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Related Experiment Videos

[How do cancers resist to chemotherapy?].

M F Poupon1

  • 1Institut Curie Biologie, Paris, France.

Pathologie-Biologie
|December 1, 1992
PubMed
Summary
This summary is machine-generated.

Cancer cells can develop resistance to chemotherapy through several mechanisms, including multidrug resistance mediated by P-glycoprotein. New research explores ways to reverse this resistance, potentially improving antitumor agent efficacy.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Cellular resistance to antitumor agents is a major challenge in cancer chemotherapy.
  • Mechanisms include decreased intracellular drug levels, multidrug resistance (MDR), agent detoxification, and target enzyme alterations.
  • Resistance can be intrinsic or acquired, with some evidence suggesting chemotherapy itself may induce resistance.

Purpose of the Study:

  • To review current understanding of cellular resistance mechanisms to antitumor agents.
  • To highlight new findings on P-glycoprotein regulation and its role in MDR.
  • To discuss strategies for overcoming P-glycoprotein-mediated resistance, including clinical trials of reversal agents.

Main Methods:

  • Review of mechanisms of cellular resistance to chemotherapy.

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  • Discussion of P-glycoprotein expression and its regulation by factors like P53 and ras.
  • Presentation of data from Phase I clinical trials using Cyclosporin A to reverse P-glycoprotein-related resistance.

    • Main Results:

    • Four primary resistance mechanisms identified: MDR (P-glycoprotein), glutathione-S-transferase detoxification, increased target enzyme production, and topoisomerase alterations.
    • P-glycoprotein expression is influenced by mutant P53, the ras oncogene, and differentiation agents.
    • Transgenic mice models demonstrate MDR1 gene transfection confers resistance; Cyclosporin A showed promise in reversing P-glycoprotein-mediated resistance in Phase I trials.

    Conclusions:

    • Understanding resistance mechanisms is crucial for improving cancer treatment outcomes.
    • P-glycoprotein plays a significant role in MDR, and its expression is subject to complex regulation.
    • Further clinical trials are necessary to validate the therapeutic potential of agents that reverse P-glycoprotein-mediated resistance.