Background. We sought to determine the significance of Ki-67, one of the tumor cell proliferation markers, as a useful prognostic factor in early breast cancer. Results. Univariate analysis determined that tumor size, lymph node involvement, histologic grade, estrogen receptor, progesterone receptor, bcl-2, and Ki-67 (C10%) were statistically significant for both overall survival (OS) and distant metastasis-free survival (DFS). Of these factors, lymph node involvement and high Ki-67 expression were identified as independent prognostic factors for OS and DFS on the basis of multivariate analysis. The survivals of intermediate-and high-risk groups according to 2007 St. Gallen consensus were further separated by Ki-67 expression level (5-year DFS rate = 91.9% vs. 86.3% for Ki-67 \ 10% and C10%, respectively in intermediate-risk group (P = .01); 5-year DFS rate = 82.5% vs. 61.4% for Ki-67 \ 10% and C10%, respectively in high-risk group (P = .01)). The survivals of low-and high-risk groups according to Adjuvant! Online were further separated by Ki-67 expression level (5-year DFS rate = 97.8% vs. 89.5% for Ki-67 \ 10% and C10%, respectively in low-risk group (P = .02); 5-year DFS rate = 9.4% vs. 82.6% for Ki-67 \ 10% and C10% in highrisk group (P = .005)). Conclusions. Ki-67 is an independent prognostic factor for DFS and OS in early breast cancer and can provide additional prognostic information on the risk stratification with the use of the 2007 St. Gallen consensus and Adjuvant! Online.

The prognostic significance of young age was found to depend on molecular subtype. An age of <35 years was a poor prognosticator in patients with the HR+/HER2-, HR+/HER2+, and HR-/HER2+ subtypes, but not in those with the TN subtype.

BackgroundThe neutrophil-lymphocyte ratio (nlr) has been reported to correlate with patient outcome in several

Although radiotherapy resistance is associated with locoregional recurrence and distant metastasis in breast cancers, clinically relevant molecular markers and critical signaling pathways of radioresistant breast cancer are yet to be defined. Herein, we show that HER2-STAT3-survivin regulation is associated with radiotherapy resistance in HER2-positive breast cancers. Depletion of HER2 by siRNA sensitized HER2-positive breast cancer cells to irradiation by decreasing STAT3 activity and survivin, a STAT3 target gene, expression in HER2-positive breast cancer cells. Furthermore, inhibition of STAT3 activation or depletion of survivin also sensitized HER2-positive breast cancer cells to irradiation, suggesting that the HER2-STAT3-survivin axis is a key pathway in radiotherapy resistance of HER2-positive breast cancer cells. In addition, our clinical analysis demonstrated the association between HER2-positive breast cancers and radiotherapy resistance. Notably, we found that increased expression of phosphorylated STAT3, STAT3, and survivin correlated with a poor response to radiotherapy in HER2-positive breast cancer tissues. These findings suggest that the HER2-STAT3-survivin axis might serve as a predictive marker and therapeutic target to overcome radiotherapy resistance in HER2-positive breast cancers.

A sonographic lesion size >20 mm can be used as another guideline for surgeons to consider sentinel lymph node biopsy in patients with DCIS diagnosed by a sonographically guided CNB.