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Effect of mutated TP53 on response of advanced breast cancers to high-dose chemotherapy

P Bertheau1, F Plassa, M Espié

  • 1Service de Pathologie and INSERM ERM 0220, Hôpital Saint-Louis, 1 Ave C, Vellefaux, 75475 Paris, Cedex 10, France.

Lancet (London, England)
|September 24, 2002
PubMed

Insights

Mutated TP53 status in breast cancer patients significantly correlates with complete response to epirubicin and cyclophosphamide chemotherapy. Inactivating the TP53 pathway may enhance treatment efficacy in advanced breast cancers.

Area of Science:

  • Oncology
  • Genetics
  • Pharmacology

Background:

  • TP53 gene status (mutated or wild type) may influence tumor response to genotoxic chemotherapy drugs, potentially affecting apoptosis and cell-cycle arrest.
  • Clinical data on TP53's role in chemotherapy response are inconclusive due to tumor and treatment heterogeneity, and varied assessment methods.

Purpose of the Study:

  • To investigate the correlation between TP53 gene status and treatment response in patients with locally advanced breast cancer.
  • To determine if TP53 pathway inactivation impacts chemotherapy efficacy in high-grade breast cancers.

Main Methods:

  • Analysis of 50 non-inflammatory, locally advanced breast cancer cases treated with high-dose epirubicin and cyclophosphamide.
  • Assessment of TP53 gene status in tumor samples.
  • Evaluation of complete response rates based on TP53 mutation status.

Main Results:

  • Eight complete responses were observed in the study cohort.
  • All complete responses occurred in the 14 patients whose tumors harbored mutated TP53 (p<0.0001).
  • A significant association was found between mutated TP53 and complete chemotherapy response.

Conclusions:

  • Inactivation of the TP53 pathway is strongly associated with a superior response to epirubicin and cyclophosphamide chemotherapy in high-grade, advanced breast cancers.
  • TP53 mutation status could serve as a predictive biomarker for chemotherapy response in this patient population.

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