[Diagnostic value of contrast-enhanced ultrasound in breast lesions of BI-RADS 4].

Objective: To investigate the value of contrast-enhanced ultrasound (CEUS) in the differential diagnosis of BI-RADS 4 breast masses. Methods: A total of 72 patients were collected from the First Hospital of Shanxi Medical University from January 2016 to December 2017.79 breast masses were confirmed by biopsy or surgical pathology.All the masses were classified by BI-RADS according to conventional ultrasound and CEUS was performed in parallel.Based on the results of the CEUS predictive model, the benign and malignant features of the breast BI-RADS type 4 tumors were re-determined: (1) conventional ultrasound BI-RADS classification+ CEUS predictive model: both of them were malignant when malignant; (2) re-adjusting BI-RADS classification by CEUS predictive model: if the malignant CEUS predictive model, upgrade a class, if the benign CEUS predictive model, downgrade a class.The diagnostic efficiency of the two methods in breast masses of BI-RADS 4 was compared. Results: (1) There were 36 malignant masses and 43 benign masses in 79 breast masses.Diagnostic sensitivity, specificity, accuracy, positive predictive value and negative predictive value of the conventional ultrasound BI-RADS classification, CEUS predictive model, conventional ultrasound BI-RADS classification+ CEUS predictive model and the adjusted BI-RADS classification were 86.1%, 65.1%, 74.7%, 67.4%, 84.8%; 88.9%, 76.7%, 82.3%, 76.2%, 89.2%; 80.6%, 86.0%, 83.5%, 82.9%, 84.1%; 97.2%, 76.7%, 86.1%, 77.8%, 97.1%, respectively.(2) The area under the receiver operating characteristic (ROC) curve of conventional ultrasound BI-RADS classification, CEUS predictive model, conventional ultrasound BI-RADS classification+ CEUS predictive model and the adjusted BI-RADS classification was 0.756, 0.828, 0.833, 0.870, respectively.Before and after the adjustment of BI-RADS classification, the difference was statistically significant (Z=2.322, P<0.05). Conclusion: The diagnostic efficiency that CEUS predictive model adjusted classification of BI-RADS 4 breast masses is better, the method can reduce unnecessary biopsy.

Expression and clinical value of the soluble major histocompatibility complex class I-related chain A molecule in the serum of patients with renal tumors.

We investigated the expression and clinical value of the soluble major histocompatibility complex class I-related chain A (sMICA) molecule in the serum of patients with renal tumors. Sixty patients diagnosed with renal tumors were enrolled in the experimental group, whereas 20 healthy volunteers served as the control group. The sMICA levels were measured via enzyme-linked immunosorbent assay, and the results were analyzed in combination with data from pathol-ogy examination. The experimental group had a statistically significant higher sMICA level (P < 0.05) than the control group. The sMICA level was higher in patients with malignant tumors than in those with be-nign tumors. We also observed a positive relationship among different tumor-node-metastasis (TNM) pathological stages with more advanced diseases exhibiting higher sMICA levels. As a tumor-associated antigen, MICA has a close relationship with renal tumorigenesis and immune es-cape. Our results indicated that sMICA levels were related to tumor pathol-ogy, TNM stage, and metastasis. Therefore, sMICA might be a potential marker for tumor characteristics, prognosis, and recurrence prediction.

A long non-coding RNA, ELFN1-AS1, sponges miR-1250 to upregulate MTA1 to promote cell proliferation, migration and invasion, and induce apoptosis in colorectal cancer.

OBJECTIVE: Long non-coding RNA (lncRNA), is essential for the development and progression of cancers. LncRNA regulates target gene expression by sponging the corresponding microRNA (miRNA) during tumorigenesis. This work aimed to explore the role of one lncRNA, ELFN1-AS1, in colorectal cancer (CRC) development and elucidate the pertinent signaling pathway. PATIENTS AND METHODS: First, we found that ELFN1-AS1 was highly abundant in the human CRC tissues and cell lines. Silence of ELFN1-AS1 expression reduced cell proliferation, colony formation, migration and invasion, while inducing apoptosis in vitro; moreover, knockdown of ELFN1-AS1 decreased the size and weight of tumor in vivo. RESULTS: Luciferase reporter assay revealed that ELFN1-AS1 interacted with miR-1205 and suppressed its expression. In addition, miR-1205 could bind to the 3' untranslated region (3'-UTR) of Metastasis Associated Protein1 (MTA1) and inhibited ELFN1-AS1 expression. More importantly, overexpression of MTA1 completely rescued the phenotype of ELFN1-AS1 knockdown. CONCLUSIONS: In sum, our study demonstrated that ELFN1-AS1 sponges miR-1205 to upregulate MTA1, which is essential for CRC cell proliferation, migration, and invasion as well as apoptosis induction.

Restoration of microRNA-373 suppresses growth of human T-cell lymphoma cells by repressing CCND1.

OBJECTIVE: Adult T cell lymphoma is a highly aggressive T-cell malignancy. This study was designed to explore the expression and functional significance of microRNA (miR)-373 in T cell lymphoma. PATIENTS AND METHODS: We analyzed the levels of CCND1 and miR-373 in T cell lymphoma tissue and the relationship of miR-373 levels with patients' prognosis. We then overexpressed miR-373 by miRNA mimics transfection and inhibited miR-373 by miRNA antisense transfection in T cell lymphoma cells. Cell survival and growth were analyzed by CCK-8 assay and MTT assay, respectively. Cell proliferation was analyzed by flow cytometry. Bioinformatics analyses were applied to predict miR-373 targets, which were then confirmed by luciferase reporter assay. RESULTS: We detected significantly higher levels of CCND1, and significantly lower levels of miR-373 in T cell lymphoma tissue, compared to the adjacent non-tumor tissue. Moreover, the low miR-373 levels were associated with poor survival of the patients. Overexpression of miR-373 significantly inhibited cell growth, while depletion of miR-373 increased cell growth in T cell lymphoma cells. Moreover, the effects of miR-373 on cell growth appeared to result from an alteration in cell proliferation. Finally, miR-373 was found to bind to the 3'-UTR of CCND1 mRNA to inhibit its translation in T cell lymphoma cells. CONCLUSIONS: Our study suggests that reduced miR-373 levels in T cell lymphoma tissue may promote T cell lymphoma growth, possibly through CCND1-mediated cell proliferation.