Triple-negative breast cancer

Purpose of review Triple-negative breast cancer has been of great interest to oncologists because these cancers do not benefit from hormonal therapies or treatments targeted against human epidermal growth factor receptor 2 receptors. The only systemic therapy currently available is chemotherapy, and prognosis remains poor. We would like to describe recent pathological and genetic advancements and their possible implications on the development of new treatment strategies. Recent findings Increasing pathological and molecular knowledge has led to a better understanding of breast cancer in general. Triple-negative breast cancer, however, remains a heterogeneous subgroup with difficult-to-define subtypes. New targeted therapies are currently being developed and researched. Summary The recent advances in pathological and molecular knowledge have changed the landscape of breast cancer, with triple-negative breast cancer emerging as a pathological and clinical heterogeneous group. The main challenge lies in the development of new tailored treatment strategies for the various subgroups, with receptor kinase inhibition as the most promising new evolution to date. Further trials are needed to validate these new treatment options.

[1]  G. Hortobagyi,et al.  Mammographic features of triple receptor-negative primary breast cancers in young premenopausal women , 2008, Breast Cancer Research and Treatment.

[2]  A. Luini,et al.  Tailored preoperative treatment of locally advanced triple negative (hormone receptor negative and HER2 negative) breast cancer with epirubicin, cisplatin, and infusional fluorouracil followed by weekly paclitaxel , 2008, Cancer Chemotherapy and Pharmacology.

[3]  Robin L. Jones,et al.  Triple negative breast cancer: molecular profiling and prognostic impact in adjuvant anthracycline-treated patients , 2008, Breast Cancer Research and Treatment.

[4]  E. Yıldırım,et al.  The prognostic importance of triple negative breast carcinoma. , 2008, Breast.

[5]  I. Ellis,et al.  Is acinic cell carcinoma a variant of secretory carcinoma? A FISH study using ETV6‘split apart’ probes , 2008, Histopathology.

[6]  Ian O Ellis,et al.  Basal-like breast cancer: a critical review. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[7]  X. Pivot,et al.  The potential of anti-vascular endothelial growth factor therapy in metastatic breast cancer: clinical experience with anti-angiogenic agents, focusing on bevacizumab. , 2008, European journal of cancer.

[8]  W. Loo,et al.  Evaluation of neoadjuvant inhibition of aromatase activity and signal transduction in breast cancer. , 2008, Cancer letters.

[9]  H. Rugo,et al.  Phase II study of sunitinib malate, an oral multitargeted tyrosine kinase inhibitor, in patients with metastatic breast cancer previously treated with an anthracycline and a taxane. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[10]  S. Barni,et al.  Targeted therapies for the treatment of breast cancer in the post-trastuzumab era. , 2008, The oncologist.

[11]  C. Reynolds,et al.  Molecular analysis of metaplastic breast carcinoma: high EGFR copy number via aneusomy , 2008, Molecular Cancer Therapeutics.

[12]  F. B. Sørensen,et al.  Estrogen receptor, progesterone receptor, HER-2, and response to postmastectomy radiotherapy in high-risk breast cancer: the Danish Breast Cancer Cooperative Group. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[13]  K. Hess,et al.  Response to neoadjuvant therapy and long-term survival in patients with triple-negative breast cancer. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[14]  S. Jeffrey,et al.  Basal carcinoma of the breast revisited: an old entity with new interpretations , 2008, Journal of Clinical Pathology.

[15]  A. Alavi,et al.  Comparison of triple‐negative and estrogen receptor‐positive/progesterone receptor‐positive/HER2‐negative breast carcinoma using quantitative fluorine‐18 fluorodeoxyglucose/positron emission tomography imaging parameters , 2008, Cancer.

[16]  A. Tutt,et al.  Triple negative tumours: a critical review , 2007, Histopathology.

[17]  O. Nalcioglu,et al.  Magnetic resonance imaging in predicting pathological response of triple negative breast cancer following neoadjuvant chemotherapy. , 2007, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[18]  O Nalcioglu,et al.  Triple-negative breast cancer: MRI features in 29 patients. , 2007, Annals of oncology : official journal of the European Society for Medical Oncology.

[19]  J. Nevins,et al.  Validation of gene signatures that predict the response of breast cancer to neoadjuvant chemotherapy: a substudy of the EORTC 10994/BIG 00-01 clinical trial. , 2007, The Lancet. Oncology.

[20]  N. Sneige,et al.  Triple Negative Breast Carcinoma and the Basal Phenotype: From Expression Profiling to Clinical Practice , 2007, Advances in anatomic pathology.

[21]  Larry Norton,et al.  HER2 and response to paclitaxel in node-positive breast cancer. , 2007, The New England journal of medicine.

[22]  O. Fadare,et al.  The Phenotypic Spectrum of Basal-like Breast Cancers: A Critical Appraisal , 2007, Advances in anatomic pathology.

[23]  C. Jasmin,et al.  Combined paclitaxel and cetuximab achieved a major response on the skin metastases of a patient with epidermal growth factor receptor-positive, estrogen receptor-negative, progesterone receptor-negative and human epidermal growth factor receptor-2-negative (triple-negative) breast cancer. , 2007, Anti-cancer drugs.

[24]  S. Narod,et al.  Triple-Negative Breast Cancer: Clinical Features and Patterns of Recurrence , 2007, Clinical Cancer Research.

[25]  A. Stan,et al.  Predominance of the basal type and HER-2/neu type in brain metastasis from breast cancer , 2007, Modern Pathology.

[26]  Marc Tischkowitz,et al.  Use of immunohistochemical markers can refine prognosis in triple negative breast cancer , 2007, BMC Cancer.

[27]  D. Sgroi,et al.  The p63/p73 network mediates chemosensitivity to cisplatin in a biologically defined subset of primary breast cancers. , 2007, The Journal of clinical investigation.

[28]  C. Perou,et al.  The Triple Negative Paradox: Primary Tumor Chemosensitivity of Breast Cancer Subtypes , 2007, Clinical Cancer Research.

[29]  A. Vincent-Salomon,et al.  Identification of typical medullary breast carcinoma as a genomic sub-group of basal-like carcinomas, a heterogeneous new molecular entity , 2007, Breast Cancer Research.

[30]  A. Theocharis,et al.  The importance of c-Kit and PDGF receptors as potential targets for molecular therapy in breast cancer. , 2007, Current medicinal chemistry.

[31]  M. Fernö,et al.  Basal-like phenotype is not associated with patient survival in estrogen-receptor-negative breast cancers , 2007, Breast Cancer Research.

[32]  D. Easton,et al.  Basal-like grade III invasive ductal carcinoma of the breast: patterns of metastasis and long-term survival , 2007, Breast Cancer Research.

[33]  J. Weidhaas,et al.  Locoregional relapse and distant metastasis in conservatively managed triple negative early-stage breast cancer. , 2006, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[34]  A. Ashworth,et al.  EGFR amplification and lack of activating mutations in metaplastic breast carcinomas , 2006, The Journal of pathology.

[35]  S. Lakhani,et al.  Metaplastic breast carcinomas are basal‐like tumours , 2006, Histopathology.

[36]  J. Robertson,et al.  Morphological and immunophenotypic analysis of breast carcinomas with basal and myoepithelial differentiation , 2006, The Journal of pathology.

[37]  D. Birnbaum,et al.  Typical medullary breast carcinomas have a basal/myoepithelial phenotype , 2005, The Journal of pathology.

[38]  Å. Borg,et al.  Cytokeratin 5/14-positive breast cancer: true basal phenotype confined to BRCA1 tumors , 2005, Modern Pathology.

[39]  Roman Rouzier,et al.  Breast Cancer Molecular Subtypes Respond Differently to Preoperative Chemotherapy , 2005, Clinical Cancer Research.

[40]  Daniel A. Haber,et al.  Gefitinib-Sensitizing EGFR Mutations in Lung Cancer Activate Anti-Apoptotic Pathways , 2004, Science.

[41]  A. Gown,et al.  Immunohistochemical and Clinical Characterization of the Basal-Like Subtype of Invasive Breast Carcinoma , 2004, Clinical Cancer Research.

[42]  Patricia L. Harris,et al.  Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. , 2004, The New England journal of medicine.

[43]  L. Bégin,et al.  Disruption of the expected positive correlation between breast tumor size and lymph node status in BRCA1‐related breast carcinoma , 2003, Cancer.

[44]  Philip M. Long,et al.  Breast cancer classification and prognosis based on gene expression profiles from a population-based study , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[45]  Christian A. Rees,et al.  Molecular portraits of human breast tumours , 2000, Nature.

[46]  S. Küçücük,et al.  MAPK overexpression is associated with anthracycline resistance and increased risk for recurrence in patients with triple-negative breast cancer. , 2008, Annals of oncology : official journal of the European Society for Medical Oncology.

[47]  Qifeng Yang,et al.  Outcomes in young women with breast cancer of triple-negative phenotype: the prognostic significance of CK19 expression. , 2008, International journal of radiation oncology, biology, physics.

[48]  A. Rademaker,et al.  alphaB-crystallin is a novel predictor of resistance to neoadjuvant chemotherapy in breast cancer. , 2008, Breast cancer research and treatment.

[49]  Ian O Ellis,et al.  Prognostic markers in triple‐negative breast cancer , 2007, Cancer.

[50]  H. Dressman,et al.  Genomic signatures to guide the use of chemotherapeutics , 2006 .