Assessment of cellular differentiation by ABO (H) isoantigens in breast lesions.
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Gap junctions provide pathways of direct cell to cell communication in the tissues of metazoan animals. Cells joined by gap junctions share their small ions and molecules but can maintain distinctive activities through expression of different macromolecules which are too large to pass through the junctions. The junctional channels are made of a tissue invariant, evolutionarily conserved 16-18 k protein but the formation and maintenance of active coupling also requires one or more connexins, a family of tissue-specific proteins ranging in size from 21 k to 70 k. Junctions can be isolated as complexes containing both types of protein by mild procedures using high pH but the connexins can be removed by detergent, urea and protease treatment without destroying the characteristic junctional-morphology of hexagonally packed channels in the double membrane structures. There is also some evidence for the participation in the complex of tissue-specific proteoglycans which perhaps interact with the tissue-specific connexins and account for specificity of junction formation. Such specificity in mixed cultures leads to the production of communication compartments, groups of cells joined by junctions but separated by reduced trans-boundary coupling from cells in adjacent compartments. Compartmentation also occurs in vivo resulting in specific patterns of junctional communication which have been mapped in most detail in mouse skin. These mapping data and the changes which are associated with abnormal proliferation have lead to new ideas on intercellular control.(ABSTRACT TRUNCATED AT 250 WORDS)
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After four days of treatment with 10(-8) M TPA, differentiation of the human T-lymphoblastoid cell line MOLT-4 was induced along the T cell lineage, confirmed by a fall in adenosine deaminase and 5'-ectonucleotidase and a rise in purine nucleoside phosphorylase activity. TPA-treated cells became resistant to the cytotoxic effects of 1-beta-D-arabinofuranosylcytosine (Ara-C), 9-beta-D-arabinofuranosyladenine (Ara-A), and 2-chlorodeoxyadenosine. This was, in part, due to the altered cell cycle distribution (accumulation of cells in the G1 phase), since the toxicity of Ara-C and Ara-A is S phase specific. The diminished rate of Ara-C transport concomitant with Ara-CTP formation after TPA treatment is considered to be the biochemical basis for this acquired resistance.
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The development of rete testis in the rat, rabbit and guinea pig foetuses has been studied, as well as the influence of prolactin and thyrotropin on differentiation of its cells. It was shown that the rete testis tubules, as well as the seminiferous tubules develop from sex cords, which were derived from coelomic epithelium cells and gonocytes. The development of seminiferous tubules and rete testis was described at various stages of prenatal ontogenesis. Thyrotropin and prolactin exert different effects on differentiation of the rete testis cells: the former increases the mitotic activity of gonocytes and the latter increases that of epithelial cells and enhances degenerative processes in primary germ cells.
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The mechanisms and determination of differentiation of normal and cancer cells were compared by distinguishing them from the phenomena of regulation, retrodifferentiation and maturation. Reference is made to the laws of order in time and space which are superimposed on the common genetic code during the various types of differentiation. In conclusion, the particular mechanisms of malignant differentiation are discussed by taking melanoma and tumor formation by papova-viruses as examples.
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