In vitro Transformation of Syrian Hamster Embryo Cells by Diverse Chemical Carcinogens

DiPaolo, Joseph A.; Nelson, Richard L.; Donovan, Paul

doi:10.1038/235278a0

Cited by 90 publications

(21 citation statements)

References 10 publications

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“…Of the two chemicals used in the present experiment, namely dimethylnitrosamine (DMN) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), the latter has been shown repeatedly to transform fibroblast or fibroblast-like cells in vitro (Takii, Takaki and Okada, 1971;Inui, Takayama and Sugimura, 1972;DiPaolo, Nelson and Donovan, 1972). Fibroblasts exposed to DMN were shown to increase cell multiplication, resulting later in continuously growing cells.…”

mentioning

confidence: 93%

Malignant Transformation in vitro of Rat Liver Cells by Dimethylnitrosamine and N-Methyl-N′-nitro-N-Nitrosoguanidine

Montesano¹,

Vincent²,

Tomatis³

1973

Br J Cancer

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Summary.-Epithelial-like cells originating from 10-day and 8-week old BD rats were treated in vitro with dimethylnitrosamine (DMN) and N-methyl-N'-nitronitrosoguanidine (MNNG). Morphologically, no differences were seen between treated and untreated cells up to the time when the cells were transplanted into syngeneic hosts. However, the treated cells grew in soft agar and once injected subcutaneously or intraperitoneally into newborn rats, developed tumours after a latent period of 9-12 weeks. The tumours obtained with DMN-treated cells were well differentiated adenocarcinomata, whereas carcinosarcomata were observed with the MNNG-treated cells.

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mentioning

confidence: 93%

Malignant Transformation in vitro of Rat Liver Cells by Dimethylnitrosamine and N-Methyl-N′-nitro-N-Nitrosoguanidine

Montesano¹,

Vincent²,

Tomatis³

1973

Br J Cancer

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“…This model uses chemically initiated neoplastic hamster embryo cells as an alternative in vitro system the characteristics of which make it relevant for studies of the cellular and molecular biology of human carcinogenesis (DiPaolo et al, 1969a(DiPaolo et al, ,b, 1971(DiPaolo et al, , 1986. The treatment of Syrian hamster cells in vitro with chemical or physical carcinogens has been used as the experimental model in other laboratories, and proved to be e cient for the detection of non-ras transforming genes (Borek et al, 1987;Gilmer et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

The product of the cph oncogene is a truncated, nucleotide-binding protein that enhances cellular survival to stress

1999

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Cph was isolated from neoplastic Syrian hamster embryo ®broblasts initiated by 3-methylcholanthrene (MCA), and was shown to be a single copy gene in the hamster genome, conserved from yeast to human cells, expressed in fetal cells and most adult tissues, and acting synergistically with H-ras in the transformation of murine NIH3T3 ®broblasts. We have now isolated Syrian hamster full-length cDNAs for the cph oncogene and proto-oncogene. Nucleotide sequence analysis revealed that cph was activated in MCA-treated cells by a point-mutational deletion at codon 214, which caused a shift in the normal open reading frame (ORF) and brought a translation termination codon 33 amino acids downstream. While proto-cph encodes a protein (pcph) of 469 amino acids, cph encodes a truncated protein (cph) of 246 amino acids with a new, hydrophobic C-terminus. Similar mechanisms activated cph in other MCA-treated Syrian hamster cells. The cph and proto-cph proteins have partial sequence homology with two protein families: GDP/GTP exchange factors and nucleotide phosphohydrolases. In vitro translated, gel-puri®ed cph proteins did not catalyze nucleotide exchange for H-ras, but were able to bind nucleotide phosphates, in particular ribonucleotide diphosphates such as UDP and GDP. Steady-state levels of cph mRNA increased 6.7-fold in hamster neoplastic cells, relative to a 2.2-fold increase in normal cells, when they were subjected to a nutritional stress such as serum deprivation. Moreover, cphtransformed NIH3T3 cells showed increased survival to various forms of stress (serum starvation, hyperthermia, ionizing radiation), strongly suggesting that cph participates in cellular mechanisms of response to stress.

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“…Further dilutions were made with fresh complete medium to obtain the concentrations needed. Final concentrations of carcinogens used were those which, with the exception of urethane, produced neoplastic transformation of hamster cells in culture (DiPaolo, Donovan and Nelson, 1969;DiPaolo, Nelson and Donovan, 1972).…”

Section: Methodsmentioning

confidence: 99%

Chromosome Bands Induced in Human and Syrian Hamster Cells by Chemical Carcinogens

DiPaolo¹,

Popescu²

1974

Br J Cancer

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Summary.-After 24 hours of treatment of human peripheral leucocyte cultures or Syrian hamster embryonic secondary cultures with some known chemical carcinogens at concentrations that produce transformation in vitro of hamster cells, the chromosomes of both types of cells exhibited typical G banding. Chromosome bands did not result with urethane, a compound which does not produce cytotoxicity or cause transformation by direct exposure of cells. Non-carcinogenic chemicals which do not inhibit cell multiplication also failed to produce bands. Cytogenetic analysis following removal of the carcinogens from the cultures indicated non-banded uniformly stained chromosomes. It is concluded that metaphases with chromosome bands are more likely to be the result of nonspecific toxicity rather than being related to the carcinogenic properties of the chemicals.

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In vitro Transformation of Syrian Hamster Embryo Cells by Diverse Chemical Carcinogens

Cited by 90 publications

References 10 publications

Malignant Transformation in vitro of Rat Liver Cells by Dimethylnitrosamine and N-Methyl-N′-nitro-N-Nitrosoguanidine

Malignant Transformation in vitro of Rat Liver Cells by Dimethylnitrosamine and N-Methyl-N′-nitro-N-Nitrosoguanidine

The product of the cph oncogene is a truncated, nucleotide-binding protein that enhances cellular survival to stress

Chromosome Bands Induced in Human and Syrian Hamster Cells by Chemical Carcinogens

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