Read e-book online Biology of Tumors: Surfaces, Immunology, and Comparative PDF

By James C. Robbins, Garth L. Nicolson (auth.), Frederick F. Becker (eds.)

ISBN-10: 1468427369

ISBN-13: 9781468427363

ISBN-10: 1468427385

ISBN-13: 9781468427387

As was once proven within the first volumes of this sequence, nice strides were made in picking the various brokers or periods of drugs liable for carcinogenesis and in delineating their interactions with the mobile. sincerely, the purpose of such reports is that, as soon as pointed out, those brokers may be eradicated from the surroundings. but, regardless of those advances and the removal of a few vital carcinogenic brokers, one significant issue exists. it's a consistent display screen of all oncologic research and diminishes the significance of each scan and of each medical remark. As we famous past, that challenge is our lack of ability to outline the malignant telephone. it truly is via stories of the basic biology of tumors that we search this definition. an unlimited quantity of knowledge has been collected which describes what this cellphone does and-to a lesser extent-how it does it. however the why evades us. we have now been not able to outline the malignant phone, store in huge phrases via evaluating it to its general counterpart. the foremost challenge seems to be that the malignant cellphone does lots. it's a chimera, mystifyingly composed of standard actions and buildings, of phenotypic schizophrenia with embryonic, fetal, and grownup charac­ teristics and, sometimes, a touch of an unclassifiable potential specified to malignant cells.

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1974; Rozengurt and Jimenez de Asua, 1973). The rapid increase in sugar transport with serum addition or with transformation also seems not to depend on cAMP changes (Hatanaka, 1974; Kletzien and Perdue, 1974a,b). Dibutyryl cAMP does reduce the 2-deoxyglucose transport of polyoma-transformed 3T3 cells to the 3T3 level and stop the growth of the transformed cells, but the growth restriction is not a restoration of the non transformed-type density-dependent inhibition (Grimes and Schroeder, 1973).

Cells are treated with galactose oxidase, which oxidizes carbon atom 6 of nonreducing terminal galactose and galactosamine residues to the aldehyde, and the resulting aldehydes are then reduced back to [3H]galactose and [3H]galactosamine by tritiated sodium borohydride. Inability of the galactose oxidase to penetrate easily into healthy cells limits incorporation of tritium to glycolipids and glycoproteins exposed on the cell surface. Using this technique, Gahmberg and Hakomori (197 Sa) have found that, while polyoma-transformed NIL contains much less higher neutral glycolipid than NIL, the remaining glycolipid molecules are more accessible to (or reactive with) added galactose oxidase.

For example, the glycoprotein of vesicular stomatitis virus grown in BHK cells gives glycopeptides of the same size distribution as those of virus grown in polyoma-transformed BHK, but the sugar composition and sensitivity to a mixture of glycosidases are different (Moyer and Summers, 1974). Differences have been found in the mixture of carbohydrate-peptide linkage regions of glycopeptides isolated from growing vs. , 1973). , 1969), and there is a report that while glycoproteins spontaneously released by transformed BHK cells are more glycosylated than those released by normal cells the remaining membrane proteins are less glycosylated in the transformed cells (Chiarugi and Urbano, 1972).

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Biology of Tumors: Surfaces, Immunology, and Comparative Pathology by James C. Robbins, Garth L. Nicolson (auth.), Frederick F. Becker (eds.)

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