By John A. Kellen (auth.), John A. Kellen (eds.)
Nullius in verba. . . fact might be confirmed no longer through phrases. Horace (Epistles) Few learn introductions apart from publication reviewers, who are looking to take a shortcut and stay away from interpreting the e-book itself. in spite of the fact that, culture calls for that the preface make public why the e-book used to be written in any respect (this isn't really purported to contain strong purposes equivalent to augmenting the ego of the editor and authors). often, the inflationary tendency to submit in verbose size is in clash with industry forces and curiosity. doubtless, multidrug resistance is a "fashionable" subject, yet there are lots of models displayed at the cat-walk of clinical literature. one could rationalize that the forces using our hindrance with multi drug resistance replicate the disappointment of pharmaceutical businesses and oncologists alike: once a brand new anticancer drug enters medical trials, melanoma cells begin eluding extinction with their complex and winning mechanisms. Many offers were offered and spent, basically to verify the futility of our efforts to defeat this mobile Darwinism. Our scientific and clinical education makes it demanding, if no longer most unlikely, to just accept that the survival of a malignant mobile, on my own or as a part of a tissue, is a part of the continuance of lifestyles. when you consider that publicity to noxious and deadly elements is unavoidable, cells were pressured to boost a mess of mechanisms to avoid access or speed up go out of such fabrics from intracellular space.
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Extra resources for Alternative Mechanisms of Multidrug Resistance in Cancer
Mechanisms of Multidrug Resistance 25 Table 5. Manipulation ofPKC activity by various compounds with the goal to influence MDR. , 1994 REFERENCES Ahmad S, Mineta T, Martuza RL, Glazer R1 (1994): Antisense expression of protein kinase C alpha inhibits the growth and tumorigenicity of human glioblastoma cells. Proc AACR 35:445 Bates SE, Le JS, Dickstein B, Spolyar M, Fojo AT (1993): Differential Modulation of P-Glycoprotein Transport by Protein Kinase Inhibition. Biochemistry 37:9156-9164 Dekker LV, Parker PJ (1994): Protein kinase C - a question of specificity.
1989). Indeed, many MDR cell lines show considerable increase 24 John A. , 1993). , 1994). , 1993). , 1992). , 1994). , 1994b). , 1989). Manipulation of PKC by activators and inhibitors have clinical potential as anticancer agents per se or in conjunction with other MDR mechanisms. On Table 5 a brief review of such agents is listed, without claim to be complete. The importance of PKC is reflected in the need for Chapter 9 devoted to this topic. Mechanisms of Multidrug Resistance 25 Table 5. Manipulation ofPKC activity by various compounds with the goal to influence MDR.
They demonstrated that cyclophosphamideinduced inhibition of weight gain in rats was enhanced by the depletion GSH by diethyl maleate. Adams et al. (1985) found that, following cyclophosphamide treatment in mice, there was a depletion of both GSH content and GST activity in the bone marrow. , 1986). , 1980; Revis and Marusic, 1978). Thus, a role for GSH as a determinant of therapeutic efficacy has been demonstrated for a number of antineoplastic agents. The observation that a reduction in intracellular GSH levels may result in the sensitization of drug-resistant tumor cells has led to the initiation of approaches to modulate GSH levels in aneffort to improve the therapeutic efficacy of drugs such as alkylating agents.
Alternative Mechanisms of Multidrug Resistance in Cancer by John A. Kellen (auth.), John A. Kellen (eds.)