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Molecular Oncology, Markers, Clinical Correlates |
, MIB-1, p53, and c-erbB-2 in Inflammatory Breast Cancer
Cancer Therapeutics Branch [N. J. M., X. Y., A. L. P., S. M. Sw.], Cell and Cancer Biology Branch [I. R. L.], Laboratory of Pathology [M. J. M., S. M. H.], and Biostatistics and Data Management Section [S. M. St.], Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20889; National Surgical Adjuvant Breast and Bowel Project Operation Center, Pittsburgh, Pennsylvania [S. P.]; Georgetown University, Washington, DC [D. P. H.]; Centre Ibn Zohr, Tunis, Tunisia [N. M.]; and George Washington University School of Public Health and Health Services, Washington, DC [P. H. L.]
Purpose and Experimental Design: The purpose is to define intratumoral microvessel density (MVD) and potential biological markers that correlate with inflammatory breast cancer (IBC), we examined MVD, estrogen receptor a (ER) status, MIB-1 proliferation index, p53, and c-erbB-2 by immunohistochemistry in archival specimens from 67 women diagnosed with breast cancer with or without the inflammatory phenotype at the Institut Salah Azaiz (Tunis, Tunisia).
Results: The moderate (25–50/x400 field) to high microvessel count (>50/x400 field) was observed in 23 (51%) of 45 IBC tumors compared with 3 (14%) of 22 non-IBC tumors (P = 0.0031; 
2 test). The presence of ER was found in 6 (14%) of 44 cases versus 7 (32%) of 22 cases in IBC and non-IBC, respectively (P = 0.10). In this series of 67 patient tumors, the median MVD count in ER-negative breast tumors was 21, whereas the median count was 4 in ER-positive breast tumors (P = 0.08; Wilcoxon rank-sum test). However, MIB-1, p53, and c-erbB-2 were not significantly different between IBC and non-IBC tumors. The intratumoral MVD between IBC and non-IBC was still statistically significant after adjustment for multiple comparisons (P = 0.02; Bonferroni test).
Conclusions: These data suggest that there is an increased MVD in breast cancer with the inflammatory phenotype as compared with breast cancer without the inflammatory phenotype.
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