A Neo-Adjuvant Study of Sequential Epirubicin and Docetaxel in Combination With Capecitabine in Patients With Locally Advanced Breast Cancer
- Describe the pathologic response rate in chemotherapy-naive women with locally advanced
breast cancer (stage IIIA or IIIB) after 6 courses of sequential neoadjuvant therapy
with epirubicin hydrochloride and a combination of docetaxel with capecitabine .
- Describe the adverse events of sequential epirubicin hydrochloride and a combination of
docetaxel with capecitabine in this patient population.
- Identify by transcriptional profiling the differential expression of candidate gene
products that confer chemosensitivity to epirubicin hydrochloride, docetaxel, and
- Correlate the differential expression of known genetic polymorphisms of intracellular
regulators involved in the metabolism of epirubicin hydrochloride, docetaxel, and
capecitabine with adverse events and tumor response.
- Assess individual patient variation in clinical (toxicity and/or activity), in
pharmacologic (pharmacokinetic/pharmacodynamic parameters), and/or biologic
(correlative laboratory study results) responses to epirubicin hydrochloride,
docetaxel, and capecitabine due to genetic differences in proteins involved in drug
response (transport, metabolism and/or mechanism of action).
OUTLINE: Patients receive epirubicin hydrochloride IV on day 1. Treatment repeats every 2
weeks for 3 courses. Beginning 2 weeks after last dose of epirubicin hydrochloride, patients
receive docetaxel IV over 1 hour on day 1 and oral capecitabine twice daily on days 1-14.
Treatment with docetaxel and capecitabine repeats every 3 weeks for 3 courses. Patients then
Blood samples are collected at baseline for pharmacogenetic studies. Tumor tissue samples
are collected at baseline and periodically during treatment for correlative laboratory
After completion of study treatment, patients are followed every 3 months until disease
progression and then every 6 months for up to 5 years.
Masking: Open Label, Primary Purpose: Treatment
Pathologic response rate
Julian R. Molina, MD, PhD
United States: Food and Drug Administration