Showing papers on "Carcinogenesis published in 1970"

Studies on the mechanism of skin tumor promotion.

Abstract: At a level which was effective as a skin tumor promoter, croton oil increased the rate of incorporation of tritiated precursors into mouse skin macromolecules. After a single application of croton oil, the early 2- to 3-fold stimulation of RNA and protein synthesis and the 60% inhibition of DNA synthesis was followed by a 3-fold stimulation of DNA synthesis at 18 hr. The rates of macromolecular synthesis returned to normal levels within 7 days. A single application of cantharidin, a weak tumor promoter, stimulated both DNA and RNA synthesis in mouse skin. Treatment with either croton oil or cantharidin stimulated the synthesis of rapidly labeled RNA when measured 2 hr after treatment; stimulation of RNA synthesis may be important in the process of promotion. When an incision was made in initiated skin, tumors developed along the line of wound healing. Because croton oil, cantharidin, and other promoters cause hyperplasia and because wound healing causes a local stimulation of mitosis, a stimulation of cell division may be involved in promotion. A possible molecular mechanism of skin carcinogenesis is discussed.

Group-Specific Antigen Expression During Embryogenesis of the Genome of the C-Type RNA Tumor Virus: Implications for Ontogenesis and Oncogenesis

Abstract: Tests for the group-specific antigen of the C-type RNA tumor virus showed that mouse embryos of all strains tested, at some stage of development in utero, revealed detectable titers of group-specific antigen in one or more of their tissues; younger, rather than older, embryos were likely to be positive, particularly in those strains which normally reveal little or no expression of the RNA genome postnatally. The antigens were found in embryos of low-leukemia strains, free of infectious virus. These new findings support a previously stated hypothesis that the genome of RNA tumor viruses, mostly switched off for infectious virus expression, is vertically transmitted as part of the natural genetic apparatus of normal mouse cells. Since group-specific antigens have also been described in chick embryos and immunological tolerance to homologous group-specific antigens has been demonstrated in hamsters and cats as well as in mice and chickens, the hypothesis has been extended to include vertebrate cells in general. Finally, the high incidence and titers of the group-specific antigen suggest that the genes for RNA tumor virus, which later in life act as determinants of cancer, may be important also as gene determinants in the developing embryo.

Acute Changes in Nucleic Acid and Protein Synthesis in the Mouse Bladder Epithelium Induced by Three Bladder Carcinogens

Abstract: Summary The effect of a single oral dose of 4-ethylsulfonylnaphthalene-1-sulfonamide, 2-acetylaminofluorene, and 3-aminodibenzofuran on DNA, RNA, and protein synthesis in the urinary bladder and liver of the mouse has been investigated. Each chemical stimulated RNA and DNA synthesis in the bladder, but the magnitude and timing of the response was different in each case. Administration of 4-ethylsulfonylnaphthalene-1-sulfonamide in the diet produced an increase in DNA synthesis in the mouse bladder which lasted for 4 weeks, whereas with 2-acetylaminofluorene, increased DNA synthesis occurred only during the first week. The effect of 4-ethylsulfonyl-naphthalene-1-sulfonamide on nucleic acid synthesis was specific for the bladder, whereas 2-acetylaminofluorene stimulated both RNA and DNA synthesis in the liver and 3-aminodibenzofuran induced a small increase in DNA synthesis in male, but not in female, mouse liver.

Genetics and Cancer

Abstract: Certain genetic disorders in man may serve as models for the study of carcinogenesis, which may, in turn, lead to new means of prevention and treatment. In some disorders, there is an increased probability that normal cells will be transformed into cancer cells. In others, cancer seems to result from defective host resistance to transformed cells. In still other genetic disorders, the role of chromosomal abnormality and of viral infection in the origin of cancer can be investigated.

Expression of proliferating cell nuclear antigen in lung cancer.

Abstract: Background: Since an important component of carcinogenesis is unregulated growth, many investigators have reported the methods to detect cell proliferation in tissues including PCNA. PCNA is a 36 Kd intranuclear polypeptide and plays a critical role in cell proliferation. Thus progressive dysregulation of proliferation during carcinogenesis can be directly visualized in the paraffin embedded tissue using immunohistochemistry for PCNA which has an advantage of simplicity and maintenance of tissue architecture. The heterogeneity of PCNA expression is known to be related with proliferating fraction, histologic grade, DNA ploidy, and susceptibility of anticancer drugs, etc. We analyzed the biologic significance of the expression of PCNA in lung cancer tissues. Method: 43 lung cancer tissues, which were resected by surgery and were embedded in paraffin, were stained immunohistochemically by one hour MicroProbe System and the results were corelated with cell type, stage, site and survival. Result: 1) Suamous cell type showed high positivity (89%) than in adenocarcinoma (54%). 2) No significant difference related to tumor stage was noticed. 3) No significant difference between primary site and metastatic site was noticed. 4) No significant difference in 12-month survival between positive group and negative group was noticed. Conclusion: From this study, we concluded that imunohistochemistry for PCNA expression of routinely processed tissue is a simple technique for the assessment of proliferation in non-small cell lung cancer. Whether the labelling index has an independent prognostic value and deserves special attention in pathobiological evaluation in lung cancer remains to be investigated from large series with longer follow-up and to be correlated with multiple biological markers.