Abstract

Abstract Aim: To assess neoangiogenesis in relation to breast density (BD), calcitonin gene related peptide (CGRP), cell proliferation seeking radiotracer 99mTc-(V)DMSA uptake (SMM) in invasive ductal associated with extensive in situ carcinoma (DCIS + IDC) and in pure invasive breast carcinoma (IDC). Methods: 20 patients with histologically confirmed mixed DCIS + IDC (n=10) and pure IDC (n=10) were submitted preoperatively to mammography and scintimammography. The percentage of breast density (BD) and the percentage of tracer uptake (SMM) were calculated with computer assisted methods. CGRP and the number of newly formed blood vessels (NBV) were immunohistochemicaly assessed. NBV, BD, CGRP, and SMM were compared (t-test) between the two groups. Linear regression analysis was performed between NBV, BD, CGRP and SMM in both groups. Results: NBV, BD, CGRP and SMM were significantly higher in mixed DCIS + IDC as compared to pure IDC (32.1±10.4 vs 24.3±5 p=0.048, 35.2 ± 6.9 vs 25.6±10.7 p=0.028, 25.5±7.6 vs 17±7.8 p=0.024, 26.75±4.09 vs 11.34±8.5 p=0.0009). NBV was strongly correlated with BD and CGRP in the DCIS component of the mixed group (r=0.933 p<0.001, r=0.793 p<0.01 respectively). BD was also significantly correlated with CGRP and SMM in the DCIS component of the same group (r=0.974 p<0.001, r=0.728 p<0.05 respectively). In contrast, no significant correlation(NS) was found between NBV and BD, CGRP or between BD and CGRP, SMM in both the IDC component of mixed group and pure IDC group (r=0.388 NS, r=0.391 NS, r= − 0.597 NS, r= − 0.352 NS in the IDC component of mixed group; r=0.584 NS, r= 0.297 NS, r= − 0.574 NS, r= −0.294 NS in pure IDC respectively). Conclusion: Mixed DCIS + IDC lesions exhibit significantly increased NBV, BD, CGRP and SMM values as compared to those of IDC lesions. The strong correlation between neoangiogenesis and the other parameters in the mixed group indicates that the mixed DCIS + IDC constitutes a strictly different entity from pure IDC, more aggressive and probably originates from the stroma through the CGRP pathway. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2381.

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