultured. These rapidly growing cells produced benign tumors when grafted to nude mice and possessed a heterozygous mutation in the c-Ha-ras gene with an A----T transversion in codon 61. Fibroblast-conditioned low Ca2+ medium prevented cell death, focus formation, c-Ha-ras gene mutation, and tumorigenicity. Thus, suboptimal culture conditions favored a spontaneous mutation in codon 61 of the c-Ha-ras gene of keratinocytes. When a v-Ha-ras gene was introduced into normal keratinocytes by a replication-defective retrovirus, the recipient cells produced papillomas in vivo, and after 2 mo, 60% of the tumors converted to squamos cell carcinomas. None of the 22 converted tumors had an endogenous c-Ha-ras gene mutation at codon 61. However, the A----T transversion mutation developed when these carcinoma cells were cultured in low Ca2+ medium but not in fibroblast-conditioned medium. Cells with both an exogenous v-Ha-ras and an activated c-Ha61-ras gene produced undifferentiated, rapidly lethal carcinomas, while cells with only v-Ha-ras maintained the squamous carcinoma phenotype. Undifferentiated carcinomas also developed when the v-Ha-ras gene was introduced into papilloma cells with a chemically induced endogenous c-Ha61-ras gene mutation. These results suggest that mutation in the c-Ha-ras gene can contribute to initiation, malignant conversion, and malignant progression in skin carcinogenesis, and gene dosage may determine the phenotype expressed.

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Section: Dna Analysismentioning

confidence: 99%

Spontaneous Ha‐ras Gene Activation in Cultured Primary Murine Keratinocytes: Consequences of Ha‐ras Gene Activation in Malignant Conversion and Malignant Progression

Greenhalgh

Welty

Strickland

et al. 1989

Molecular Carcinogenesis

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“…Northern analysis. Five microgramsof poly(A)+ RNA was separated on a 1 % formaldehydeiagarose gel, transferred t o nitrocellulose, and hybridized t o the following oncogenespecific probes: a BamHl fragment of pl1-4 (p53) from A. Levine [12]; an FcoRI fragment of Ki-MuSV clone HiHi3 (Ki-ras) [13], a Pstl fragment of p-fos-1 (fix) [14], and an EcoRl fragment o f Ha-MuSV clone B59 (Ha-ras) [15] from R. Muller; a Pstlfragment of pMycPst (myc) [161, a Pvull fragment of p52 c (N-ras) 1171. a Hindlll fragment of PAL1 (int-1) [18], and a SalllEcoRI fragment of pMetH (met) (191 from ATCC (Rockville, MD); a SmallEcoRI fragment of 6929 (L-myc) from 1. Minna [20]; an SstlliXhol fragment of 361 1 (raf), and a Hindlll fragment of A-MuLV (a60 from Oncor (Gaithersburg, MD); and an Xhol fragment of pHFl (actin) from K. Nelson [21].…”

Section: Walker and Ne7tesheimmentioning

confidence: 99%

Cellular oncogene expression in cell lines derived from tumors produced by transformed rat tracheal epithelial cells

Walker

Nettesheim

1989

Molecular Carcinogenesis

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Five tumor-derived cell lines established from transformed rat tracheal epithelial (RTE) cells were examined for activated oncogenes using the NIH 3T3 assay, and the expression of 11 cellular oncogenes in the transformed cells was quantitated and compared with expression in normal RTE cells. DNA from the tumor-derived cell lines lacked transforming activity, but expression of several oncogenes (fos, abl, Ki-ras, Ha-ras, and p53) was higher in the transformed cells than in normal RTE cells.

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“…DNA probes and hybridization 32P-labeled DNA probes were prepared by nick translation of the following clones: the 450 bp BS-9 fragment for H-ras (Ellis et al, 1980), the 3.2 kb fragment for cmvc from mouse (Shen-Ong. et al.…”

Section: Formaldehyde-agarose Gel Electrophoresis Andmentioning

confidence: 99%

Specific gene expression during compensatory renal hypertrophy in the rat

Beer

Zweifel

Simpson

et al. 1987

Journal Cellular Physiology

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The compensatory growth of the kidney which is induced by unilateral nephrectomy is a highly regulated process resulting principally in hypertrophy of the remaining kidney. The events which regulate this process are unknown. We have examined the levels of transcripts for the proto-oncogenes, myc, H-ras, K-ras, and fos, and the cellular genes, H4 histone, ornithine aminotransferase, and gamma-glutamyl transpeptidase, following unilateral nephrectomy in the rat. The pattern of expression of c-myc, c-H-ras, and c-K-ras during compensatory growth of the kidney differs from the pattern of expression of these proto-oncogenes during liver regeneration, in which, unlike the kidney, hyperplasia rather than hypertrophy predominates. The lack of change in the abundance of these proto-oncogene transcripts following unilateral nephrectomy suggests a primary relationship between the expression of these proto-oncogenes and DNA synthesis and indicates there may be separate signals for cell growth, one to double cell size and one to replicate DNA. Increased mRNA transcripts for the enzymes ornithine aminotransferase and gamma-glutamyl transpeptidase were induced in the contralateral kidney after nephrectomy. The time course of expression for these two enzymes differs. The early expression of the gamma-glutamyl transpeptidase gene may indicate an involvement of this glutathione-metabolizing enzyme during renal compensatory growth, while the function of the delayed increase in ornithine aminotransferase transcripts in the remaining kidney is not apparent.

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Dual evolutionary origin for the rat genetic sequences of Harvey murine sarcoma virus

Cited by 347 publications

References 43 publications

Spontaneous Ha‐ras Gene Activation in Cultured Primary Murine Keratinocytes: Consequences of Ha‐ras Gene Activation in Malignant Conversion and Malignant Progression

Spontaneous Ha‐ras Gene Activation in Cultured Primary Murine Keratinocytes: Consequences of Ha‐ras Gene Activation in Malignant Conversion and Malignant Progression

Cellular oncogene expression in cell lines derived from tumors produced by transformed rat tracheal epithelial cells

Specific gene expression during compensatory renal hypertrophy in the rat

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