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This article is part of the supplement: Symposium Mammographicum 2004

Oral presentation

Scintimammographic findings with 99mTc-(V)DMSA and 99mTc-MIBI in usual-type ductal epithelial hyperplasia (HUT) and apocrine metaplasia (AM) of the breast, in relation with the cell proliferation index (Ki-67) and the presence of estrogen receptors (ERs)

V Papantoniou1, J Koutsikos1, M Bembi2, M Sotiropoulou3, S Tsiouris1, E Mainta1, V Valotasiou1, D Lazaris4 and CH Zerva1

1Nuclear Medicine Department, Alexandra University Hospital, Athens, Greece

2Obstetrics & Gynaecology Department, IASO Hospital, Athens, Greece

3Pathology Department, Alexandra University Hospital, Athens, Greece

4Obstetrics & Gynaecology Department, Alexandra University Hospital, Athens, Greece

from Symposium Mammographicum 2004
Edinburgh, UK. 19th – 20th July 2004

Breast Cancer Res 2004, 6(Suppl 1):P16doi:10.1186/bcr835

Published: 14 July 2004

Aim

The aim of this study was to assess retrospectively the ability of 99mTc-(V)DMSA and 99mTc-MIBI to recognize benign breast lesions such as HUT and AM, with elevated proliferative activity at different ER status, which have different probabilities to progress into invasive tumors.

Patients and methods

Twenty-one patients with histologically confirmed HUT and/or AM were submitted preoperatively to (V)DMSA and/or MIBI scintimammography, 10 min and 60 min after administration of 925–1100 MBq each radiotracer. Immunohistochemical staining was performed using the avidin–biotin method to determine Ki-67 and ER positivity. Lesion to background ratios (L/B) were calculated and compared (t test) with Ki-67 and ER values in HUT and AM with both tracers (Ki-67 >3% and ER >15% were considered positive).

Results

Histology demonstrated HUT in 11 patients and AM in 10 patients. Mean L/B ratios for (V)DMSA and MIBI in HUT and AM were 1.71 ± 0.44 (range 1.0–2.6), 1.2 ± 0.23 (range 1.0–1.6), 1.1 ± 0.06 (range 1.0–1.2) and 1.15 ± 0.05 (range 1.05–1.2), respectively. Ki-67 for HUT ranged from 1 to 20% (mean ± standard deviation [SD], 6.25 ± 5.7) and ER from 0 to 90% (mean ± SD, 43.8 ± 5.7). Ki-67 for AM ranged from 1 to 15% (mean ± SD, 4.83 ± 4.7). In patients with HUT and Ki-67 <3% the mean L/B (V)DMSA ratio was 1.13 ± 0.10, while in those with HUT and Ki-67 >3% it was 1.89 ± 0.35 (P = 0.0012). In patients with HUT and ER <15% the mean (V)DMSA L/B ratio was 1.66 ± 0.47, while in ER >15% it was 1.73 ± 0.43 (not statistically different). L/B MIBI ratios were not significantly different in the groups with higher or lower Ki-67 and ER values in patients with HUT (1.48 ± 0.45 for Ki-67 <3% and 1.25 ± 0.15 for Ki-67 >3%). AM did not show any statistical difference between L/B (V)DMSA and MIBI in the groups with higher and lower Ki-67 and ER expression.

Conclusion

(V)DMSA uptake in HUT seems to be related to Ki-67 activity and could be a useful indicator of the probability of these lesions to progress to atypical hyperplasia, ductal carcinoma in situ or invasive tumors.

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