BackgroundThe false negative rate of sentinel lymph node biopsy (SLNB) is 5-10%, and results in improper patient management. The study was to assess the value of ultrasound-suspicious axillary lymph node biopsy (USALNB) in patients with early breast cancer, and to compare SLNB combined with USALNB (SLNB + USALNB) with SLNB alone.MethodsFrom January 2010 to July 2013, 216 patients with early breast cancer were enrolled consecutively at the Department of Breast and Thyroid Surgery, Qianfoshan Hospital, Shandong University. All patients underwent wire localization of the suspicious node by color Doppler ultrasonography, followed by SLNB 2–3 hours later, suspicious node lymphadenectomy, and level ≥ II axillary dissection (as the gold standard). The predictive values of node status between SLNB + USALNB and SLNB alone were compared.ResultsThe success rate of SLNB was 99.1% (214/216). After axillary dissection, 71 patients were confirmed with axillary lymph node metastases by pathological examinations. Eight false negatives were observed using SLNB alone, resulting in sensitivity of 88.7%, specificity of 100%, false negative rate of 11.3%, and false positive rate of 0% in predicting the axillary node status. SLNB + USALNB resulted in sensitivity of 97.2%, specificity of 100%, false negative rate of 2.8%, and false positive rate of 0%. The false negative rate of SLNB + USALNB was significantly different from that of SLNB alone (P = 0.031).ConclusionsSLNB + USALNB seems to be a low-risk procedure that might be useful in reducing the false negative rate of SLNB, improving the accuracy of axillary nodes evaluation in early breast cancer.
Resistance to trastuzumab is frequently observed during the treatment of patients with human epidermal growth factor 2 (HER2)-positive metastatic breast cancers. The aim of the present study was to determine if the phosphorylated proline-rich Akt substrate of 40 kDa (phospho-PRAS40Thr246), a novel biomarker for phosphoinositol-3 kinase (PI3K) pathway activation, could predict the response of HER2-positive metastatic breast cancers to treatment with trastuzumab. Formalin-fixed, paraffin-embedded tumor tissue samples were retrospectively collected from 55 trastuzumab-treated patients. Next, the expression of phospho-PRAS40Thr246 and phosphatase and tensin homolog (PTEN) was assessed by immunohistochemistry. In total, five common phosphoinositol-3 kinase α catalytic subunit mutations, namely E542K, E545K, E545D, H1047R and H1047L, were identified by the amplification-refractory mutation system, using the allele-specific polymerase chain reaction. The activation of the PI3K pathway, as determined by low PTEN expression or the presence of oncogenic PIK3CA mutations, was observed in 49.1% (27 cases) of the 55 HER2-positive metastatic breast cancer tissues. In total, 40% of the tumors were defined as being phospho-PRAS40Thr246-positive. Furthermore, the results revealed that phospho-PRAS40Thr246 expression was associated with the PI3K pathway activation status and an increased risk of tumor progression in HER2-positive metastatic breast cancer patients who had received trastuzumab-based therapy. Therefore, phospho-PRAS40Thr246 expression levels may reflect the PI3K pathway activation status and act as a biomarker for HER2-amplified breast cancer patients who are unlikely to respond to trastuzumab-based therapy.
Emerging evidence suggests that long non-coding RNAs (lncRNAs) play pivotal roles in cancer progression, including in intrahepatic cholangiocarcinoma (IHCC). The overexpression of lncRNA ZEB1 antisense 1 (ZEB1-AS1) has been discovered in several types of cancer; however, the clinical significance and functional role of ZEB1-AS1 in IHCC have not yet been determined. In the present study, ZEB1-AS1 was found to be upregulated in IHCC cell lines and tissues. A high ZEB1-AS1 expression was associated with clinical progression and a poor survival of patients with IHCC, and was identified as an independent risk factor for a poor prognosis. In addition, ZEB1-AS1 promoted the proliferation and metastasis of IHCC cells both in vitro and in vivo. ZEB1-AS1 was demonstrated to increase the expression of ZEB1 by sponging miR-200a and to thereby accelerate epithelial-mesenchymal transition (EMT). On the whole, the findings of the present study demonstrate that ZEB1-AS1 promotes proliferation and metastasis in IHCC, and induces EMT through the miR-200a/ZEB1 signaling pathway. ZEB1-AS1 may thus be a promising prognostic biomarker and essential therapeutic target for IHCC.
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