To evaluate and compare the performance of synthetic magnetic resonance imaging (SyMRI) in classifying benign and malignant breast lesions and predicting the expression status of immunohistochemistry (IHC) markers. We retrospectively analysed 121 patients with breast lesions who underwent dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) and SyMRI before surgery in our hospital. DCE-MRI was used to assess the lesions, and then regions of interest (ROIs) were outlined on SyMRI (before and after enhancement), and apparent diffusion coefficient (ADC) maps to obtain quantitative values. After being grouped according to benign and malignant status, the malignant lesions were divided into high and low expression groups according to the expression status of IHC markers. Logistic regression was used to analyse the differences in independent variables between groups. The performance of the modalities in classification and prediction was evaluated by receiver operating characteristic (ROC) curves. In total, 57 of 121 lesions were benign, the other 64 were malignant, and 56 malignant lesions performed immunohistochemical staining. Quantitative values from proton density-weighted imaging prior to an injection of the contrast agent (PD-Pre) and T2-weighted imaging (T2WI) after the injection (T2-Gd), as well as its standard deviation (SD of T2-Gd), were valuable SyMRI parameters for the classification of benign and malignant breast lesions, but the performance of SyMRI (area under the curve, AUC = 0.716) was not as good as that of ADC values (AUC = 0.853). However, ADC values could not predict the expression status of breast cancer markers, for which SyMRI had excellent performance. The AUCs of androgen receptor (AR), estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER-2), p53 and Ki-67 were 0.687, 0.890, 0.852, 0.746, 0.813 and 0.774, respectively. SyMRI had certain value in distinguishing between benign and malignant breast lesions, and ADC values were still the ideal method. However, to predict the expression status of IHC markers, SyMRI had an incomparable value compared with ADC values.

Breast cancer (BC) is a malignant tumor that occurs in the epithelial tissue of the breast gland. Long non-coding RNA (lncRNA) small nucleolar RNA host gene 3 (SNHG3) has been found to promote BC cell proliferation and invasion by regulating the microRNA (miR)-101/zinc-finger enhancer binding axis in BC. Herein, the objective of the present study is to evaluate the effect of lncRNA SNHG3 on BC cell proliferation and metastasis with the Notch signaling pathway.

The present study aimed to investigate the underlying regulatory mechanism of MYCL proto‑oncogene (MYCL) in triple‑negative breast cancer (TNBC) progression. In vitro experiments were performed to confirm the functional roles of MYCL in TNBC, and its effects on the JAK/STAT3 pathway through flow cytometric analysis, colony formation, wound healing and Transwell assays. In addition, the GSE45498 dataset demonstrated that MYCL was upregulated in TNBC and that it was significantly related to poor survival of patients with TNBC. Knockdown of MYCL induced the apoptosis, and suppressed the proliferation, migration and invasion of TNBC cells by inhibiting the JAK/STAT3 pathway. Notably, MYCL could activate the JAK/STAT3 pathway, whereas inhibition of the JAK/STAT3 pathway could eliminate the effect of MYCL on TNBC cells. Knockdown of MYCL also suppressed the growth of TNBC xenograft tumors. In conclusion, MYCL could promote TNBC progression by activating the JAK/STAT3 pathway.