TY - JOUR
T1 - Relationship between tumour shrinkage and reduction in Ki67 expression after primary chemotherapy in human breast cancer
AU - Bottini, A.
AU - Berruti, A.
AU - Bersiga, A.
AU - Brizzi, M. P.
AU - Bruzzi, P.
AU - Aguggini, S.
AU - Brunelli, A.
AU - Bolsi, G.
AU - Allevi, G.
AU - Generali, D.
AU - Betri, E.
AU - Bertoli, G.
AU - Alquati, P.
AU - Dogliotti, L.
PY - 2001/10/19
Y1 - 2001/10/19
N2 - The association between tumour shrinkage and reduction in kinetic cell activity after primary chemotherapy in human breast cancer is still a matter of investigation. 157 patients with T2-4, N0-1, M0 breast cancer received primary chemotherapy consisting of either the CMF regimen + tamoxifen (the first consecutive 76 cases) or the single agent epirubicin (the subsequent 81), Ki67, p53, bcl2, c-erbB2 and steroid hormone receptors were evaluated immunohistochemically in tumour specimens obtained before chemotherapy and at surgery. Tumour shrinkage of >50% occurred in 72.4% of patients. Ki67 expression significantly decreased after chemotherapy; the reduction correlated with tumour response in both univariate (P <0.005) and multivariate analysis (P = 0.02). p53, bcl-2, steroid hormone receptor and c-erbB2 immunostaining were scarcely affected. Baseline bcl2 (P = 0.04) and c-erbB2 (P = 0.02) were directly and inversely associated with the reduction in Ki67 immunostaining, respectively, Baseline p53 expression (P <0.01) was directly related with Ki67 expression at residual tumour, whereas oestrogen receptor expression (P <0.001) was inversely related. Ki67 at residual tumour was a better predictor for relapse-free survival (RFS) than baseline Ki67. Clinical response (P <0.03), but not reduction in Ki67, was a significant independent predictor for disease recurrence. Chemotherapy was found to induce tumour shrinkage and to reduce the number of cells in the cell cycle, but its effect on tumour biology/aggressiveness was minimal. Reduction in Ki67 immunostaining correlated with clinical response but failed to be related to RFS, Ki67 expression at surgery rather than at baseline appears to be a better predictor for disease relapse.
AB - The association between tumour shrinkage and reduction in kinetic cell activity after primary chemotherapy in human breast cancer is still a matter of investigation. 157 patients with T2-4, N0-1, M0 breast cancer received primary chemotherapy consisting of either the CMF regimen + tamoxifen (the first consecutive 76 cases) or the single agent epirubicin (the subsequent 81), Ki67, p53, bcl2, c-erbB2 and steroid hormone receptors were evaluated immunohistochemically in tumour specimens obtained before chemotherapy and at surgery. Tumour shrinkage of >50% occurred in 72.4% of patients. Ki67 expression significantly decreased after chemotherapy; the reduction correlated with tumour response in both univariate (P <0.005) and multivariate analysis (P = 0.02). p53, bcl-2, steroid hormone receptor and c-erbB2 immunostaining were scarcely affected. Baseline bcl2 (P = 0.04) and c-erbB2 (P = 0.02) were directly and inversely associated with the reduction in Ki67 immunostaining, respectively, Baseline p53 expression (P <0.01) was directly related with Ki67 expression at residual tumour, whereas oestrogen receptor expression (P <0.001) was inversely related. Ki67 at residual tumour was a better predictor for relapse-free survival (RFS) than baseline Ki67. Clinical response (P <0.03), but not reduction in Ki67, was a significant independent predictor for disease recurrence. Chemotherapy was found to induce tumour shrinkage and to reduce the number of cells in the cell cycle, but its effect on tumour biology/aggressiveness was minimal. Reduction in Ki67 immunostaining correlated with clinical response but failed to be related to RFS, Ki67 expression at surgery rather than at baseline appears to be a better predictor for disease relapse.
KW - CMF
KW - Epirubicin
KW - Ki67
KW - Tamoxifen
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U2 - 10.1054/bjoc.2001.2048
DO - 10.1054/bjoc.2001.2048
M3 - Article
C2 - 11710821
AN - SCOPUS:0035914249
VL - 85
SP - 1106
EP - 1112
JO - British Journal of Cancer
JF - British Journal of Cancer
SN - 0007-0920
IS - 8
ER -