Role of expression of cell cycle inhibitor p27 and MIB-1 in predicting lymph node metastasis in male breast carcinoma
- PMID: 11896756
- DOI: 10.1046/j.1524-4741.2002.08206.x
Role of expression of cell cycle inhibitor p27 and MIB-1 in predicting lymph node metastasis in male breast carcinoma
Abstract
Tumor expression of the proliferation marker (MIB-1) and the cell cycle-related protein (p27) may predict the biologic behavior of various human tumors. The purpose of this study was to evaluate the role of p27 and MIB-1 expression in predicting lymph node metastasis in male breast carcinomas (MBCs). We studied 67 patients with invasive MBC who had undergone modified radical mastectomy. Pathologic lymph node status was correlated with the p27 protein and the MIB-1 proliferation index. These factors were studied immunohistologically by standard methods. Men in this study ranged from 36 to 92 years of age (mean, 63 years); 43 (64%) were T1 lesions, and 24 (36%) were T2 lesions. Twenty-nine patients (43%) had positive nodes. p27 was expressed in 43 tumors (64%) and MIB-1 in 13 tumors (19.4%). Tumors with positive p27 showed positive lymph nodes in 10 cases (23%). In contrast, p27-negative tumors had positive lymph nodes in 18 cases (75%). Tumors positive for MIB-1 show positive lymph nodes in 11 cases (85%). However, when MIB-1 was negative, only 16 patients (30%) had positive lymph nodes. Multivariate logistic regression analysis confirmed the utility of MIB-1 overexpression in predicting lymph node metastasis ( p < 0.0006). Also, decreased p27 protein expression strongly correlates with lymph node metastasis ( p < or = 0.0001). Furthermore, when p27 was negative and MIB-1 was positive, 100% of the patients had positive lymph nodes. In contrast, when p27 was positive and MIB-1 was negative, only 12% of patients had positive lymph nodes. The reduced expression of the p27 protein and the overexpression of the MIB-1 proliferation index in this study show a significant correlation in predicting lymph nodes metastasis in MBCs.
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