A tumor sample drawn at the time of pre-treatment biopsy will be frozen and used to perform oligonucleotide based microarrays (Affymetrix). This technique allows the evaluation of thousands of genes and ultimately provides us with the tumor genetic profile. Homogeneous genetic profiles (genetic clusters) that might be identified, will be correlated with the efficacy of single-agent epirubicin. This correlation will allow us to address the secondary end-point of this study, which is the identification of other genes or eventually a genetic profile playing a role in the determination of sensitivity to anthracyclines. Among the genes that could interfere with sensitivity to anthracyclines, p-53 seems to deserve special attention. Indeed, "in-vitro" data suggest that at least some p-53 mutated tumors are poorly sensitive to anthracyclines, primarily because anthracycline-induced apoptosis is prevented. Interestingly, p-53 mutated tumors display frequently HER-2 gene amplification and therefore topo II a gene amplification (23). Accordingly, p-53 mutations could hamper response to anthracyclines even in tumors carrying topo II a gene amplification. This hypothesis will also be explored in the present study, because p-53 mutations will be evaluated by DNA sequencing, and the efficacy of epirubicin in topo II a amplified and non-amplified tumors will be correlated with p-53 status.