Cell Transformation modifiers

The mechanism of vanadium interaction with growth and differentiation pathways has been extensively studied [70], In tissue culture systems, vanadium has been shown to inhibit growth and, in some cases, modify DNA synthesis to block the G2-to-M transition. Cells blocked at M phase are susceptible to apoptosis, which can be stimulated by vanadium compounds. Vanadium compounds have also been shown to have mitotic effects stimulating growth, cell proliferation, or cell transformation. In some cases, vanadium compounds were able to promote cellular differentiation. Clearly, the addition of vanadium compounds would not have all of these... 

The viruses may be conceived as particles attaching themselves to particular receptors of the succeptible cells. These receptors may be chemical configurations that combine with either viruses or allied substances of similar composition. After due attachment the viruses gain entry into the cell and subsequently multiply. Thus the newly constituted viruses are eventually realised from the cell to paraciticize other cells of the host. In such transformation the metabolic activity of the host cell is modified in some manner. 

The incidence of ovarian tumors in mice, guinea pigs, and rabbits increased after 3 years of chronic irradiation at doses as low as 1.1 mGy daily (Lorenz et al. 1954). Unlike other tumors, the induction of ovarian tumors depended on a minimum total dose and seemed to be independent of a daily dose (Lorenz et al. 1954). Radiation-induced neoplastic transformation of hamster cells may be associated initially with changes in expression of the genes modifying cytoskeletal elements (Woloschak et al. 1990b). 

Atherosclerotic lesions are thought to arise from transport and retention of plasma LDL through the endothelial cell layer into the extracellular matrix of the subendothelial space. Once in the artery wall, LDL is chemically modified through oxidation and nonenzymatic glycation. Mildly oxidized LDL then recruits monocytes into the artery wall. These monocytes then become transformed into macrophages that accelerate LDL oxidation. 

The intracellular distribution of steroid hormone receptors has long been the object of controversy. The first theoretical formulation on the intracellular location of the ERs was elaborated by Jensen in 1968 and is known as the two-step theory. Its execution was based entirely on biochemical observations obtained by means of tritium-marked estradiol. The ERs, in cells not exposed to hormones, are found abundantly in the soluble cell fraction, or cytosol (Fig. 1.1). Treatment with hormones confines the receptors to the particulated or nuclear fraction and causes their disappearance from the cytosol. The two-step theory established that the receptor is found in the cytoplasm naturally and upon the arrival of a hormone it is transformed into a complex hormone-receptor (first step) capable of translocating itself to the nucleus and of modifying gene expression (second step). 

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