Breast carcinoma arising in a fibroadenoma: A case series of 16 patients and review of the literature.

Breast carcinoma arising from a fibroadenoma is an uncommon entity and is frequently detected incidentally during pathological examination or excisional biopsy of a benign breast tumor. Due to only sporadic cases being reported, evidence-based guidelines are not well-established to date. The present report describes 16 patients diagnosed with breast carcinoma arising within a fibroadenoma in the Third Hospital of Nanchang (Nanchang, China) between January 2019 and December 2021 and discusses the clinicopathological characteristics, imaging findings and treatment. The age of patients at diagnosis ranged between 19 and 58 years and a well-defined asymptomatic mass was the most common clinical presentation. Carcinoma occurring in fibroadenoma generally mimics a benign tumor and potential carcinomatous changes may not be detected. Pathologically, carcinoma in situ was the predominant subtype in the present study. Additionally, ductal carcinoma in situ was more common compared with lobular carcinoma in situ in the present case series. Regarding the molecular phenotypes, the majority of cases were categorized as luminal subtype, although other subtypes such as triple-negative and HER2 positive breast cancer were also identified. In the present study, seven patients were treated with breast-conserving surgery and nine patients were treated with mastectomy. Sentinel lymph node biopsy was performed in all patients and none exhibited axillary node metastasis. Additionally, six patients underwent radiotherapy and two received chemotherapy. During the follow-up, all patients were alive and no evidence of disease relapse was observed. In summary, clinicians should be aware of the possibility of carcinoma within a fibroadenoma, which could alter the therapeutical course. Adequate biopsy or excision should be performed in patients with indicators of malignant transformation in a presumed benign breast tumor.

Encapsulated papillary carcinoma of the breast: A single institution experience.

Encapsulated papillary carcinoma (EPC) is a relatively rare form of breast cancer. To date, no evidence-based guidelines for the treatment of EPC have been established. Between January 2015 and December 2021, patients with histologically confirmed EPC of the breast were recorded in a database by The Third Hospital of Nanchang City (Nanchang, China). A total of 46 patients with EPC were retrieved from the database. Age at diagnosis ranged from 41-88 years (median age, 62 years). A total of 21 of these patients had pure EPC, 6 patients had EPC associated with ductal carcinoma in situ and 19 patients had EPC associated with invasive carcinoma. The majority of EPC cases were low nuclear grade, hormone receptor-positive and human epidermal growth factor receptor-2-negative. Additionally, myoepithelial cells were always absent in the papillae of the EPC. All patients underwent lumpectomy or mastectomy with sentinel lymph node biopsy, and almost all of the patients received adjuvant hormonal therapy. Adjuvant chemotherapy was only suggested to 4 patients who were diagnosed with axillary lymph node involvement. Subsequently, the clinicopathological features of non-invasive EPC were compared with invasive EPC. The results indicated that larger tumor sizes and axillary lymph node metastases were more common in invasive tumors. During the follow-up, only 2 patients with invasive EPC experienced recurrence or metastasis. In conclusion, a substantial proportion of invasive EPC cases display aggressive characteristics and metastatic potential, despite it being considered a subtype of carcinoma in situ with excellent prognosis, and local surgical resection is the initial method of treatment. Therefore, adjuvant endocrine therapy, radiotherapy and chemotherapy should be considered in select patients, especially in those diagnosed with invasive EPC tumors.

Nomogram for Predicting Overall Survival and Assessing the Survival Benefit of Adjuvant Treatment in pT1-2N0M0 Triple-Negative Breast Cancer: A Surveillance, Epidemiology, and End Results-Based Study.

Background: Accurate survival prediction of triple-negative breast cancer (TNBC) is essential in the decision-making of adjuvant treatment. The aim of this prospective study was to develop a nomogram that predicts overall survival and assists adjuvant treatment formulation. Methods: A total of 16,977 patients with pT1-2N0M0 TNBC between 2010 and 2015 from the SEER database were enrolled. Independent prognostic factors associated with overall survival (OS) were identified using univariate and multivariate Cox regression hazards method and utilized to compose the nomogram. The survival benefit of adjuvant treatment on OS were analyzed after stratification by nomogram sum-score. Results: Patients were randomized 7:3 into the training and validation cohorts. Multivariate analysis revealed that age at diagnosis, grade, tumor size, laterality, and mastectomy type were independent prognostic factors of OS and were integrated to develop a nomogram for predicting prognosis. Patients were stratified into 3 prognostic subgroups according to the sum-score of our nomogram. There were no significant differences found in OS between surgery alone and other adjuvant treatment strategies in low risk group. In moderate risk group, patients receiving chemotherapy or the combination of chemotherapy and radiotherapy showed better OS than those receiving surgery alone or radiotherapy alone. For patients in high risk group, the combination of chemotherapy and radiotherapy could maximally improve the overall survival rate of patients. Conclusion: A novel nomogram for OS prediction and risk stratification in patients with pT1-2N0M0 TNBC was developed. This cohort study reveals the prognostic roles of different adjuvant treatment strategies in subgroups, which may provide a reference for the decision-making of postoperative treatment, eventually improving prognosis for individual patients.

Knockdown of LINC00665 inhibits proliferation and invasion of breast cancer via competitive binding of miR-3619-5p and inhibition of catenin beta 1.

BACKGROUND: Long intergenic non-protein coding RNA00665 (LINC00665) plays a crucial tumorigenic role in many cancers, such as gastric cancer and lung adenocarcinoma. However, its role and mechanism of action in the progression of breast cancer (BC) are unknown. METHODS: LINC00665 expression levels were determined using quantitative polymerase chain reaction analysis with BC tissues and cell lines. BC cell proliferation was tested by performing 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays, whereas BC cell migration and invasion capabilities were analyzed by performing transwell migration assays. Percentages of apoptotic cells were measured by flow cytometry. Interactions between LINC00665 and miR-3169-5p were examined by performing luciferase reporter assays, and the expression levels of proteins, such as ß-catenin, were examined by western blot analysis. RESULTS: LINC00665 was expressed at high levels in BC tissues and cells. Upregulated LINC00665 expression correlated with tumor size and tumor, node, and metastasis stages, but not with the age of patients. LINC00665 knockdown inhibited BC cell proliferation, migration, and invasion, whereas it promoted apoptosis. Moreover, bioinformatics analysis and the luciferase reporter assay revealed that LINC00665 bound the microRNA (miR) miR-3619-5p. miR-3619-5p expression correlated negatively with LINC00665 expression in BC tissues. miR-3619-5p overexpression inhibited BC cell proliferation, migration, and invasion, but promoted apoptosis. Simultaneous knockdown of LINC00665 and miR-3619-5p led to increased cell proliferation, migration, and invasion, and inhibited apoptosis. Additionally, catenin beta 1, which encodes the ß-catenin protein, was the target gene of miR-3619-5p. ß-catenin expression clearly decreased after LINC00665 knockdown and miR-3619-5p overexpression, but increased after simultaneous knockdown of LINC00665 and miR-3619-5p. CONCLUSION: LINC00665 knockdown inhibited BC cell proliferation and invasion by binding miR-3619-5p and inhibiting ß-catenin expression.

Long non coding RNA NRON inhibited breast cancer development through regulating miR-302b/SRSF2 axis.

AIMS: Long noncoding RNA NRON has been investigated in various tumors, such as hepatocellular carcinoma. However, the role of lncRNA NRON in breast cancer remains unclear. The aim of this study was to explore the function and mechanism of lncRNA NRON in breast cancer. MATERIALS AND METHODS: Overexpression and knockdown vectors were constructed. Proliferation and invasion were measured to evaluate the function of lncRNA NRON. A dual-luciferase reporter assay was utilized to analyze the potential binding target of lncRNA NRON. A rescue experiment was performed to verify the relationship between lncRNA NRON and SRSF2. RESULTS: Our results showed that the expression of lncRNA NRON was significantly downregulated in breast cancer tissues. Overexpression of lncRNA NRON significantly inhibited proliferation and invasion in breast cancer cell lines. Knockdown of lncRNA NRON promoted breast cancer development. We also provided evidence that lncRNA NRON negatively regulated miR-302b. Moreover, we identified SRSF2 as a downstream target of miR-302b. CONCLUSION: Overall, we performed a comprehensive analysis to indicate that the lncRNA NRON/miR-302b/SRSF2 axis plays an important role in breast cancer. Our study is the first to prove that lncRNA NRON functions as a tumor suppressor in breast cancer.

Long intergenic noncoding RNA 00641 inhibits breast cancer cell proliferation, migration, and invasion by sponging miR-194-5p.

Long noncoding RNAs have an essential role in the tumorigenesis of breast cancer (BC). Nonetheless, the consequences of long intergenic noncoding RNA 00641 (LINC00641) in BC remain unidentified. This study shows that LINC00641 expression level was decreased in BC tissues. LINC00641 expression level was negatively related to tumor size, lymph-node metastasis, as well as clinical stage. LINC00641 overexpression inhibited cell proliferation, migration, and invasion but stimulated apoptosis in BC cells. LINC00641 overexpression also remarkably reduced BC growth and metastasis in vivo. LINC00641 acts as a competitive endogenous RNA to sponge miR-194-5p. miR-194-5p level was higher in BC tissues and cells compared with normal-adjacent tissues and normal breast epithelial cell. miR-194-5p expression was negatively correlated with LINC00641 expression in BC tissues. miR-194-5p overexpression reversed the effects of LINC00641 on cell proliferation, cycle, apoptosis, migration, as well as invasion. In conclusion, LINC00641 inhibits BC cell proliferation, migration, as well as invasion by sponging miR-194-5p.

miR-613 inhibits proliferation and invasion of breast cancer cell via VEGFA.

MicroRNAs (miRNAs) play important roles in the pathogenesis of many types of cancers by negatively regulating gene expression at posttranscriptional level. However, the role of microRNAs in breast cancer, has remained elusive. Here, we identified that miR-613 inhibits breast cancer cell proliferation by negatively regulates its target gene VEGFA. In breast cancer cell lines, CCK-8 proliferation assay indicated that the cell proliferation was inhibited by miR-613, while miR-613 inhibitor significantly promoted the cell proliferation. Transwell assay showed that miR-613 mimics significantly inhibited the migration and invasion of breast cancer cells, whereas miR-613 inhibitors significantly increased cell migration and invasion. Luciferase assays confirmed that miR-613 directly bound to the 3' untranslated region of VEGFA, and western blotting showed that miR-613 suppressed the expression of VEGFA at the protein levels. This study indicated that miR-613 negatively regulates VEGFA and inhibits proliferation and invasion of breast cancer cell lines. Thus, miR-613 may represent a potential therapeutic molecule for breast cancer intervention.

The inconsistency of molecular subtypes between primary foci and metastatic axillary lymph nodes in Luminal A breast cancer patients among Chinese women, an indication for chemotherapy?

Patients with Luminal A breast cancer often have favorable prognosis, but some of these patients still have lymph node metastases, it remains unclear what the role of adjuvant chemotherapy is in Luminal A subtype with lymph node metastases. The aim of this study was to find a new method to distinguish which Luminal A patient can be benefited from chemotherapy. We retrospectively investigated the inconsistency of molecular subtypes between primary foci and metastatic axillary lymph nodes in Luminal A breast cancer patients, and analyzed the clinicopathologic characteristics, Recurrence score (RS), disease-free survival (DFS), and overall survival (OS) in 146 Luminal A breast cancer patients. The discordance of molecular subtypes between primary foci and metastatic lymph nodes were explored by univariate and multivariate logistic regression. The DFS and OS were calculated by the Kaplan-Meier survival curves, and the Cox regression analyses were performed to identify independent prognostic factors for DFS and OS. In our results, the inconsistency was found in 55 patients (55/146, 37.67 %). Lymphatic vascular invasion (OR 6.402, 95 % CI 2.371-17.287, P < 0.001), lymph node stage (OR 2.147, 95 % CI 1.095-4.209, P = 0.026), and histological grade (OR 3.319, 95 % CI 1.101-8.951, P = 0.032) were significantly related to the inconsistency. The inconsistent group (non-Luminal A variations) had a poor prognosis compared with the consistent group, the DFS between the two groups was significantly different (P = 0.022), but the OS did not have obvious difference (P = 0.140). Moreover, the inconsistency was associated with high RS (P = 0.036). In conclusion, more aggressive molecular subtypes in metastatic lymph nodes, which associated with poor prognosis, were observed in Luminal A breast cancer patients, which indicate that chemotherapy is necessary for these patients.

Clinical effects of immunotherapy of DC-CIK combined with chemotherapy in treating patients with metastatic breast cancer.

This study aimed to analyze the clinical effects of dendritic cell (DC) and cytokine-induced killer (CIK) immunotherapy combined with chemotherapy on patients with metastatic breast cancer. Twenty patients were included into this study who were diagnosed as metastatic breast cancer (MBC). DC and CIK were augmented by in vitro culture and then rein fused into body through vein.The pain relief rate (RR), toxic and side effects of chemotherapy, immunity functions and living quality of patients were observed. DC and CIK cells were induced by the autologous peripheral blood mononuclear cells (PBMC). Meanwhile, flow cytometry was used to measure T cell subsets and natural killer T (NKT) cells in patients in the two groups before and after the biological treatment. After DC and CIK were rein fused into the patients body, no severe side-effect was found. It was also found that cellular immunotherapy combined with chemotherapy the immunotherapy of cells improved the immunity, the living quality of patients and the disease control rate (DCR). In conclusion, cellular immunotherapy produces small side effects; it combined with chemotherapyis able to improve the DCR and living quality of patients and prolong their lives.

Analysis of miR-205 and miR-155 expression in the blood of breast cancer patients.

The purpose of this study was to identify and validate circulating microRNAs (miRNAs) in human plasma for use as breast cancer (BC) biomarkers and to analyze their relationship to clinicopathologic features and its preliminary biological function. Genome-wide expression profiling of miRNAs in BC was investigated by microarray analysis. miR-155 was up-regulated greater than two-fold in BC compared with Normal Adjacent Tissue (NAT), whereas let-7b, miR-381, miR-10b, miR-125a-5p, miR-335, miR-205 and miR-145 were down- regulated greater than two-fold. Our hypothesis was that circulating miRNAs are also present and differentially expressed in the serum of BC patients compared to controls. Using real-time PCR (RT-PCR), we analyzed miR-205 and miR-155 in archived serum from 30 participants, 20 with breast cancer and 10 healthy people. miR-205 was down-regulated in BC patient serum while miR-155 was up-regulated. Furthermore, we analyzed the relationship between the expression levels of these two miRNAs and the clinicopathologic parameters of BC patients. High expression of miR155 was associated with clinical stage, molecular type, Ki-67 and p53 in BC patients (P<0.05). By contrast, we found no significant correlation between miR-205 and BC patient clinicopathologic parameters. Functional analysis showed that ectopic expression of miR-205 significantly inhibits cell proliferation and promotes apoptosis. miR-205 was down-regulated and miR-155 was up-regulated in BC patient serum. miR-155 was positive correlated with clinical stage and ki-67 and negatively correlated with p53 status.