By John A. Kellen (auth.), John A. Kellen (eds.)
Nullius in verba. . . fact might be proven no longer by means of phrases. Horace (Epistles) Few learn introductions aside from booklet reviewers, who are looking to take a shortcut and steer clear of examining the publication itself. even though, culture calls for that the preface make public why the e-book used to be written in any respect (this isn't really imagined to contain robust purposes equivalent to augmenting the ego of the editor and authors). usually, the inflationary tendency to post in verbose size is in clash with industry forces and curiosity. doubtless, multidrug resistance is a "fashionable" subject, yet there are numerous models displayed at the cat-walk of medical literature. you'll rationalize that the forces riding our situation with multi drug resistance mirror the disappointment of pharmaceutical businesses and oncologists alike: once a brand new anticancer drug enters scientific trials, melanoma cells commence eluding extinction with their problematic and winning mechanisms. Many can provide were offered and spent, in basic terms to verify the futility of our efforts to defeat this mobile Darwinism. Our clinical and clinical education makes it difficult, if now not 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. due to the fact publicity to noxious and deadly ingredients is unavoidable, cells were pressured to enhance a large number of mechanisms to avoid access or speed up go out of such fabrics from intracellular space.
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Extra info for Alternative Mechanisms of Multidrug Resistance in Cancer
BBRC 197:702-708 Biedler JL, Meyers MB (1988): Multidrug resistance (vinca alkaloids, actinomycin D, and anthracycline antibiotics). In: Drug Resistance in Mammalian Cells (Ed. Gupta RS) Vol II pp 57-88 CRC Press, Boca Raton Chiou S-K, Rao L, White E (1994): Bc1-2 Blocks p53-Dependent Apoptosis. Mol Cell Bioi 14:2556-2563 Dickstein B, Valverius EM, Wosikowski K, Saceda M, Pearson JW, Martin MB, Bates SE (1993): J Cell Physiol 157:110-118 Huang A, Wright JA (1994): Fibroblast growth factor mediated alterations in drug resistance, and evidence of gene amplification.
The regulation of GST is complex as they are subject to both developmental control and tissue specific expression. Pickett and his colleagues have identified cis-acting elements in the 5' flanking region of the rat Ya subunit gene. , 1991). , 1990, 1991). , 1990). Friling et al. (1990, 1992) have identified an additional cis-acting element in the 5' flanking region of the murine Ya subunit which was designated the electrophilic-responsive element (EpRE). , 1992). In addition to activation of EpRE, Bergelson et al.
Presented at the 34th Ann Meet Can Fed Bioi Soc (Kingston, Ont Canada, June 1991) Cole SPC, Chanda ER, Dicke FP, Gerlach JH, Mirski SEL (1991): Non-Pglycoprotein-mediated Multidrug Resistance in a SmaIl Cell Lung Cancer Cell Line: Evidence for Decreased Susceptibility to Druginduced DNA Damage and Reduced Levels of Topoisomerase II. Cancer Res 51:3345-3352 Danks MK, Schmidt CA, Deneka DA, Beck WT (1989): Altered interaction of ATP with DNA topoisomerase II from VM-26-resistant CEM cells. Proc AACR 30:524 Deffie AM, Goldenberg GJ (1989): Altered levels of expression of DNA Topoisomerase II in ADR-sensitive and -resistant P388 murine leukemia cells.
Alternative Mechanisms of Multidrug Resistance in Cancer by John A. Kellen (auth.), John A. Kellen (eds.)