These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Multidrug resistance of acute leukemia and a strategy to overcome it. Author: Motoji T, Motomura S, Wang YH. Journal: Int J Hematol; 2000 Dec; 72(4):418-24. PubMed ID: 11197207. Abstract: A representative cause of multidrug resistance (MDR) is expression of the MDR gene (mdr1) and its product P-glycoprotein (P-gp). The function of P-gp is thought to be the extrusion of anticancer drugs from the cell against a concentration gradient. In acute myelogenous leukemia (AML), P-gp expression in leukemic blast cells at initial presentation has been reported to be 20% to 40%. The remission rate of acute leukemia patients is significantly lower in P-gp+ patients than in P-gp- patients. A significantly shorter survival and relapse-free survival in P-gp+ AML patients compared with P-gp- patients has been reported. Intracellular daunorubicin/Rhodamine123 content in P-gp+ leukemic blast cells is significantly lower than in P-gp- leukemic blast cells. By using a leukemic blast colony assay, lowered sensitivity to the anticancer drug was revealed not only in leukemic blast cells but also in leukemic progenitors. One method to overcome MDR with a possibility of clinical application is to use drugs that interfere with the function of P-gp. The addition of MS-209 in vitro as an MDR-reversing agent significantly enhanced the intracellular daunorubicin/Rhodamine 123 accumulation and the retention of P-gp+ leukemic blast cells to a level similar to that of P-gp- blast cells. Recent clinical trials using MDR-reversing agents have demonstrated some encouraging results in P-gp+ patients but not in P-gp- patients.[Abstract] [Full Text] [Related] [New Search]