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Retinoid resistance in leukemic cells

M Kizaki1, H Ueno, H Matsushita

  • 1Division of Hematology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.

Leukemia & Lymphoma
|May 1, 1997
PubMed
Summary

Acute promyelocytic leukemia (APL) patients often relapse due to all-trans retinoic acid (RA) resistance. Drug metabolism, including increased cytochrome P-450 and CRABP, appears to be a key factor in developing this resistance.

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Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • Acute promyelocytic leukemia (APL) shows high initial response rates to all-trans retinoic acid (RA).
  • However, acquired resistance to RA frequently develops in APL patients, leading to relapse despite initial treatment success.

Purpose of the Study:

  • To investigate the underlying mechanisms of acquired all-trans retinoic acid (RA) resistance in acute promyelocytic leukemia (APL) cells.
  • To explore potential molecular and pharmacological factors contributing to treatment failure.

Main Methods:

  • Analysis of retinoid receptor gene mutations in RA-resistant APL cell lines (UF-1).
  • Assessment of changes in all-trans RA metabolism, including plasma concentrations, and the role of enzymes like cytochrome P-450, CRABP, and P-glycoprotein.

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Main Results:

  • No point mutations were found in the RAR-alpha gene's ligand-binding domain of RA-resistant UF-1 cells.
  • Continuous all-trans RA treatment led to reduced plasma RA concentrations.
  • Induction of cytochrome P-450, CRABP, and P-glycoprotein was observed, contributing to lower active retinoid levels.

Conclusions:

  • Acquired resistance to all-trans RA in APL is not solely due to mutations in the RAR-alpha gene.
  • Altered drug metabolism, including increased expression of metabolizing enzymes and transporters, plays a significant role in the development of RA resistance in APL.