Multidrug Resistance in Acute Myeloid Leukemia: Potential New Therapeutics

The results demonstrated in the article by Kersemans et al show that there may be a treatment to overcome multidrug resistance in acute myeloid leukemias and perhaps other types of hematologic cancers

J. H. Weisburg

2008

Scholarcy highlights

  • In acute myeloid leukemias, multidrug resistance is frequently, but not always, caused by the MDR1 gene product, a 170- to 180kDa glycoprotein known as P-glycoprotein or human MDR1 protein previous research
  • See page 1546 increased intracellular pH and decreased plasma membrane potentials, another explanation of the MDR mechanism of Pgp is the alteredpartition model. This model takes into account how the alterations in intracellular pH and membrane potential that accompany the overexpression of Pgp indirectly affect the partitioning of the drugs, but Pgp does not directly pump the drugs out of the cell
  • Other drug-resistance proteins, which are associated with hematologic cancers that use similar mechanisms, include the MDR-associated protein, the lung resistance protein, and the breast cancer resistance protein previous research
  • Several groups have shown that MDR cells seem to be resistant to several forms of immunologic therapies, including complementmediated cytotoxicity, immunotoxin, gelonin attached to monoclonal antibodies, interleukin 2, and drug immunoconjugates
  • Auger electrons from the 111In were cytotoxic to the parental HL60 cell line and drug-resistant HL60-MX-1 cell line and to the primary AML specimens that were expressing a diversity of MDR phenotypes
  • These results suggest that 111In-anti-CD33 monoclonal antibodies that are modified with an nuclear localizing sequence may be a new treatment for patients who have drug-resistant myeloid leukemias
  • The results demonstrated in the article by Kersemans et al show that there may be a treatment to overcome multidrug resistance in acute myeloid leukemias and perhaps other types of hematologic cancers

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