Format

Send to

Choose Destination
J Breast Cancer. 2013 Mar;16(1):40-9. doi: 10.4048/jbc.2013.16.1.40. Epub 2013 Mar 31.

STAT3, a Poor Survival Predicator, Is Associated with Lymph Node Metastasis from Breast Cancer.

Author information

1
Department of Thyroid and Breast Surgery, Western China Hospital of Sichuan University, Chengdu, China.

Abstract

PURPOSE:

The aim of this study is to explore signal transducer and activator of transcription 3 (STAT3) expression in breast cancer and to analyze the detailed mechanism that STAT3 contributes to the progression of breast cancer.

METHODS:

We retrospectively analyzed the clinicopathologic characteristics and overall survival (OS) of 140 breast cancer patients after curative surgery, and detected STAT3 expression, phosphorylated STAT3 (pSTAT3) expression, Ki-67 expression, vascular endothelial growth factor (VEGF)-C and -D expression in breast cancer tissues, and adjacent nontumor tissues. Survival analysis and relationship analysis were adopted for demonstrated the important mechanism of STAT3 contribution to progression of breast cancer.

RESULTS:

STAT3 expression, pSTAT3 expression, Ki-67 expression, VEGF-C expression, and VEGF-D expression in breast cancer tissues were significantly higher than those in adjacent nontumor tissues, respectively. With survival analysis, only number of lymph node metastasis (N stage) was identified as the independent predictors of the OS of breast cancer patients. Besides, we demonstrated there was the most prominent correlation between STAT3 expression and lymph node metastasis in breast cancer tissues by using the multinominal regression method.

CONCLUSION:

STAT3, a poor survival biomarker potential association with lymph node metastasis, was suitable for predication the OS of breast cancer patients after curative resection.

KEYWORDS:

Breast neoplasms; Neoplasm metastasis; Prognosis; STAT3 transcription factor

Supplemental Content

Full text links

Icon for Korean Breast Cancer Society Icon for PubMed Central
Loading ...
Support Center