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Anthracycline resistance: the problem and its current definition

¹Division of Medical Oncology, Istituto Nazionale per lo Studio e la Cura dei Tumori, Milan, Italy.

Seminars in Oncology

|August 1, 1997

Summary

Anthracycline chemotherapy for breast cancer faces challenges due to drug resistance. Understanding resistance mechanisms like P-glycoprotein and topoisomerase II is crucial for improving treatment outcomes and predicting patient response.

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Area of Science:

Oncology
Pharmacology
Molecular Biology

Background:

Anthracyclines have been a cornerstone in breast cancer treatment since the 1970s.
Despite combination regimens improving outcomes, modest survival and relapse rates persist, particularly in metastatic disease.
Drug resistance, both intrinsic and acquired, is a primary driver of clinical failure in breast cancer treatment.

Purpose of the Study:

To review the known mechanisms of anthracycline resistance in breast cancer.
To evaluate the clinical relevance of P-glycoprotein (Pgp)-mediated multidrug resistance.
To explore other potential mechanisms of resistance, such as alterations in topoisomerase II.

Main Methods:

Review of in vitro and in vivo studies on P-glycoprotein inhibitors.

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Analysis of clinical trial data regarding the efficacy of Pgp inhibitors.

Examination of studies correlating gene expression (MDR1) with treatment outcomes.

Investigation of non-efflux pump resistance mechanisms, including topoisomerase II activity.

Main Results:

In vitro efficacy of Pgp inhibitors has not consistently translated to clinical benefit.
Pgp inhibition may increase vulnerability of certain tissues (e.g., brain) to cytotoxic drugs.
Correlation between MDR1 gene overexpression and treatment failure in human tumors remains unclear.
Changes in topoisomerase II activity represent another significant mechanism of anthracycline resistance.

Conclusions:

A significant gap exists between laboratory findings on drug resistance and clinical outcomes.
Current laboratory studies cannot reliably predict clinical efficacy, cross-resistance, or treatment failure mechanisms.
Further research is needed to clarify the clinical contribution of multidrug resistance and other mechanisms to anthracycline resistance in breast cancer.