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 selecting a few of the brokers or periods of drugs chargeable for carcinogenesis and in delineating their interactions with the phone. sincerely, the purpose of such stories is that, as soon as pointed out, those brokers may be eradicated from the surroundings. but, regardless of those advances and the removing of a few vital carcinogenic brokers, one serious problem exists. it's a consistent visual display unit of all oncologic research and diminishes the significance of each test and of each scientific commentary. As we famous previous, that challenge is our lack of ability to outline the malignant mobile. it's via reports of the basic biology of tumors that we search this definition. an unlimited volume of knowledge has been collected which describes what this telephone does and-to a lesser extent-how it does it. however the why evades us. now we have been not able to outline the malignant mobilephone, shop in large phrases by way of evaluating it to its general counterpart. the main challenge seems to be that the malignant mobilephone does lots. it's a chimera, mystifyingly composed of ordinary actions and buildings, of phenotypic schizophrenia with embryonic, fetal, and grownup charac teristics and, sometimes, a touch of an unclassifiable potential designated to malignant cells.
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1972), and Coggin and Anderson (1974). Another property of cells after transformation is an increase in agglutinability by plant lectins, proteins and glycoproteins that bind specific saccharide determinants (for review, see Nicolson, 197Aa; Burger, 1973; Lis and Sharon, 1973). Aub et al. (1963, 1965a,b) found that a wheat germ (Triticum vulgaris) preparation agglutinated certain transformed cells but not their normal counterparts. Burger and Goldberg (1967) purified the agglutinating activity and characterized the responsible molecule as a lectin, wheat germ agglutinin (WGA), that binds to cell surface N-acetyl-n-glucosamine-like residues.
1974; Rozengurt and Jimenez de Asua, 1973). The hypothesis of Pardee et al. (1974) should probably be adapted, therefore, to include other controls of cAMP level or other effectors between a primary membrane change and transport activity. While it is not possible at present to demonstrate a primary cellular change among the many changes found with malignancy, the hypotheses of Holley (1972) and of Pardee et al. (1974) have helped greatly in focusing attention on cell surface changes in cancer.
1970). , 1974b) cell lines. , 1974b; Poste, 1972). 3. Transport Cells, both prokaryotic and eukaryotic, have specific mechanisms for transporting polar small molecules through the apolar plasma membrane. Without these transport systems, polar nutrients would enter the cell quite slowly, and polar waste products would tend to accumulate (see Oxender, 1972, for a general transport review). Viral transformation of cultured animal cells increases some but not all transport activities in every case examined to date.