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

As used to be proven within the first volumes of this sequence, nice strides were made in picking out the various brokers or sessions of gear liable for carcinogenesis and in delineating their interactions with the telephone. essentially, the purpose of such reviews is that, as soon as pointed out, those brokers will be eradicated from the surroundings. but, regardless of those advances and the removing of a few very important carcinogenic brokers, one significant issue exists. it's a consistent display screen of all oncologic examine and diminishes the significance of each test and of each scientific remark. As we famous previous, that challenge is our lack of ability to outline the malignant mobilephone. it's via reports of the basic biology of tumors that we search this definition. an unlimited volume of knowledge has been accumulated which describes what this phone 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 cellphone, keep in huge phrases by means of evaluating it to its basic counterpart. the most important challenge seems to be that the malignant mobilephone does loads. it's a chimera, mystifyingly composed of ordinary actions and constructions, of phenotypic schizophrenia with embryonic, fetal, and grownup charac­ teristics and, sometimes, a touch of an unclassifiable means specific to malignant cells.

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A given transforming virus may lead to reductions in different transferase activities in different cell lines, and even more than one activity in a particular line. Glycosyltransferase activity increases have been reported for confluent hamster cells compared to sparse (Kijimoto and Hakomori, 1971), but these changes were not found with mouse cells (Brady and Fishman, 1974). In sum, part but not all of the conclusions reached from the study of NIL cell glycolipids seem applicable to other systems (discussed below).

These results were also found with SV3T3 cells (Nicolson, 1974b). Mobile lectin sites are directly involved in the agglutination of cells at room temperature, but the clusters seem to arise from a uniform distribution by lectin-induced effects on the cell surface. Inbar and Sachs (1973) and Nicolson (1973b) used fluorescent Con A to show that transformed cells have inherently dispersed distributions of their Con A binding sites at low temperature (or on aldehyde-fixed cells), and these dispersed sites can rearrange into clusters at or above room temperature in the presence of Con A.

Using Con A-peroxidase techniques, Martinez-Palomo et al. (1972) and Bretton et al. (1972) found that normal, polyoma-, and SV40-transformed hamster cell lines bind Con A-peroxidase, but the peroxidase product is generally more patchy on the transformed cells labeled at room temperature than at O°C. Also, two adenovirus12 hamster tumor lines of differing malignancy were discontinuously labeled with Con A-peroxidase compared to the normal parental line (Huet and Bernhard, 33 SURFACES OF NORMAL AND TRANSFORMED CELLS 34 c.

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