Classical multidrug resistance in acute myeloid leukaemia

Research output: Contribution to journalArticle

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Abstract

Approximately 15-30% of acute myeloid leukaemia (AML) patients are primarily resistant to chemotherapy, and 60-80% of patients who achieve complete remission will inevitably relapse and succumb to their disease. The multidrug resistant (MDR) phenotype has been suspected as a major mechanism of therapy failure in AML; it is one of the best understood mechanisms of resistance to anticancer drugs. The classical MDR phenotype is characterized by the reduced ability of cells to accumulate drugs as compared to normal cells. The increased drug efflux is due to the activity of a 170 kDa glycoprotein, the P-glycoprotein (Pgp), a unidirectional drug-efflux pump which is encoded by the MDR1 gene. While studies of myeloid leukaemia and myeloma have provided the best evidence for the potential association between Pgp expression and clinical outcome, the lack of standardized methods for MDR detection and, perhaps even more importantly, inconsistencies in the interpretation of MDR expression data account for divergent results in the literature. The clinicians' strong interest in MDR stems from the availability of agents capable of interfering with MDR, at least in vitro. If these laboratory results were reproducible in vivo, reversal of MDR would offer a rare opportunity to incorporate laboratory experience into the clinical management of patients.

Original languageEnglish (US)
Pages (from-to)53-60
Number of pages8
JournalMedical Oncology
Volume14
Issue number1
DOIs
StatePublished - Mar 1997

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Multiple Drug Resistance
Acute Myeloid Leukemia
P-Glycoprotein
Pharmaceutical Preparations
Phenotype
Myeloid Leukemia
Glycoproteins
Recurrence
Drug Therapy
Genes
Therapeutics

Keywords

  • acute myeloid leukaemia
  • multidrug resistance

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Classical multidrug resistance in acute myeloid leukaemia. / Paietta, Elisabeth M.

In: Medical Oncology, Vol. 14, No. 1, 03.1997, p. 53-60.

Research output: Contribution to journalArticle

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