Sonographically guided vacuum-assisted breast biopsy for complete excision of presumed benign breast lesions.

OBJECTIVES: Benign breast disease has a high prevalence and a substantial impact on women's quality of life. Excisional biopsy is still frequently used for the diagnosis of breast masses in China. We report our experience with percutaneous removal of presumed benign lesions under sonographic guidance with a multidirectional handheld vacuum-assisted biopsy device and evaluate this procedure as an alternative approach in the diagnosis and treatment of clinically benign breast lesions. METHODS: A total of 1766 sonographically guided vacuum-assisted excision procedures were performed on 738 patients with clinically benign breast lesions between February 2008 and October 2011. RESULTS: The mean patient age ± SD was 35.86 ± 11.2 years. The mean diameter of the lesions was 1.25 ± 0.70 cm. The mean number of cores needed to achieve removal was 11.6 ± 4.8. Fifty-nine percent of cases (436 of 738) had multiple breast lesions. There were no serious adverse events. There were only 37 cases with substantial bleeding. No cases had wound infection. Hematoma occurred in 62 cases (8%), but none needed surgical intervention. Skin damage occurred in only 5 cases (0.7%) and 14 cases (1.9%) had a vasovagal response. Most of the specimens (1755 of 1766 [99.4%]) were benign. Postoperative pain was minimal, and better cosmetic results were obtained than with conventional open biopsy. CONCLUSIONS: Percutaneous excisional biopsy with a sonographically guided vacuum-assisted core device is a safe and effective approach for accurate diagnosis and complete removal of presumed benign breast masses.

An autophagy inhibitor enhances the inhibition of cell proliferation induced by a proteasome inhibitor in MCF-7 cells.

The ubiquitin-proteasome system and the autophagy-lysosome pathway are the two main routes for eukaryotic intracellular protein clearance. Inhibition of proteasome activity leads to cell death. Due to the dual roles of autophagy in tumor cell survival and death, the effect of suppression of autophagy on breast cancer cells remains to be elucidated. We investigated whether inhibition of the proteasome is capable of inducing autophagy, and we assessed the effect of combined inhibition of the proteasome and autophagy on human breast cancer MCF-7 cells. The proteasome inhibitor bortezomib was used to induce autophagy in MCF-7 cells, and the effect of autophagy on the proliferation of MCF-7 cells was investigated using the autophagy inhibitor 3-MA. Cell viability was measured by MTT assay. The expression of autophagy­related proteins was determined by Western blot analysis and the GFP-LC3 redistribution was detected using a fluorescence microscope after MCF-7 cells were infected with a GFP-LC3-expressing adenovirus. MCF-7 cell proliferation was inhibited and autophagy was activated in the same dose­dependent manner. Bortezomib induced a dose­dependent increase in LC3-II. However, when MCF-7 cells were co-treated with bortezomib and 3-MA, 3-MA blocked the increase in LC3-II protein expression and led to a significant inhibition of cell proliferation. Inhibition of the proteasome may induce autophagy in human breast cancer MCF-7 cells and 3-MA could inhibit autophagy induced by the proteasome inhibitor. A combination of 3-MA and bortezomib increases cell death. These findings indicate that suppression of the two intracellular degradation systems may shed new light on breast cancer control.