Uptake in vivo and in vitro of actinomycin D by mouse leukemias as factors in survival

Kessel, David; Wodinsky, I

doi:10.1016/0006-2952(68)90170-6

Cited by 38 publications

(13 citation statements)

References 15 publications

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“…Two transmembrane xenobiotic transporter proteins, P glycoprotein (Pgp) and the multidrug resistance protein (MRP), cause multidrug resistance when transfected into drug-sensitive cells in culture (1)(2)(3)(4)(5). Despite these findings, the role these transporters play in clinical drug resistance exhibited by human breast cancer is unclear; hence, alternate or additional drug resistance mechanisms operative in this disease have been sought.…”

mentioning

confidence: 99%

A multidrug resistance transporter from human MCF-7 breast cancer cells

Doyle

Yang

Abruzzo

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

2,036

1,579

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MCF-7/AdrVp is a multidrug-resistant human breast cancer subline that displays an ATP-dependent reduction in the intracellular accumulation of anthracycline anticancer drugs in the absence of overexpression of known multidrug resistance transporters such as P glycoprotein or the multidrug resistance protein. RNA fingerprinting led to the identification of a 2.4-kb mRNA that is overexpressed in MCF-7/AdrVp cells relative to parental MCF-7 cells. The mRNA encodes a 663-aa member of the ATP-binding cassette superfamily of transporters that we term breast cancer resistance protein (BCRP). Enforced expression of the full-length BCRP cDNA in MCF-7 breast cancer cells confers resistance to mitoxantrone, doxorubicin, and daunorubicin, reduces daunorubicin accumulation and retention, and causes an ATP-dependent enhancement of the efflux of rhodamine 123 in the cloned transfected cells. BCRP is a xenobiotic transporter that appears to play a major role in the multidrug resistance phenotype of MCF-7/AdrVp human breast cancer cells.

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mentioning

confidence: 99%

A multidrug resistance transporter from human MCF-7 breast cancer cells

Doyle

Yang

Abruzzo

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

2,036

1,579

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“…The primary approach to this problem has been to isolate lines of cultured cells selected for resistance to various anticancer drugs. In studies using mouse and Chinese hamster cells (1)(2)(3)(4), as well as human cells (5)(6)(7)(8)(9), recently reviewed by Beck & Danks (10) and Sugimoto & Tsuruo (11), the isolation of tissue culture cells with a broad pattern of cross-resistance to many natural product anticancer drugs was frequently reported. This resistance is due to decreased accumulation of drugs in cells because of an energy-depen dent drug transport protein.…”

Section: The Clinical Problem and Phenotype Of Multidrug Resistancementioning

confidence: 99%

Biochemistry of Multidrug Resistance Mediated by the Multidrug Transporter

Gottesman

Pastan²

1993

Annu. Rev. Biochem.

3,322

1,863

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“…It is clear that the conversion of FU to nucleotide derivatives is a prerequisite for antineoplastic activity (see Section 111) and that, conversely, failure of tumor to convert FU to nucleotide would be associated with drug resistance. In early work aimed at testing this concept, a significant correlation was found between the extent of anabolism of FU and FUdR at a fued time point in a series of murine tumors and the effectiveness of these drugs in extending the lifespan of animals bearing these tumors (281,291). It was also reported (219) that peak levels of FdUMP in a FU-sensitive murine adenocarcinoma of the colon were twice as high as peak levels of this metabolite in a similar murine colonic adenocarcinoma that was insensitive to FU; it was suggested that t h s difference was sufficient to explain the difference between drug sensitivity and drug refractoriness.…”

Section: A Fdump Levelsmentioning

confidence: 99%