Clinical Significance of Contrast-Enhanced Ultrasound Galactography in Pre-operative Diagnosis of Patients With Pathologic Nipple Discharge.

OBJECTIVE: The aim of the work described here was to investigate the feasibility and diagnostic value of using contrast-enhanced ultrasound (CEUS) galactography with SonoVue in patients with pathologic nipple discharge (PND). METHODS: Twenty-eight patients who underwent breast surgery for PND from May 2019 to August 2021 were included. Routine ultrasound, ductoscopy and CEUS galactography were performed successively. Lesions were diagnosed and localized. The sensitivity, specificity and pre-operative localization value of each examination method were evaluated on post-operative pathology. RESULTS: CEUS galactography was successfully conducted in all 28 patients and revealed negative ductal ectasia, filling stop and filling defect. Ductoscopy revealed positive nodules in 21 cases and negative nodules in 7 cases. A total of 18 nodules were found by routine ultrasound, and the relationship between all nodules and the discharge duct was confirmed after CEUS galactography. Compared with the other two methods, CEUS galactography had higher sensitivity, positive predictive value and negative predictive value (100%, 81.82% and 100%, respectively), while it has the same specificity as routine ultrasound (both 60%). The pre-operative location of the nipple duct was consistent with the intra-operative findings in 28 patients after CEUS galactography. CONCLUSION: The ultrasound contrast agent SonoVue can be used for CEUS galactography in patients with PND. CEUS galactography can improve the detection of ductal nodules and locate the nipple discharge duct pre-operatively. As the technique does not emit radiation and SonoVue is easily metabolized and safe, CEUS galactography is better than conventional imaging for PND patients.

A Prospective Randomized Clinical Study of Minimally Invasive Video-assisted Thyroidectomy for Papillary Thyroid Microcarcinoma.

BACKGROUND: The purpose of this study was to observe the effectiveness of minimally invasive video-assisted thyroidectomy (MIVAT) in treating papillary thyroid microcarcinoma (PTMC). METHODS: A total of 224 patients with PTMC who met the inclusion and exclusion criteria were selected from the Department of General Surgery, Beijing Friendship Hospital, Capital Medical University, between January 2017 and December 2019. They were randomized into the MIVAT group or traditional open operation group. For both groups, we observed the number of lymph node dissections, amount of intraoperative blood loss, duration of the operation, length of the incision, and number of injuries to the recurrent laryngeal nerve. RESULTS: The average operation time (132.8±29.4 min) in the MIVAT group was significantly higher than that in the open surgery group (83.8±14.29 min) ( P =0.026). The length of incision (2.8±0.6 cm) in patients in the MIVAT group was significantly shorter than that in patients in the open group (7.4±1.1 cm) ( P =0.000). No significant differences were observed in the number of lymph node dissections ( P =0.712), the amount of intraoperative bleeding ( P =0.581), and the number of recurrent laryngeal nerve injuries ( P =0.634). The average follow-up was 5 years, and both groups had no recurrence. CONCLUSIONS: In the treatment of PTMC, MIVAT had similar outcomes as traditional open operations, although the operation time was longer. However, the length of the incision was significantly shorter and thus provided cosmetic advantages for patients.

PBX3-activated DLG1-AS1 can promote the proliferation, invasion, and migration of TNBC cells by sponging miR-16-5p.

DLG1-AS1 and PBX3 have been identified as acting as an oncogene in cervical cancer. However, they have not been well explored in triple-negative breast cancer (TNBC). As TNBC is one of the malignancies causing increasing death throughout the world, this study aimed to probe into the regulatory relationship between DLG1-AS1 and PBX3 in TNBC cells. In this study, real-time quantitative PCR (qRT-PCR) and western blot experiments were conducted to investigate the RNA and protein levels of genes of interest in TNBC cells. Functional experiments were implemented, such as 5-ethynyl-2'-deoxyuridine (EdU), transwell, and wound healing assays, to assess the changes in TNBC cell phenotype. Chromatin immunoprecipitation, luciferase reporter, RNA binding protein immunoprecipitation, and RNA pull-down assays were conducted to investigate the binding relationships among subject genes. The results show that DLG1-AS1 and PBX3 displayed high expression in TNBC cells, and PBX3 worked as the transcriptional activator of DLG1-AS1. Also, DLG1-AS1 served as an oncogene in TNBC cells and as a sponge for miR-16-5p to up-regulate JARID2. Meanwhile, JARID2 and PBX3 exerted oncogenic effects on TNBC cell growth. In conclusion, PBX3-activated DLG1-AS1 can promote the proliferation, invasion, and migration of TNBC cells by sponging miR-16-5p and elevating JARID2 expression.

Oncological outcome of single-port insufflation endoscopic nipple-sparing mastectomy versus open mastectomy in early breast cancer patients: a study protocol for a randomised controlled trial.

INTRODUCTION: Breast cancer is the most prevalent cancer and the leading cause of cancer-related death in women. Conventional open mastectomy (C-OM) is one of the most common procedures for breast cancer, which involves the removal of the nipple-areola complex and a large proportion of the breast skin, leading to poor cosmetic effect and restriction of upper extremity function. Single-port insufflation endoscopic nipple-sparing mastectomy (SIE-NSM) could conceal the incision along the wrinkles in the axilla, preserve all the breast skin and nipple-areola complex and provide a better cosmetic outcome and quality of life. This trial aims to investigate the oncological safety between SIE-NSM and C-OM in early breast cancer patients. METHODS AND ANALYSIS: This is a single centre, non-blinded, randomised controlled trial (RCT) and will be conducted at Beijing Friendship Hospital. Patients will be enrolled in the inpatient ward. Breast surgeons will notify patients who meet the inclusion and exclusion criteria with the instruction of this RCT. Patients will be randomly assigned to C-OM or SIE-NSM with a 3:1 allocation as per a computer-generated randomisation schedule. Patients will be followed-up for 12 months for analysing surgical outcomes. The primary outcome is the local recurrence rate at a 12-month follow-up. The secondary outcome is the distant metastasis rate, cosmetic satisfaction score and psychosocial well-being score after a 12-month follow-up. To ensure the accuracy of the cosmetic satisfaction score and psychosocial well-being score, the standard scale, Breast-Q score, will be applied. ETHICS AND DISSEMINATION: This study will be conducted according to the medical ethics committee of the Beijing Friendship Hospital and according to the principles of the Declaration of Helsinki. All patients will receive clear instruction of their disease and treatment plan. Informed consent will be obtained from all patients when they agree to comply with our research plan. The results will be disseminated at academic presentations and publications in peer-reviewed journals. The raw data will be confidentially stored in our electronic data capture database. Data will not be shared unless an appropriate data request is submitted after the trial completion and peer-review journal publication. TRIAL REGISTRATION NUMBER: NCT04461847.

Circular RNA RHOT1 promotes progression and inhibits ferroptosis via mir-106a-5p/STAT3 axis in breast cancer.

To explore the effect of circRHOT1 on breast cancer progression and the underlying mechanism. Significantly, our data revealed that the depletion of circRHOT1 was able to repress the proliferation and induce the apoptosis of breast cancer cells. CircRHOT1 knockdown could remarkably inhibit the invasion and migration in the breast cancer cells. Meanwhile, the depletion of circRHOT1 enhanced the erastin-induced inhibition effect on cell growth of breast cancer cells. The circRHOT1 knockdown notably increased the levels of reactive oxygen species (ROS), iron, and Fe2+ in breast cancer cells. Mechanically, circRHOT1 was able to sponge microRNA-106a-5p (miR-106a-5p) and inhibited ferroptosis by down-regulating miR-106a-5p in breast cancer cells. Besides, miR-106a-5p induced ferroptosis by targeting signal transducer and activator of transcription 3 (STAT3) in the system. Moreover, the overexpression of STAT3 and miR-106a-5p inhibitor could reverse circRHOT1 knockdown-mediated breast cancer progression. Functionally, circRHOT1 promoted the tumor growth of breast cancer in vivo. In conclusion, we discovered that circRHOT1 contributed to malignant progression and attenuated ferroptosis in breast cancer by the miR-106a-5p/STAT3 axis. Our finding provides new insights into the mechanism by which circRHOT1 promotes the development of breast cancer. CircRHOT1 and miR-106a-5p may serve as potential targets for breast cancer therapy.

TXR1 and TSP1 expression varies by the molecular subtypes of breast cancer patients who received previous docetaxel-based first-line chemotherapy.

The expression of taxol resistance gene 1 and thrombospondin 1 remains unknown in human breast cancer tissues. In the current study, we sought to measure the mRNA expression levels of taxol resistance gene 1 and thrombospondin 1 in breast cancer tissue and adjacent normal tissue specimens and further analyzed their expression according to the molecular subtypes and age of breast cancer patients who had received taxane-containing regimens. Archived breast cancer and adjacent non-tumor tissue specimens were obtained at Beijing Friendship Hospital, Beijing, China. The mRNA transcript levels of taxol resistance gene 1, thrombospondin 1 and multi-drug resistance 1 were determined by quantitative RT-PCR. Taxol resistance gene 1 and multi-drug resistance 1 protein levels were measured by immunoblotting assays. Forty-nine archived breast cancer tissue specimens were included. The majority of the specimens (65.3%) were of the molecular subtype A followed by triple negative breast cancer (14.3%). The mRNA transcript levels of taxol resistance gene 1 , thrombospondin 1 and multi-drug resistance 1 in breast cancer tissues were higher than those of adjacent normal tissues. The mRNA expression of TXR1 in the HER2 subtype (4.513 ± 0.810) was the highest and in the Luminal B subtype was the lowest (3.103 ± 0.417) among the four molecular subtypes. The HER2 subtype also had the highest mRNA expression of thrombospondin 1(4.827 ± 0.927) and the Luminal B subtype had the lowest TSP1 mRNA level (3.197 ± 0.565) among the four molecular subtypes. Our study represents the first attempt in delineating taxol resistance gene 1 and thrombospondin 1 expression in breast cancer and we demonstrate that taxol resistance gene 1 and thrombospondin 1 expression may vary according to the molecular subtypes of breast cancer.

Preliminary results for treatment of early stage breast cancer with endoscopic subcutaneous mastectomy combined with endoscopic sentinel lymph node biopsy in China.

BACKGROUND AND OBJECTIVES: To evaluate efficacy and aesthetic outcome for combined endoscopic subcutaneous mastectomy (E-SM) and endoscopic sentinel lymph node biopsy (E-SLNB) in early stage breast cancer patients. METHODS: Combined E-SM+E-SLNB was compared to modified radical resection in a cohort of Chinese patients (n = 49) with stages I and II breast cancer. Patient satisfaction with the aesthetic results was assessed 1 year after surgery with a 5-item-by-4-step scoring system for evaluating cosmetic outcomes. RESULTS: All patients were alive 1 year following surgery with no locoregional recurrence or distant metastases and without any critical complications. The average length of incision was less in patients receiving E-SM+E-SLNB (4.4 vs. 19.4 cm; P < 0.001), but time in surgery was longer (131.6 vs. 99.2 min; P = 0.024). After 1 year, nearly all E-SM+E-SLNB patients rated satisfaction with their appearance as excellent or good (23/24; 95.8% vs. 19/25; 76.0%; P < 0.001), and exhibited less disturbance of sensory (P < 0.001) and motor function (P = 0.014) relative to modified radical resection. CONCLUSIONS: E-SM+E-SLNB provides significant aesthetic and functional advantages for patients with early stage breast cancer without compromising medical efficacy as assessed at 16 months postsurgery. J. Surg. Oncol. 2016;113:616-620. © 2016 Wiley Periodicals, Inc.

Vascular endothelial growth inhibitor affects the invasion, apoptosis and vascularisation in breast cancer cell line MDA-MB-231.

BACKGROUND: Breast cancer is one of the most common malignant female diseases worldwide. It is a significant threat to every woman's health. Vascular endothelial growth inhibitor (VEGI) is known to be abundant in endothelial cells. According to previous literature, overexpression of VEGI has been shown to inhibit tumor neovascularisation and progression in cellular and animal models, but there has been limited research on the significance of VEGI in the breast cancer. METHODS: In our study, cell lines MDA-MB-231 were first constructed in which VEGI mediated by lentivirus over-expressed. The effects of VEGI over-expression on MDA-MB-231 cells were investigated both in vitro and in vivo. The expression of VEGI in the MDA-MB-231 cells after infection of lentivirus was analyzed using real-time PCR and Western blotting. The effect of the biological characteristics of MDA-MB-231 cells was assessed by growth, invasion, adhesion, and migration assay with subcutaneous tumor-bearing nude mice models. Then the growth curves of the subcutaneous tumors were studied. Expressions of VEGI, CD31 and CD34 in the tumors were analyzed by immunohistochemistry and apoptosis was detected by flow cytometry and immunohistochemistry. RESULTS: Infection of MDA-MB-231 cells within the lentivirus resulted in approximately a 1 000-fold increase in the expression of VEGI. As can be seen in the invasion, adhesion and migration assay, the over-expression of VEGI can inhibit the ability of MDA-MB-231 cells during migration, adhesion and invasion. The volume of the subcutaneous tumor in the over-expression group was distinctly and significantly less than that of the control groups. Immunohistochemistry analysis of the tumor biopsies clearly showed the expression of VEGI in the over-expression group increased while CD31 and CD34 decreased significantly. In vitro and in vivo, the early apoptosis rate and the apoptosis index were increased within the VEGI over-expression group as compared with the control group. CONCLUSIONS: Taken together, recombinant lentivirus that were successfully constructed, demonstrated up-regulated VEGI gene expression in breast cancer cells. Lentivirus-mediated over-expression of VEGI weakened the ability of the breast cancer cell migration, adhesion and invasion. Over-expression of VEGI diminished the tumorigenic capacity of breast cancer cells in vivo. Up-regulation of VEGI gene expression however inhibited breast cancer MDA-MB-231 cell in the early apoptosis.