The mathematical prediction model that incorporates five variables including breast cancer molecular subtype demonstrates excellent diagnostic performance in assessing the risk of non-sentinel lymph node metastasis in sentinel lymph node-positive patients. The prediction model could be of help surgeons in evaluating the risk of non-sentinel lymph node involvement for breast cancer patients; however, the model requires further validation in prospective studies.
The aim of the present study was to evaluate the association between mammographic features and clinicopathological characteristics in invasive ductal carcinoma. A total of 231 patients were retrospectively reviewed from January, 2011 to December, 2012. Statistical analysis was performed using Fisher's exact test, χ test, Spearman's correlation and logistic regression, as appropriate. Of the 231 patients who underwent mammography, malignant calcifications were significantly more frequent in carcinomas that were human epidermal growth factor receptor 2 (HER2)-positive (P=0.001) or had a >2 cm size tumor (P=0.006). The pleomorphic-type was correlated with a p53-positive status (P=0.039) or lymph node metastasis (P=0.048), whereas the indistinct amorphous-type was associated with a HER2-positive status (P=0.026). An evident mass was frequently observed in higher Ki-67 expression-level tumors (P=0.002). In conclusion, the aforementioned correlations are noteworthy as they potentially reflect tumor attributes and may serve as a guide for treatment.
Breast cancer (BC) is a common malignancy which is the most frequently diagnosed cancer in women all over the worldwide. This study aimed to investigate the roles of miR‐1469 in the development of BC, as well as its regulatory mechanism. The expression levels of miR‐1469 in BC tissues, serum, and cell lines were determined. Effects of overexpression of miR‐1469 on MCF7 cell viability, colony‐forming ability, apoptosis, migration, and invasion were then investigated. Furthermore, the potential target of miR‐1469 in MCF7 cells was explored. Besides, the association between miR‐1469, PTEN/PI3K/AKT, and Wnt/β‐catenin pathways was elucidated. Notably, confirmatory experiments by downregulation of miR‐1469 in SK‐BR‐3 cells were further performed. The miR‐1469 expression was significantly downregulated in BC tissues, serum, and cell lines. The overexpression of miR‐1469 significantly inhibited the proliferation, arrested cell‐cycle at G2/M phase, increased apoptosis, suppressed migration, and invasion of MCF‐7 cells. In addition, HOXA1 was verified as a direct target of miR‐1469, and the effects of overexpression of miR‐1469 on the malignant behaviors of MCF7 cells were significantly counteracted by overexpression of HOXA1 concurrently. Furthermore, the overexpression of miR‐1469 suppressed the activation of PTEN/PI3K/AKT and Wnt/β‐catenin pathways, which was reversed overexpression of HOXA1 concurrently. Besides, confirmatory experiments showed that the inhibition of miR‐1469 promoted the malignant behaviors of SK‐BR‐3 cells, which was inversed after miR‐1469 inhibition and HOXA1 knockdown at the same time. Our findings reveal that downregulation of miR‐1469 may promote the development of BC by targeting HOXA1 and activating PTEN/PI3K/AKT and Wnt/β‐catenin pathways. MiR‐1469 may serve as a promising target for BC therapy.
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