• Triple-negative breast cancer
• Tumor-associated stroma
• Tumor-infiltrating lymphocytes

• Humans
• Triple Negative Breast Neoplasms/pathology
• Triple Negative Breast Neoplasms/mortality
• Triple Negative Breast Neoplasms/surgery
• Triple Negative Breast Neoplasms/immunology
• Female
• Prognosis
• Middle Aged
• Lymphocytes, Tumor-Infiltrating/pathology
• Lymphocytes, Tumor-Infiltrating/immunology
• Stromal Cells/pathology
• Adult
• Aged
• Retrospective Studies
• Progression-Free Survival

• Biomarkers
• Breast cancer
• Next Generation
• Personalized Therapy
• TNBC

• Humans
• Triple Negative Breast Neoplasms/diagnosis
• Triple Negative Breast Neoplasms/therapy
• Triple Negative Breast Neoplasms/genetics
• Triple Negative Breast Neoplasms/metabolism
• Biomarkers, Tumor/genetics
• Female
• Prognosis
• Circulating Tumor DNA/blood
• Circulating Tumor DNA/analysis
• Circulating Tumor DNA/genetics
• Exosomes/metabolism
• Exosomes/genetics

• NO donor
• anti-metastasis
• aurovertin
• ferroptosis
• triple negative breast cancer

• Animals
• Female
• Humans
• Mice
• Antineoplastic Agents/pharmacology
• Antineoplastic Agents/chemistry
• Antineoplastic Agents/chemical synthesis
• Antineoplastic Agents/therapeutic use
• Apoptosis/drug effects
• Cell Line, Tumor
• Cell Proliferation/drug effects
• Drug Discovery
• Drug Screening Assays, Antitumor
• Ferroptosis/drug effects
• Mice, Inbred BALB C
• Mice, Nude
• Molecular Structure
• Nitric Oxide Donors/pharmacology
• Nitric Oxide Donors/chemistry
• Nitric Oxide Donors/therapeutic use
• Nitric Oxide Donors/chemical synthesis
• Structure-Activity Relationship
• Triple Negative Breast Neoplasms/drug therapy
• Triple Negative Breast Neoplasms/pathology
• Triple Negative Breast Neoplasms/metabolism
• Oxadiazoles/chemistry
• Oxadiazoles/pharmacology
• Pyrans/chemistry
• Pyrans/pharmacology

• B lymphocytes
• T lymphocytes
• multispectral immunofluorescence
• prognosis
• triple negative breast cancer
• tumor associated macrophages

• National Natural Science Foundation of China
• Zhejiang Provincial Nature Science Foundation of China
• Zhejiang Provincial Project for Medical and Health Science and Technology
• Zhejiang Province Traditional Chinese Medicine Science and Technology Program

• VC2
• breast cancer
• herpes
• oncolytic virus
• virotherapy

• P20 GM103424 NIGMS NIH HHS
• P20 GM130555 NIGMS NIH HHS
• P20 GM135000 NIGMS NIH HHS
• National Institute of General Medical Sciences

In patients with triple-negative breast cancer (TNBC), high tumour mutation burden and aberrant oncogene expression profiles are some of the causes of poor prognosis. Therefore, it is necessary to identify aberrantly expressed oncogenes, since they have the potential to serve as therapeutic targets. Transient receptor potential channel 5 opposite strand (TRPC5OS) has been previously shown to function as a novel tumour inducer. However, the underlying mechanism of TRPC5OS function in TNBC remain to be elucidated. Therefore, in the present study TRPC5OS expression was first measured in tissue samples of patients with TNBC and a panel of breast cancer cell lines (ZR-75-1, MDA-MB-453, SK-BR-3, JIMT-1, BT474 and HCC1937) by using qRT-PCR and Western blotting. Subsequently, the possible effects of TRPC5OS on MDA-MB-231 cells proliferation were determined using Cell Counting Kit-8 and 5-Ethynyl-2′-deoxyuridine assays after Lentiviral transfection of MDA-MB-231. In addition, potential interaction partners of TRPC5OS were explored using liquid chromatography-mass spectrometry (LC-MS)/MS. Gene expression patterns following TRPC5OS overexpression were also detected in MDA-MB-231 cells by using High-throughput sequencing. Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) analysis were then used to systematically verify the potential interactions among the TRPC5OS-regulated genes. The potential relationship between TRPC5OS-interacting proteins and gene expression patterns were studied using Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) analysis. TRPC5OS expression was found to be significantly higher in TNBC tumour tissues and breast cancer cell lines compared with luminal tumour tissues and ZR-75-1. In addition, the overexpression of TRPC5OS significantly increased cell proliferation. High-throughput sequencing results revealed that 5,256 genes exhibited differential expression following TRPC5OS overexpression, including 3,269 upregulated genes and 1,987 downregulated genes. GO analysis results indicated that the functions of these differentially expressed genes were enriched in the categories of ‘cell division’ and ‘cell proliferation’ regulation. KEGG analysis showed that the TRPC5OS-regulated genes were associated with processes of ‘homologous recombination’ and ‘TNF signalling pathways’. Subsequently, 17 TRPC5OS-interacting proteins were found using LC-MS/MS and STRING analysis. The most important protein among interacting proteins was ENO1 which was associated with glycolysis and regulated proliferation of cancer. In summary, data from the present study suggest that TRPC5OS overexpression can increase TNBC cell proliferation and ENO1 may be a potential target protein mediated by TRPC5OS. Therefore, TRPC5OS may serve as a novel therapeutic target for TNBC.

• bioinformatics analysis
• proliferation
• transient receptor potential channels 5 opposite strand
• triple-negative breast cancer

• Breast MRI
• Breast cancer
• Deep learning
• Neural network
• Triple-negative breast cancer

• Humans
• Female
• Multiparametric Magnetic Resonance Imaging
• Triple Negative Breast Neoplasms/diagnostic imaging
• Breast Neoplasms/diagnostic imaging
• Breast Neoplasms/pathology
• Artificial Intelligence
• Deep Learning
• Retrospective Studies
• Fibroadenoma/diagnostic imaging
• Sensitivity and Specificity
• Contrast Media
• Magnetic Resonance Imaging/methods
• Magnetic Resonance Spectroscopy

• Breast
• breast neoplasm
• drug therapy
• magnetic resonance ımaging
• neoadjuvant therapy
• radiology.

• artificial intelligence
• prognosis
• risk factor
• signaling pathways
• triple negative breast cancer

Breast cancer is a genetically heterogeneous disease with different molecular biological and clinical characteristics. The available knowledge about the genetic heterogeneity of the most aggressive molecular subtype of breast cancer—triple-negative—has led to discoveries in drug treatment. Identification of the molecular-genetic phenotype of breast cancer is an important prognostic factor of the disease and allows personalization of the patient’s treatment.

Understanding of the genetic mechanisms and identification of the biological markers of tumor progression that form the individual molecular phenotype of transformed cells can characterize the degree of tumor malignancy, the ability to metastasize, the hormonal sensitivity, and the effectiveness of chemotherapy, etc. Breast cancer (BC) is a genetically heterogeneous disease with different molecular biological and clinical characteristics. The available knowledge about the genetic heterogeneity of the most aggressive molecular subtype of breast cancer—triple-negative (TN)—has led to discoveries in drug treatment, including the use of DNA damaging agents (platinum and PARP inhibitors) for these tumors, as well as the use of immunotherapy. Most importantly, the ability to prescribe optimal drug treatment regimens for patients with TNBC based on knowledge of the molecular-genetic characteristics of this subtype of BC will allow the achievement of high rates of overall and disease-free survival. Thus, identification of the molecular-genetic phenotype of breast cancer is an important prognostic factor of the disease and allows personalization of the patient’s treatment.

• CNA
• microarray analysis
• prognosis
• triple-negative breast cancer

Triple-negative breast cancer (TNBC) is an aggressive disease. Recent studies have identified genome instability-derived genes for patient outcomes. However, most of the studies mainly focused on only one or a few genome instability-related genes. Prognostic potential and clinical significance of genome instability-associated genes in TNBC have not been well explored.

In this study, we developed a computational approach to identify TNBC prognostic signature. It consisted of (1) using somatic mutations and copy number variations (CNVs) in TNBC to build a binary matrix and identifying the top and bottom 25% mutated samples, (2) comparing the gene expression between the top and bottom 25% samples to identify genome instability-related genes, and (3) performing univariate Cox proportional hazards regression analysis to identify survival-associated gene signature, and Kaplan–Meier, log-rank test, and multivariate Cox regression analyses to obtain overall survival (OS) information for TNBC outcome prediction.

From the identified 111 genome instability-related genes, we extracted a genome instability-derived gene signature (GIGenSig) of 11 genes. Through survival analysis, we were able to classify TNBC cases into high- and low-risk groups by the signature in the training dataset (log-rank test p = 2.66e−04), validated its prognostic performance in the testing (log-rank test p = 2.45e−02) and Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) (log-rank test p = 2.57e−05) datasets, and further validated the predictive power of the signature in five independent datasets.

The identified novel signature provides a better understanding of genome instability in TNBC and can be applied as prognostic markers for clinical TNBC management.

• TNBC
• copy number variation
• genome instability
• mutation
• prognosis

In this study, we investigated CD20+ TILs in triple-negative breast cancer (TNBC) and their relationship with T lymphocyte subsets (CD4+, CD8+, CD25+, and FOXP3+), including their combined prognostic value using an immunohistochemical staining method.

We investigated 107 patients with TNBC for whom a full-face section stained by hematoxylin and eosin between 2006 and 2018 at Dokkyo Medical University Hospital was available.

The strongest association of infiltrating CD20+ TILs was with CD4+ TILs. There was a significant relationship between CD20+ and CD4+ TILs (r = 0.177; p < 0.001), CD8+ TILs (r = 0.085; p = 0.002), and FOXP3+ TILs (r = 0.0043; p = 0.032). No significant relationships were observed between the CD20+ and CD25+ TILs (r = 0.012; p = 0.264). Multivariate analysis revealed that only the CD20+/FOXP3 ratio was an independent factor for relapse-free survival (p < 0.001) and overall survival (p < 0.001). Patients with tumors highly infiltrated by CD4+, CD8+, and CD20+ TILs had a good prognosis. In contrast, those with tumors weakly infiltrated by CD20+ TILs but highly infiltrated by CD25+ and FOXP3+ TILs had a poor prognosis.

CD20+ TILs may support an increase in CD4+ and CD8+ TILs, which altered the anti-tumor response, resulting in a positive prognosis. CD20+ TILs correlated with FOXP3+ Treg lymphocytes, which were reported to be correlated with a poor prognosis. Our study suggested that TIL-B cells have dual and conflicting roles in TIL-T immune reactions in TNBC.

• Breast
• Triple-negative cancer
• Tumor-infiltrating B lymphocytes
• Tumor-infiltrating T lymphocytes

• drug discovery
• diseases

• Antineoplastic Agents/pharmacology
• Antineoplastic Agents/therapeutic use
• Base Sequence
• Cell Line, Tumor
• Cell Proliferation/drug effects
• Curcumin/chemistry
• Curcumin/pharmacology
• Curcumin/therapeutic use
• Disease Progression
• Gene Expression Regulation, Neoplastic/drug effects
• Humans
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Neoplastic Stem Cells/drug effects
• Neoplastic Stem Cells/metabolism
• Proto-Oncogene Proteins c-akt/metabolism
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• Signal Transduction/drug effects
• Sirolimus/pharmacology
• TOR Serine-Threonine Kinases/metabolism
• Transcription, Genetic/drug effects
• Triple Negative Breast Neoplasms/drug therapy
• Triple Negative Breast Neoplasms/genetics

• UL1 TR000124 NCATS NIH HHS
• SC1 CA200517 NCI NIH HHS
• U54 CA143930 NCI NIH HHS
• U54 CA143931 NCI NIH HHS
• SC1 GM121202 NIGMS NIH HHS
• SC2 CA235066 NCI NIH HHS
• UL1 TR001881 NCATS NIH HHS
• SC1 GM135050 NIGMS NIH HHS
• U56 CA101599 NCI NIH HHS
• U54 MD007598 NIMHD NIH HHS
• Center for Strategic Scientific Initiatives, National Cancer Institute (NCI Center for Strategic Scientific Initiatives)
• Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)

• Breast
• CD4
• CD8
• FOXP3
• Triple negative cancer

• Adult
• Aged
• Aged, 80 and over
• Breast/cytology
• Breast/immunology
• Breast/pathology
• Breast/surgery
• CD4-Positive T-Lymphocytes/immunology
• CD8-Positive T-Lymphocytes/immunology
• Carcinoma/immunology
• Carcinoma/mortality
• Carcinoma/pathology
• Carcinoma/surgery
• Disease-Free Survival
• Female
• Forkhead Transcription Factors/metabolism
• Humans
• Lymphocytes, Tumor-Infiltrating/immunology
• Lymphocytes, Tumor-Infiltrating/metabolism
• Mastectomy
• Middle Aged
• Neoplasm Recurrence, Local/epidemiology
• Neoplasm Recurrence, Local/immunology
• Prognosis
• Triple Negative Breast Neoplasms/immunology
• Triple Negative Breast Neoplasms/mortality
• Triple Negative Breast Neoplasms/pathology
• Triple Negative Breast Neoplasms/surgery

Breast cancer is a global health problem – it is the most common malignancy among women. Triple negative breast cancers (TNBC) account for 10–20% of female breast cancer. Most TNBC cases confer poor prognosis. Brain metastasis appears in more than 15% in the triple negative breast cancer population, which causes serious decrease in survival. Changes of immunophenotype are not uncommon in breast cancer, offering new therapeutic options in cases where targetable proteins or pathways are being identified.

After five lines of chemotherapy and 82 months following the first diagnosis, our patient with brain metastatic triple negative breast cancer had human epidermal growth factor receptor 2 (HER2) genetic heterogeneity in the metastatic tissue sample interpreted as HER2 status conversion. After the removal of the metastasis, we started first line therapy for metastatic HER2 positive cancer with trastuzumab and paclitaxel. After the first cycle of trastuzumab, on day 8, she had a seizure, and neurosurgical examination showed an abscess-like lesion. The punctate proved to be sterile by microbiological and pathological examination, so we continued cytostatic therapy without the anti-HER2 antibody. 3 months later, we could not identify the previous abscess-like lesion in the control computer tomography (CT) scan, and our patient had no neurological deficits.

We emphasize the importance of regular tissue confirmation of predictive markers in progressive tumorous disease even if our presented case is not unequivocally a “conversion case”. Tumor subtype is determined according to algorithms and definitions published in guidelines, nevertheless, use of different guidelines may lead to controversial interpretation in cases where HER2 genetic heterogeneity is present. Furthermore, we suggest that seronegative, aseptic intracranial fluid effusion after the removal of a brain metastasis may possibly be a side effect of trastuzumab.

• Abscess-like lesion
• Brain metastasis
• HER-2 immunophenotype switch
• Trastuzumab
• Triple negative breast cancer

Tumor-associated macrophages (TAMs) have recently been reported as an important factor in tumor growth and the progression of cancer. The prognostic significance of localizations and densities of TAMs in triple negative cancer (TNC) of the breast is not well understood. The aim of this study was to assess the localizations and densities of the TAMs subtype in TNC and examine their clinicopathological features. The study was based on 107 TNC cases operated on at Dokkyo Medical University Hospital using the pan-macrophage marker CD68 and the M2 macrophage marker CD163 in the tumor stroma (TS) and tumor nest (TN), respectively, and examined the clinicopathological significance. Multivariate Cox regression analyses revealed that age and CD163+ TAMs in both the TS and TN were independent prognostic factors for relapse-free survival and overall survival. No correlation was found between the number of CD68+ cells or the CD163/CD68 ratio either in TS or TN, or clinicopathological features. Our study found that infiltration of CD163+ TAMs, rather than CD68+, in both TS and TN was associated with poor prognosis in TNC patients by multivariate analysis. This suggests that CD163+ TAMs may affect the prognosis of TNC by not only regulating the immune reaction by TAMs in TS, but also because of their direct influence on TN.

• Breast
• CD163
• CD68
• Triple-negative cancer
• Tumor-associated macrophages

• Antineoplastic agents
• Cisplatin
• DNA repair
• Triple negative breast neoplasms

• Akt
• apatinib
• breast tumor
• docosahexaenoic acid
• targeted molecular therapy

• Metastasis
• Molecular mechanisms
• Recurrence
• Treatment methods
• Triple negative breast cancer

• DNA methylation
• TNBC
• gene expression
• therapeutic targets

• SRG2017-00097-FHS Universidade de Macau
• SMW The Faculty of Health Sciences, University of Macau

• OlympiAD
• breast cancer
• olaparib

• BRCA mutation
• diagnosis and therapy of TNBC
• subtyping of TNBC
• triple-negative breast cancer

• breast cancer
• neoadjuvant chemotherapy
• neutrophil-to-lymphocyte ratio
• pathological response
• prognosis

• Breast Neoplasms/blood
• Breast Neoplasms/drug therapy
• Chemotherapy, Adjuvant/statistics & numerical data
• Disease-Free Survival
• Female
• Humans
• Inflammation Mediators/blood
• Inflammation Mediators/metabolism
• Lymphocytes/metabolism
• Neutrophils/metabolism
• Odds Ratio
• Prognosis
• Proportional Hazards Models

Triple-negative breast cancer (TNBC) is sometimes mistaken for fibroadenoma due to its tendency to show benign morphology on breast ultrasound (US) albeit its aggressive nature. This study aims to develop a radiomics score based on US texture analysis for differential diagnosis between TNBC and fibroadenoma, and to evaluate its diagnostic performance compared with pathologic results. We retrospectively included 715 pathology-proven fibroadenomas and 186 pathology-proven TNBCs which were examined by three different US machines. We developed the radiomics score by using penalized logistic regression with a least absolute shrinkage and selection operator (LASSO) analysis from 730 extracted features consisting of 14 intensity-based features, 132 textural features and 584 wavelet-based features. The constructed radiomics score showed significant difference between fibroadenoma and TNBC for all three US machines (p < 0.001). Although the radiomics score showed dependency on the type of US machine, we developed more elaborate radiomics score for a subgroup in which US examinations were performed with iU22. This subsequent radiomics score also showed good diagnostic performance, even for BI-RADS category 3 or 4a lesions (AUC 0.782) which were presumed as probably benign or low suspicious of malignancy by radiologists. It was expected to assist radiologist’s diagnosis and reduce the number of invasive biopsies, although US standardization should be overcome before clinical application.

• AR testing
• BRCA
• germline mutation
• poly (adenosine diphosphate–ribose) polymerase 1 inhibitors
• programmed cell death ligand 1
• rebiopsy

• breast cancer-specific survival
• nodal status
• overall survival
• triple-negative breast cancer
• tumor size

• Metastatic breast cancer
• antiHer2 therapy
• endocrine therapy
• immunotherapy
• targeted therapies

The aim of the study was to estimate the implications of androgen receptor (AR) expression in estrogen receptor (ER)-positive subset of invasive breast carcinoma patients.

We assessed the AR expression in a subset of 96 predominantly ER-positive invasive breast carcinomas and correlated this expression pattern with several clinical and pathologic parameters: histologic type and grade, tumor size, lymph node status, progesterone receptor (PgR) status, and human epidermal growth factor receptor type 2 (HER2) overexpression and evaluated the association of these parameters with 10-year survival using univariate and multivariate analyses. Data used for analysis were derived from medical records. Immunohistochemical analysis for AR, ER, PgR, and HER2 were carried out and semiquantitative evaluation of stainings was performed.

AR expression was demonstrated in 43.7% of patients. AR was significantly related to well-differentiated tumors and positive PgR/HER2 status. No statistical difference was demonstrated in AR expression in relation to tumor size, lymph node status, menopausal status, and tumor histologic type. AR expression was not an independent prognostic factor related to 10-year survival in ER-positive cancers. In multivariate analyses, older age at diagnosis, larger tumor size, and positive lymph node status were significantly associated with poorer 10-year survival.

AR expression is significantly associated with ER/PgR/HER2 status and positively related to well-differentiated tumors. Although AR status in ER-positive cancers is not an independent prognostic factor, it might provide important additional information on prognosis and become a promising object for targeted therapy.

To quantify the effect of traditional prognostic factors [nodal status, estrogen-receptor (ER), progesterone-receptor (PR), human epidermal growth factor receptor 2 (HER2)] on long-term outcome of patients with early breast cancer (EBC), treated in clinical practice over a period of about twenty years.

1198 consecutive patients were identified. Median DFS (disease-free survival): ER+/PR±/HER2−, 165 months (mo) if node-negative (N0) and 114mo if node-positive (N+) (p < 0.001); triple-negative (TN), 109mo if N0 and 65mo if N+ (p 0.144); ER+/PR±/HER2+ in patients not-treated with adjuvant trastuzumab (T−), not reached if N0 and 114mo if N+ (p 0.297); ER+/PR±/HER2+ in patients treated with trastuzumab (T+), 95mo if N0 and 85mo if N+ (p 0.615); ER−/PR−/HER2+ T−, not reached if N0 and 26mo if N+ (p 0.279); ER−/PR−/HER2+ T+, not reached if N0 and 66mo if N+ (p 0.014). Median OS (overall survival): ER+/ PR±/HER2−, 166mo if N0 and 144mo if N+ (p 0.028); TN, 158mo if N0 and 96mo if N+ (p 0.384); ER+/PR±/HER2+ T−, not reached if N0 and 157mo if N+ (p 0.475), ER+/PR±/HER2+ T+, not reached if N0 and 106mo if N+ (p 0.436); ER−/PR−/HER2+ T−, not reached if N0 and 34mo if N+ (p 0.273); ER−/PR−/HER2+ T+, not reached neither if N0 nor if N+ (p 0.094).

Disease-free survival (DFS) and overall survival (OS) were evaluated according to tumor characteristics, based on information retrospectively retrieved from patients’ medical records.

Pathological tumor characteristics and nodal status still represent useful tools in treatment selection and follow-up decision making of EBC patients in clinical practice.

• 20-year follow-up
• clinical practice
• clinicopathological prognostic factors
• early breast cancer
• survival

• classification
• functions
• long noncoding RNAs
• triple negative breast cancer

• Breast cancer
• MRI
• Meta-analysis
• NAC
• pCR

• Basal-like type breast cancer
• Breast cancer
• Breast conserving surgery
• Mastectomy
• Postoperative radiotherapy
• Triple negative breast cancer

• B-mode ultrasound
• Retraction pattern
• Strain elastography
• Three-dimensional ultrasound
• Triple negative breast cancer

• Adult
• Aged
• Breast Neoplasms/diagnostic imaging
• Diagnosis, Differential
• Elasticity Imaging Techniques/methods
• Female
• Humans
• Image Interpretation, Computer-Assisted/methods
• Imaging, Three-Dimensional/methods
• Middle Aged
• Multimodal Imaging/methods
• Reproducibility of Results
• Sensitivity and Specificity
• Triple Negative Breast Neoplasms/diagnostic imaging
• Ultrasonography, Mammary/methods
• Young Adult

• hormone receptor-negative breast cancer
• metastatic breast cancer
• triple-negative breast cancer

Centrosome amplification (CA), a cell-biological trait, characterizes pre-neoplastic and pre-invasive lesions and is associated with tumor aggressiveness. Recent studies suggest that CA leads to malignant transformation and promotes invasion in mammary epithelial cells. Triple negative breast cancer (TNBC), a histologically-aggressive subtype shows high recurrence, metastases, and mortality rates. Since TNBC and non-TNBC follow variable kinetics of metastatic progression, they constitute a novel test bed to explore if severity and nature of CA can distinguish them apart. We quantitatively assessed structural and numerical centrosomal aberrations for each patient sample in a large-cohort of grade-matched TNBC (n = 30) and non-TNBC (n = 98) cases employing multi-color confocal imaging. Our data establish differences in incidence and severity of CA between TNBC and non-TNBC cell lines and clinical specimens. We found strong correlation between CA and aggressiveness markers associated with metastasis in 20 pairs of grade-matched TNBC and non-TNBC specimens (p < 0.02). Time-lapse imaging of MDA-MB-231 cells harboring amplified centrosomes demonstrated enhanced migratory ability. Our study bridges a vital knowledge gap by pinpointing that CA underlies breast cancer aggressiveness. This previously unrecognized organellar inequality at the centrosome level may allow early-risk prediction and explain higher tumor aggressiveness and mortality rates in TNBC patients.

• centrosome amplification
• disease prognosis
• metastasis
• triple negative breast cancer

• cyclophosphamide
• disease-free survival
• epirubicin
• fluorouracil
• lymph node status
• overall survival
• triple negative breast cancer

• Cyclin
• Epidermal growth factor receptor
• Triple negative breast cancer
• Vascular endothelial growth factor
• p53

Magnetic resonance imaging (MRI) is highly sensitive in identifying residual breast cancer following neoadjuvant chemotherapy (NAC), and consequently is a commonly used imaging modality in locally advanced breast cancer patients. In these patients, tumor response is an important prognostic indicator. However, discrepancies between MRI findings and surgical pathology are well documented. Overestimation of residual disease by MRI may result in greater surgery than is actually required while underestimation may result in insufficient surgery. Thus, it is important to understand when MRI findings are reliable and when they are less accurate. MRI most accurately predicts pathology in triple negative, Her2 positive and hormone receptor negative tumors, especially if they are of a solid imaging phenotype. In these cases, post-NAC MRI is highly reliable for surgical planning. Hormone receptor positive cancers and those demonstrating non mass enhancement show lower concordance with surgical pathology, making surgical guidance more nebulous in these cases. Radiologists and surgeons must assess MRI response to NAC in the context of tumor subtype. Indiscriminate interpretations will prevent MRI from achieving its maximum potential in the pre-operative setting.

• Breast
• Magnetic resonance imaging
• Neoadjuvant chemotherapy
• Biomarkers
• Phenotypes

• Breast cancer cell
• EGFR
• HER2
• Triple negative breast cancer

• Breast cancer
• HER2
• Molecular imaging
• Molecular target therapy
• PET

• Triple-negative
• breast cancer
• prognosis
• survival