By John A. Kellen (auth.), John A. Kellen (eds.)

Nullius in verba. . . fact might be demonstrated now not by means of phrases. Horace (Epistles) Few learn introductions with the exception of e-book reviewers, who are looking to take a shortcut and steer clear of interpreting the publication itself. despite the fact that, culture calls for that the preface make public why the e-book was once written in any respect (this isn't presupposed to comprise robust purposes reminiscent of augmenting the ego of the editor and authors). usually, the inflationary tendency to submit in verbose size is in clash with marketplace forces and curiosity. doubtless, multidrug resistance is a "fashionable" subject, yet there are various models displayed at the cat-walk of medical literature. possible rationalize that the forces riding our crisis with multi drug resistance mirror the disappointment of pharmaceutical businesses and oncologists alike: once a brand new anticancer drug enters medical trials, melanoma cells begin eluding extinction with their problematic and winning mechanisms. Many provides were presented and spent, simply to substantiate the futility of our efforts to defeat this mobile Darwinism. Our scientific and medical education makes it difficult, if no longer most unlikely, to just accept that the survival of a malignant cellphone, by myself or as a part of a tissue, is a part of the continuance of lifestyles. considering the fact that publicity to noxious and deadly components is unavoidable, cells were compelled to increase a mess of mechanisms to avoid access or speed up go out of such fabrics from intracellular space.

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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. , 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.

Kellen Meyers MB, Yu P, Mendelsohn J (1993): Crosstalk between epidennal growth factor receptor and P-glycoprotein in actinomycin D - resistant Chinese hamster lung cells. Biochem PharmacoI46:1841-1848 Oesterreich S, Wing Ch-N, Qiu M, Hilsenback SG, Osborne CK, Fuqua SAW (1993): The Small Heat Shock protein hsp27 is Correlated with Growth and Drug Resistance in Human Breast Cancer Cell Lines. Cancer Res 53:4443-4448 Pallares-Trujillo J, Domenech C, Grau-Oliete MR, Rivera-Fillat MP (1993): Role of cell cholesterol in modulating vincristine uptake and resistance.

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. CLINICAL ROLE OF GST In vitro and preclinical studies suggest that modulation of drug resistance can be accomplished through alterations in either GSH pools through the use of agents such as buthionine sulfoximine or GSH- Glutathione S-Transferases in MDR 49 monoethyl ester; or by altering GST activity with a variety of agents designed to inhibit these enzymes.

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Alternative Mechanisms of Multidrug Resistance in Cancer by John A. Kellen (auth.), John A. Kellen (eds.)
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