Clinicopathological characteristics and prognostic significance of casting-type calcifications in patients with invasive breast cancer presenting with microcalcification.

To explore the clinicopathological characteristics and prognostic significance of casting-type calcification (CC) in patients with breast cancer presenting with microcalcification on mammography. Data on patients with invasive breast cancer who had mammographic calcification was retrospectively analyzed. The chi-square test was utilized to assess the clinicopathological characteristics of two forms of CC-related breast cancer. The examination of prognostic variables was conducted using Kaplan-Meier and Cox regression analyses. A total of 427 eligible patients were included in this study. Chi-square analysis indicated that the presence of CC was associated with estrogen receptor (ER) negativity (P = 0.005), progesterone receptor (PR) negativity (P < 0.001), and epidermal growth factor receptor 2 (HER-2) positivity (P < 0.001); among these, the association was stronger with the CC-predominant type. After a median follow-up of 82 months, those with CC had a worse 5-year recurrence-free survival (RFS) (77.1% vs. 86.9%, p = 0.036; hazard ratio [HR], 1.86; 95% confidence interval [CI] 1.04-3.31) and overall survival (OS) (84.0% vs. 94.4%, p = 0.007; HR, 2.99; 95% CI 1.34-6.65) rates. In COX regression analysis, such differences were still observed in HER-2 positive subgroups (RFS: HR: 2.45, 95% CI 1-5.97, P = 0.049; OS: HR: 4.53, 95% CI 1.17-17.52, P = 0.029). In patients with invasive breast cancer exhibiting calcifications on mammography, the presence of CC, especially the CC-predominant type, is linked to a higher frequency of hormone receptor negativity and HER-2 positivity. The presence of CC is associated with an unfavorable 5-year RFS and OS rates.

Relevance and mechanism of STAT3/miR-221-3p/Fascin-1 axis in EGFR TKI resistance of triple-negative breast cancer.

The epidermal growth factor receptor 1 (EGFR) plays a crucial role in the progression of various malignant tumors and is considered a potential target for treating triple-negative breast cancer (TNBC). However, the effectiveness of representative tyrosine kinase inhibitors (TKIs) used in EGFR-targeted therapy is limited in TNBC patients. In our study, we observed that the TNBC cell lines MDA-MB-231 and MDA-MB-468 exhibited resistance to Gefitinib. Treatment with Gefitinib caused an upregulation of Fascin-1 (FSCN1) protein expression and a downregulation of miR-221-3p in these cell lines. However, sensitivity to Gefitinib was significantly improved in both cell lines with either inhibition of FSCN1 expression or overexpression of miR-221-3p. Our luciferase reporter assay confirmed that FSCN1 is a target of miR-221-3p. Moreover, Gefitinib treatment resulted in an upregulation of phosphorylated signal transducer and activator of transcription 3 (p-STAT3) in MDA-MB-231 cells. Using Stattic, a small-molecule inhibitor of STAT3, we observed a significant enhancement in the inhibitory effect of Gefitinib on the growth, migration, and invasion of MDA-MB-231 cells. Additionally, Stattic treatment upregulated miR-221-3p expression and downregulated FSCN1 mRNA and protein expression. A strong positive correlation was noted between the expression of STAT3 and FSCN1 in breast cancer tissues. Furthermore, patients with high expression levels of both STAT3 and FSCN1 had a worse prognosis. Our findings suggest that elevated FSCN1 expression is linked to primary resistance to EGFR TKIs in TNBC. Moreover, we propose that STAT3 regulates the expression of miR-221-3p/FSCN1 and therefore modulates resistance to EGFR TKI therapy in TNBC. Combining EGFR TKI therapy with inhibition of FSCN1 or STAT3 may offer a promising new therapeutic option for TNBC.

The impact of Angiopoietin-2 genetic polymorphisms on susceptibility for malignant breast neoplasms.

Breast cancer causes morbidity and mortality among women worldwide, despite much research illuminating the genetic basis of this disease. Anti-angiogenesis therapies have been widely studied, although the association between angiopoietin-2 (ANGPT2) single nucleotide polymorphisms (SNPs) and breast cancer subtypes remains unclear. This case-control study included 464 patients with malignant breast neoplasms and 539 cancer-free females. We explored the effects of ANGPT2 SNPs on the susceptibility for a malignant breast neoplasm in a Chinese Han population. Five ANGPT2 SNPs (rs2442598, rs734701, rs1823375, 11,137,037, and rs12674822) were analyzed using TaqMan SNP genotyping. Carriers of the variant GG allele of rs1823375 were less likely than wild-type carriers to be diagnosed with clinically staged breast cancer, while females with human epidermal growth factor receptor 2 (HER2)-enriched disease carrying the CG or the CG+GG genotype at rs1823375 were significantly less likely than CC genotype carriers to be of lymph node status N1-N3. We also found that the T-T-C-A-T ANGPT2 haplotype significantly increased the risk for developing a malignant breast neoplasm by 1.385-fold (95% CI: 1.025-1.871; p < 0.05). Our study is the first to document a correlation between ANGPT2 polymorphisms and the development and progression of a malignant breast neoplasm in females of Chinese Han ethnicity.

Theaflavin Attenuates TBHP-Induced Endothelial Cells Oxidative Stress by Activating PI3K/AKT/Nrf2 and Accelerates Wound Healing in Rats.

The treatment of wounds remains a clinical challenge because of poor angiogenesis under the wound bed, and increasingly, the patients' need for functional and aesthetically pleasing scars. Previous reports have shown that Theaflavin can induce angiogenesis and terminate the progression of ischemic cardiovascular disease, but limited therapy is available for the management of cutaneous wounds. In this study, our in vitro work discovered that human umbilical vein endothelial cells (HUVECs) exposed to Theaflavin can alleviate apoptosis and cell dysfunction induced by tert-butyl hydroperoxide (TBHP). The cellular activity of HUVECs were assessed by cell tube formation, migration and adhesion. Mechanistically, Theaflavin protected HUVECs from TBHP-stimulated cell apoptosis through the activation of the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/nuclear factor (erythroid-derived 2)-like 2 (Nrf2) axis, so Nrf2 silencing can partly eliminate the cytoprotective effect of Theaflavin treatment. In in vivo experiments, administering Theaflavin orally can enhance vascularization in regenerated tissues and accelerate wound healing. In summary, our data served as a novel evidence for the wound healing treatment with Theaflavin, and certified the potential mechanism of Theaflavin, which can be used as a potential agent for cutaneous wound therapy.

Upregulated WTAP expression appears to both promote breast cancer growth and inhibit lymph node metastasis.

It is unclear as to whether Wilms' tumor 1-associated protein (WTAP) promotes or suppresses breast cancer. This immunohistochemistry analysis explored levels of WTAP expression in 347 cases of breast cancer and analyzed the relationship between WTAP expression and the clinicopathological characteristics and prognosis of breast cancer patients. The rate of high WTAP expression was significantly higher in breast cancer tissue than in adjacent normal breast tissue (37.5% vs 0.0%; P < 0.001). WTAP expression was positively associated with tumor size and grade, and negatively associated with axillary lymph node metastasis, estrogen and progesterone receptor status. Rates of high WTAP expression were 66.1% in triple-negative breast cancer (TNBC) tissue and 31.3% in non-TNBC tissue. In multiple logistic regression analysis, independent predictors of WTAP expression in breast cancer included larger tumor size (odds ratio = 1.907; 95% confidence interval: 1.185-3.067; P = 0.008), lymph node metastasis (0.597; 0.373-0.956; P = 0.032) and TNBC status (3.735; 2.056-6.784; P < 0.001). No clear relationship was observed between patient prognosis and WTAP expression. We suggest that WTAP expression is upregulated in breast cancer and appears to both promote tumor growth and inhibit lymph node metastasis.

p-STAT3 expression in breast cancer correlates negatively with tumor size and HER2 status.

ABSTRACT: Although some studies have reported the expression and clinical significance of phosphorylated signal transducer and activator of transcription 3 (p-STAT3) in breast cancer tissues, it is still controversial whether p-STAT3 play a role in promoting or suppressing cancer. Here, we used immunohistochemistry analysis to explore expression of p-STAT3 in 407 cases of breast cancer, and analyzed the relationship between p-STAT3 expression and the clinicopathological characteristics and prognosis of breast cancer patients. Positive p-STAT3 expression was seen in 112 cases (27.5%) of breast cancer. p-STAT3 expression was negatively correlated with tumor size, tumor stage and human epidermal growth factor receptor 2 (HER2) status, and the positive rate of p-STAT3 was lowest in HER2-enriched subtype breast cancer (15.3%), while other subtypes were luminal B (23.0%), luminal A (30.2%), and triple-negative breast cancer (TNBC) (37.5%). Logistic regression model multivariate analysis showed that the independent correlation factor of p-STAT3 expression in breast cancer was tumor size (OR = 0.187, 95% CI = 0.042-0.839, P = .029) and HER2 status (OR = 0.392, 95% CI = 0.216-0.710, P = .002). In this study, no clear relationship was observed between patients' prognosis and expression of p-STAT3. Therefore, we suggest that p-STAT3 expression in breast cancer is negatively correlated with tumor size and HER2 status, but appears to have no effect on survival.

Downregulated METTL14 Expression Correlates with Breast Cancer Tumor Grade and Molecular Classification.

It is unclear whether the methyltransferase-like 14 (METTL14) protein promotes or suppresses cancer growth. We examined the association between METTL14 expression, cancer progression, and patient prognosis in a total of 398 breast cancer tissue specimens. Significantly fewer cancer tissue specimens compared with normal breast tissue expressed high levels of METTL14 (52.8% vs. 75.0%). METTL14 expression was negatively associated with tumor grade and positively associated with patient age, estrogen, and progesterone receptor status. High METTL14 expression was more common in luminal A and luminal B tissue (75.9% and 60.8%, respectively), compared with human epidermal growth factor receptor 2- (HER2-) enriched and triple-negative breast cancer (TNBC) samples (38.2% and 18.6%, respectively). In multiple logistic regression analysis, independent predictors of METTL14 expression in breast cancer included higher tumor grade (odds ratio (OR) = 0.494, 95% confidence interval (CI): 0.289-0.844; P = 0.010), TNBC subtype (OR = 0.109, 95% CI: 0.054-0.222; P < 0.001), and HER2-enriched subtype (OR = 0.298, 95% CI: 0.156-0.567; P < 0.001). No clear relationship was observed between patient prognosis and METTL14 expression. It appears that downregulated METTL14 expression in breast cancer is associated with tumor grade and molecular classification.

A new clinical prognostic nomogram for liver cancer based on immune score.

BACKGROUND: Increased attention is being paid to the relationship between the immune status of the tumor microenvironment and tumor prognosis. The application of immune scoring in evaluating the clinical prognosis of liver cancer patients has not yet been explored. This study sought to clarify the association between immune score and prognosis and construct a clinical nomogram to predict the survival of patients with liver cancer. METHODS: A total of 346 patients were included in our analysis datasets downloaded from The Cancer Genome Atlas (TCGA) dataset. A Cox proportional-hazards regression model was used to estimate the adjusted hazard ratios (HRs). A nomogram was built based on the results of multivariate analysis and was subjected to bootstrap internal validation. The predictive accuracy and discriminative ability were measured by the concordance index (C-index) and the calibration curve. Through the functional analysis of differential expression of genes with different immune scores, the target genes were screened out. RESULTS: In comparison with patients with low immune scores, those with intermediate and high immune scores had significantly improved survival time [HR and 95% confidence interval (CI): 0.54 (0.30-0.97) and 0.51 (0.27-0.97), respectively]. The C-index for survival time prediction was 0.66 (95% CI: 0.60-0.71). The calibration plot for the probability of survival at three or five years showed good agreement between prediction by the nomogram and actual observations. The top 10 hub genes were CXCL8(chemokine (C-X-C motif) ligand 8), SYK(spleen tyrosine kinase), CXCL12(chemokine (C-X-C motif) ligand 12), CXCL10 (chemokine (C-X-C motif) ligand10), CXCL1(chemokine (C-X-C motif) ligand1), CCL5(chemokine (C-C motif) ligand 5), CCL20(chemokine (C-C motif) ligand 20), LCK, CXCL11(chemokine (C-X-C motif) ligand 11), CCR5(chemokine (C-C motif) receptor 5). More importantly, we found that the high expression of CXCL8 and CXCL1 were related to the prognosis. CONCLUSIONS: High and/or intermediate immune scores are significantly correlated with better survival time in patients with liver cancer. Moreover, nomograms for predicting prognosis may help to estimate the survival of patients. We also propose that CXCL8 and CXCL1 may be a potential therapeutic target for liver cancer treatment.

Methylation-Driven Genes Identified as Novel Prognostic Indicators for Thyroid Carcinoma.

BACKGROUND: Aberrant DNA methylation plays an crucial role in tumorigenesis through regulating gene expression. Nevertheless, the exact role of methylation in the carcinogenesis of thyroid cancer and its association with prognosis remains unclear. The purpose of this study is to explore the DNA methylation-driven genes in thyroid cancer by integrative bioinformatics analysis. METHODS: The transcriptome profiling data and DNA methylation data of thyroid cancer were downloaded from The Cancer Genome Atlas (TCGA) database. The methylmix R package was used to screen DNA methylation-driven genes in thyroid cancer. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were conducted to annotate the function of methylation-driven genes. Univariate Cox regression analyses was performed to distinguish prognosis-related methylation-driven genes. Multivariate Cox regression analyses was utilized to build a prognostic multi-gene signature. A survival analysis was carried out to determine the individual prognostic significance of this multi-gene signature. RESULTS: A total of 51 methylation-driven genes were identified. The functional analysis indicated that these genes were significantly enriched in diverse biological processes (BP) and pathways related to the malignancy processes. Four of these genes (RDH5, TREM1, BIRC7, and SLC26A7) were selected to construct the risk evaluation model. Patients in the low-risk group had an conspicuously better overall survival (OS) than those in high-risk group (p < 0.001). The area under the receiver operating characteristic (ROC) curve for this model was 0.836, suggesting a good specificity and sensitivity. Subsequent survival analysis revealed that this four-gene signature served as an independent indicator for the prognosis of thyroid cancer. Moreover, the prognostic signature was well validated in a external thyroid cancer cohort. CONCLUSION: We identified methylation-driven genes in thyroid cancer with independent prognostic value, which may offer new insight into molecular mechanisms of thyroid cancer and provide new possibility for individualized treatment of thyroid cancer patients.

Impacts of RETN genetic polymorphism on breast cancer development.

The adipokine resistin is linked with obesity, inflammation and various cancers, including breast cancer. This study sought to determine whether certain polymorphisms in the gene encoding resistin, RETN, increase the risk of breast cancer susceptibility. We analyzed levels of resistin expression in breast cancer tissue and samples from The Cancer Genome Atlas database. We also examined associations between four RETN single nucleotide polymorphisms (SNPs; rs3745367, rs7408174, rs1862513 and rs3219175) and breast cancer susceptibility in 515 patients with breast cancer and 541 healthy women without cancer. Compared with wild-type (GG) carriers, those carrying the AG genotype of the RETN SNP rs3219175 and those carrying at least one A allele in the SNP rs3219175 had a higher chance of developing breast cancer (adjusted odds ratio, AOR: 1.295, 95% confidence intervals, CI: 1.065-1.575 and 2.202, 1.701-2.243, respectively). When clinical aspects and the RETN SNP rs7408174 were examined in the breast cancer cohort, the CT genotype was linked to late-stage disease, while women with luminal A disease and at least one C allele were likely to progress to stage III/IV disease and to develop highly pathological grade III disease. Moreover, resistin-positive individuals were at greater risk than resistin-negative individuals for developing pathological grade III disease (OR: 5.020; 95% CI: 1.380-18.259). This study details risk associations between resistin and RETN SNPs in breast cancer susceptibility in Chinese Han women.

Correlation between CCL4 gene polymorphisms and clinical aspects of breast cancer.

Breast cancer is a major cause of cancer mortality amongst women. Chemokine (C-C motif) ligand 4 is encoded by the CCL4 gene; specific CCL4 gene polymorphisms are related to the risks and prognoses of various diseases. In this study, we examined whether CCL4 gene single nucleotide polymorphisms (SNPs) predict the risk and progression of breast cancer. Between 2014 and 2016, we recruited 314 patients diagnosed with breast cancer and a cohort of 209 healthy participants (controls) without a history of cancer. Genotyping of the CCL4 rs1634507, rs10491121 and rs1719153 SNPs revealed no significant between-group differences for these polymorphisms. However, amongst luminal A and luminal B subtypes, compared with patients with the AA genotype, those carrying the AG genotype at SNP rs10491121 were less likely to develop lymph node metastasis. In addition, compared with AA carriers, those carrying the AG + GG genotype at SNP rs10491121 were at lower risk of developing distant metastasis, while the presence of the AT genotype at SNP rs1719153 increased the likelihood of pathologic grade (G3 or G4) disease. Variations in the CCL4 gene may help to predict breast cancer progression and metastasis.

HMGB1 genetic polymorphisms are biomarkers for the development and progression of breast cancer.

Breast cancer is a major cause of cancer mortality worldwide. High-mobility group box protein 1 (HMGB1) is a ubiquitous nuclear protein found in all mammal eukaryotic cells that participates in tumor progression, migration and metastasis. HMGB1 overexpression has been indicated in breast cancer patients. However, scant information is available regarding the association between HMGB1 single nucleotide polymorphisms (SNPs) and the risk or prognosis of breast cancer. We report on the association between 4 SNPs of the HMGB1 gene (rs1360485, rs1045411, rs2249825 and rs1412125) and breast cancer susceptibility as well as clinical outcomes in 313 patients with breast cancer and in 217 healthy controls. Patients with one G allele in the rs1360485 or rs2249825 domains are likely to progress to T2 tumor and lymph node metastasis. In addition, the presence of one G allele in SNPs rs1360485 or rs2249825 was associated with a higher risk of progressing to T2 tumor and distant metastasis amongst HER2-enriched and triple-negative breast cancer (TNBC) tumors compared with luminal A and luminal B tumors. Furthermore, having one C allele in the rs1412125 domain increased the risk of pathologic grade 3 disease in HER2-enriched and TNBC tumors. Our results indicate that genetic variations in the HMGB1 gene may serve as an important predictor of breast cancer progression and metastasis.

miR-125b regulates the drug-resistance of breast cancer cells to doxorubicin by targeting HAX-1.

MircroRNAs (miRNAs) are considered as essential regulators in the tumorigenesis and chemoresistance of multiple cancer types. In the present study, it was demonstrated that the expression levels of miR-125b were significantly downregulated in the tissues of patients with breast cancer (BC), as well as the BC cell lines in vitro. To study the association between chemoresistance and miR-125b in BC, doxorubicin (DOX)-resistant MCF-7 (MCF-7/R) cells were established, and gain- and loss-of-function experiments were performed. It was demonstrated that the overexpression of miR-125b increased the sensitivity of MCF-7/R cells to DOX. Furthermore, it was revealed that the sensitization of miR-125b mimics to DOX-induced cell death was regulated by the hematopoietic cell-specific protein 1-associated protein X-1 (HAX-1) vector and HAX-1 small interfering RNA. These results emphasized the notable function of miR-125b and its target of HAX-1 in regulating DOX-resistance. In addition, it was demonstrated that the miR-125b mimics promoted the loss of the mitochondrial membrane potential and the generation of reactive oxygen species induced by DOX treatment in MCF-7/R cells. These data suggest that the miR-125b-HAX-1-mitochondria pathway has a notable function in the treatment of DOX-resistant BC cells, which may provide a novel target for the chemotherapy of BC.

FSCN1 gene polymorphisms: biomarkers for the development and progression of breast cancer.

Breast cancer is a major cause of cancer mortality worldwide. Fascin-1 (FSCN1) is an actin-binding protein found in mammalian cells, including endothelial, neuronal and mesenchymal cells. FSCN1 overexpression has been indicated in breast cancer patients. However, scant information is available regarding the association between FSCN1 single nucleotide polymorphisms (SNPs) and the risk or prognosis of breast cancer. We report on the association between 6 SNPs of the FSCN1 gene (rs56156320, rs8772, rs3801004, rs2966447, rs852479 and rs1640233) and breast cancer susceptibility as well as clinical outcomes in 316 patients with breast cancer and in 222 healthy controls. Carriers of the AC or AC + CC allele of the variant rs56156320 were at greater risk of breast cancer compared with wild-type (AA) carriers. Moreover, carriers of at least one G allele in rs3801004 were likely to progress to stage III/IV disease and lymph node metastasis. Individuals with at least one T allele at FSCN1 SNP rs2966447 were at higher risk of developing pathologic grade G3 disease. Furthermore, individuals bearing the C/C haplotype at SNPs rs56156320 and rs3801004 had nearly twice the risk of breast cancer. Our results indicate that genetic variations in the FSCN1 gene may serve as an important predictor of early-stage breast cancer.

EGFR conjunct FSCN1 as a Novel Therapeutic Strategy in Triple-Negative Breast Cancer.

Emerging evidence indicates that Fascin-1 (FSCN1) may possess a causal role in the development of several types of cancers and serves as a novel biomarker of aggressiveness in certain carcinomas. However, the regulatory mechanism of FSCN1 in triple-negative breast cancer (TNBC) cell invasion and migration is still largely unknown. In our study, we observed that the FSCN1 expression rates were significantly higher in invasive ductal carcinoma, compared with both usual ductal hyperplasia and ductal carcinoma in situ. FSCN1 expression was significantly higher in cases of TNBC compared with the non-TNBC subtype. Overexpression of FSCN1 promoted TNBC cell migration and invasion. Epidermal growth factor induced the expression of FSCN1 through activation of MAPK, which subsequently promoted cell migration and invasion. A significant decrease in FSCN1 expression following the co-treatment of FSCN1 siRNA and Gefitinib, compared with the separate treatment of FSCN1 siRNA or Gefitinib. Furthermore, we found that there was a significant association between FSCN1 expression and poor relapse-free survival and overall survival. Therefore, we suggest that co-targeting epidermal growth factor receptor and FSCN1 dual biomarker may be used as a novel therapeutic strategy for TNBC.

A retrospective analysis of hyperthermic intraperitoneal chemotherapy for gastric cancer with peritoneal metastasis.

Peritoneal metastasis (PM) is a poor prognostic factor in patients with gastric cancer. The aim of this study was to evaluate the efficacy and safety of hyperthermic intraperitoneal chemotherapy (HIPEC) in patients with advanced gastric cancer with PM by retrospective analysis. A total of 54 gastric cancer patients with positive ascitic fluid cytology were included in this study: 23 patients were treated with systemic chemotherapy combined with HIPEC (HIPEC+ group) and 31 received systemic chemotherapy alone (HIPEC- group). The patients were divided into 4 categories according to the changes of ascites, namely disappear, decrease, stable and increase. The disappear + decrease rate in the HIPEC+ group was 82.60%, which was statistically significantly superior to that of the HIPEC- group (54.80%). The disappear + decrease + stable rate was 95.70% in the HIPEC+ group and 74.20% in the HIPEC- group, but the difference was not statistically significant. In 33 patients with complete survival data, including 12 from the HIPEC+ and 21 from the HIPEC- group, the median progression-free survival was 164 and 129 days, respectively, and the median overall survival (OS) was 494 and 223 days, respectively. In patients with ascites disappear/decrease/stable, the OS appeared to be better compared with that in patients with ascites increase, but the difference was not statistically significant. Further analysis revealed that patients with controlled disease (complete response + partial response + stable disease) may have a better OS compared with patients with progressive disease, with a statistically significant difference. The toxicities were well tolerated in both groups. Therefore, HIPEC was found to improve survival in advanced gastric cancer patients with PM, but the difference was not statistically significant, which may be attributed to the small number of cases. Further studies with larger samples are required to confirm our data.

Fascin-1 as a novel diagnostic marker of triple-negative breast cancer.

In some cases of breast cancer, diagnosis of triple-negative breast cancer (TNBC) requires further fluorescence in situ hybridization (FISH) for determining human epidermal growth factor receptor 2 (HER2) status. However, few cases undergo FISH in China, leading to difficulty regarding subsequent treatment decisions. Here, we used immunohistochemical analysis to explore expression of fascin-1, an actin-bundling protein, as a diagnostic marker of TNBC. A total of 457 cases of breast cancer were divided into four molecular subtypes, including 82 cases (17.9%) of TNBC, 81 (17.7%) of HER2-enriched, 185 (40.5%) of luminal A, and 109 (23.9%) of luminal B. Positive fascin-1 expression was seen in 144 cases (31.5%), including 77 (16.8%) strong positive cases. Rates of positive and strong positive expression of fascin-1 were significantly higher in cases of TNBC than in the other molecular subtypes. In all cases of breast cancer, the sensitivities and specificities of positive and strong positive fascin-1 expression for predicting TNBC were 87.8% and 80.8%, and 78.0% and 96.5%, respectively. In cases of hormone receptor-negative breast cancer, the sensitivities and specificities of positive and strong positive fascin-1 expression for predicting TNBC were 87.8% and 61.7%, and 78.0% and 92.6%, respectively. In 24 cases with estrogen receptor (ER)-, PR-, and HER2 2 +  equivocal status who underwent FISH, the sensitivity and specificity of strong positive fascin-1 expression for predicting TNBC were 71.4% and 90.0%. These results suggest that strong positive fascin-1 expression can be used as a diagnostic marker of TNBC.