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C421A polymorphism in the human breast cancer resistance protein gene is associated with low expression of Q141K protein and low-level drug resistance.
- Y. Imai, M. Nakane, +5 authors Y. Sugimoto
- Medicine, BiologyMolecular cancer therapeutics
- 1 June 2002
People with C376T and/or C421A polymorphisms may express low amounts of BCRP, and this low BCRp expression might result in hypersensitivity of normal cells to such anticancer drugs as irinotecan and mitoxantrone.
A ras-related gene with transformation suppressor activity
Transport of methotrexate, methotrexate polyglutamates, and 17beta-estradiol 17-(beta-D-glucuronide) by ABCG2: effects of acquired mutations at R482 on methotrexate transport.
It is demonstrated that R482 mutations observed in drug-resistant cell lines have profound effects on the in vitro transport properties of the pump, indicating that ABCG2 is a component of the energy-dependent efflux system for certain folates and antifolates, but that its transport characteristics with respect to polyglutamates and reduced folates are not identical to those of multidrug resistance protein family members.
ABCG2 Transports Sulfated Conjugates of Steroids and Xenobiotics*
- Michiko Suzuki, Hiroshi Suzuki, Y. Sugimoto, Y. Sugiyama
- Chemistry, MedicineJournal of Biological Chemistry
- 20 June 2003
It was suggested that ABCG2 preferentially transports sulfate conjugates and that E1S and DHEAS are the potential physiological substrates for this transporter.
Phytoestrogens/Flavonoids Reverse Breast Cancer Resistance Protein/ABCG2-Mediated Multidrug Resistance
This study shows that phytoestrogens/flavonoids, such as genistein, naringenin, acacetin, and kaempferol, potentiated the cytotoxicity of SN-38 and mitoxantrone in BCRP-transduced K562 (K562/BCRP) cells and suggests that flavonoid and glycosylated flavonoids may be useful in overcoming B CRP-mediated drug resistance in tumor cells.
Breast cancer resistance protein exports sulfated estrogens but not free estrogens.
- Y. Imai, Sakiyo Asada, Satomi Tsukahara, E. Ishikawa, T. Tsuruo, Y. Sugimoto
- Chemistry, MedicineMolecular pharmacology
- 1 September 2003
It is demonstrated that BCRP does not transport either free estrone or 17beta-estradiol but exports sulfate conjugates of these estrogens.
alpha-Galactosidase A deficient mice: a model of Fabry disease.
- T. Ohshima, G. Murray, +8 authors A. Kulkarni
- Biology, MedicineProceedings of the National Academy of Sciences…
- 18 March 1997
The similarity of the pathophysiological process in the mutant mice and in patients with Fabry disease is indicated, indicating the importance of an animal model for exploring therapeutic strategies for patients withFabry disease.
Gefitinib reverses breast cancer resistance protein-mediated drug resistance.
- K. Yanase, Satomi Tsukahara, Sakiyo Asada, E. Ishikawa, Y. Imai, Y. Sugimoto
- Medicine, ChemistryMolecular cancer therapeutics
- 1 September 2004
Gefitinib inhibits the transporter function of BCRP and reverses B CRP-mediated drug resistance both in vitro and in vivo, and suggests that gefit inib may overcome BCRp- mediated drug resistance by inhibiting the pump function ofBCRP.
Estrogen-mediated post transcriptional down-regulation of breast cancer resistance protein/ABCG2.
It is shown that at physiologic levels, estrogens markedly decrease endogenous BCRP expression in the estrogen-responsive and estrogen receptor alpha (ERalpha)-positive human breast cancer MCF-7 cells, but not in estrogen-nonresponsive human cancer cells, indicating that estrogen down-regulates B CRP expression by novel posttranscriptional mechanisms.
Dominant‐negative inhibition of breast cancer resistance protein as drug efflux pump through the inhibition of S‐S dependent homodimerization
- Kumie Kage, Satomi Tsukahara, +4 authors Y. Sugimoto
- Biology, MedicineInternational journal of cancer
- 10 February 2002
It is suggested that homodimer formation is essential for B CRP drug resistance, implicating this dominant‐negative inhibition of BCRP drug efflux pump as a new strategy to circumvent drug resistance.