Titlebook: Interrelationship Among Aging, Cancer and Differentiation; Proceedings of the E Bernard Pullman,Paul O. P. Ts’o,Edmond L. Schneide Conferen

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Deceleration of Cancer Mortality Rates with Age and Time, life then plateaus, accounting for less than 12 percent of all deaths among persons over age 80. This pattern does not support a direct relationship between cancer and aging, or a simple association between cancer and cumulative exogenous or endogenous factors. Cancer deaths can be expected to repr

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Overview of the Pathobiology of Aging,s relevant to somatic mutational theories. Of special relevance to the theme of this conference is the evidence for a widespread loss of proliferative homeostasis and the evidence for chromosomal instability, both of which may contribute to the pathogenesis of neoplasia and might be related to aspec

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Regulators of Growth, Differentiation and the Reversal of Malignancy,hat uncouple growth and differentiation so as to produce malignant cells. When cells become malignant, the malignant phenotype can again be suppressed. Results on the reversibility of malignancy in different types of tumors have shown, that in addition to genes for the expression of malignancy (onco

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Transforming Genes of Human Malignancies,emarkable discoveries. A wide variety of human tumors have been shown to possess discrete genetic sequences capable of inducing the transformation of appropriate assay cells. These genes were subsequently found to be the homologues of the cell-derived oncogene sequences responsible for the transform

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Cancer Cells as Probes of Embryonic Development,ggesting that a close developmental correspondence between the field and the cancer cell is required- Inhibitors of mitosis are present in two of these embryonic fields, and in one case it is likely that the inhibitor plus cell contact is required for regulation to occur.

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Virus Transformation as a Function of Age, Differentiation and Hereditary Factors,ation of mammalian cells has been shown to occur after exposure to DNA- or RNA-oncogenic viruses, ionizing irradiation and chemical carcinogens (1–4). In most instances, dispersed monolayer cultures of freshly explanted cell strains or established cell lines have been used for such assays. Multiple

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Negative Control of Viral and Cellular Enhancer Activity by the Products of the Immortalizing E1A Gs from cellular genes. In a transient assay, we show that both E1A products repress transcription activation mediated by viral enhancers such as polyoma, SV40 and E1A, when cotransfected in HeLa cells and by the cellular enhancer of the immunoglobulin heavy chain, when cotransfected in the appropria

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