Exosomes and breast cancer: a comprehensive review of novel therapeutic strategies from diagnosis to treatment

2016 ◽  
Vol 24 (1) ◽  
pp. 6-12 ◽  
Author(s):  
C-Y Wu ◽  
S-L Du ◽  
J Zhang ◽  
A-L Liang ◽  
Y-J Liu
2020 ◽  
pp. 157-198
Author(s):  
Guifei Li ◽  
Hui Yao ◽  
Shichao Yan ◽  
Shujun Fu ◽  
Xiyun Deng ◽  
...  

2017 ◽  
Vol 9 (7) ◽  
pp. 493-511 ◽  
Author(s):  
Karima Oualla ◽  
Heba M. El-Zawahry ◽  
Banu Arun ◽  
James M. Reuben ◽  
Wendy A. Woodward ◽  
...  

Triple-negative breast cancer (TNBC) is a heterogeneous subtype of breast cancer that is defined by negative estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2) status. Treating patients with TNBC remains clinically challenging, as patients are not candidates for endocrine or HER2-directed therapy. As a result, chemotherapy with traditional agents such as anthracyclines and taxanes remains the only available option with moderate success. Recent discoveries have revealed that TNBC is a heterogeneous disease at the clinical, histological and molecular levels. The use of biomarkers to identify distinct subsets of TNBC that derive the greatest benefit from presently approved as well as novel therapeutics has become the main focus of current research. The aim of this review is to explore the clinical and biological complexity of TNBC as well as identify novel therapeutic options that target the various molecular subsets of TNBC.


2020 ◽  
Vol 21 (21) ◽  
pp. 8102 ◽  
Author(s):  
Giovanni Zarrilli ◽  
Gianluca Businello ◽  
Maria Vittoria Dieci ◽  
Silvia Paccagnella ◽  
Valentina Carraro ◽  
...  

Breast cancer evolves thanks to a dense and close interaction with the surrounding tumor microenvironment (TME). Fibroblasts, leukocytes, blood and lymphatic endothelial cells and extracellular matrix are the constituents of this entity, and they synergistically play a pivotal role in all of the stages of breast cancer development, from its onset to its metastatic spread. Moreover, it has been widely demonstrated that variations to the TME can correspond to prognosis variations. Breast cancer not only modulates the transformation of the environment within the mammary gland, but the same process is observed in metastases as well. In this minireview, we describe the features of TME within the primitive breast cancer, throughout its evolution and spread into the main metastatic sites.


2005 ◽  
Vol 12 (4) ◽  
pp. 721-747 ◽  
Author(s):  
Nicola Normanno ◽  
Massimo Di Maio ◽  
Ermelinda De Maio ◽  
Antonella De Luca ◽  
Andrea de Matteis ◽  
...  

Tamoxifen has been the mainstay of hormonal therapy in both early and advanced breast cancer patients for approximately three decades. The availability of novel compounds such as aromatase inhibitors (AIs) and fulvestrant, with different mechanism of action, is changing the scenario of endocrine treatment of postmenopausal breast cancer patients. In this review article, we have summarized the current knowledge of the mechanisms of resistance to endocrine therapy, in order to derive information that might be useful for therapeutic intervention. We propose that resistance to endocrine therapy is a progressive, step-wise phenomenon induced by the selective pressure of hormonal agents, which leads breast cancer cells from an estrogen-dependent, responsive to endocrine manipulation phenotype to a non-responsive phenotype, and eventually to an estrogen-independent phenotype. In particular, evidence suggests for each ‘action’ introduced to block estrogen stimulation of breast cancer cells (i.e. treatment with anti-estrogen), there are one or more corresponding ‘reactions’ that tumor cells can use to escape our attempts to block their growth: estrogen hypersensitivity associated with increased transcriptional activity of estrogen receptor α (ERα) and/or increased non-genomic activity of ERα, estrogen supersensitivity, increased growth factor signaling, suppression of ERα expression and finally estrogen independence. Activation of growth factor signaling is involved in each step of this phenomenon, and might ultimately substitute estrogen in sustaining the growth and the survival of breast cancer cells. In this respect, results of pre-clinical and clinical studies with AIs, fulvestrant and signaling inhibitors sustain this hypothesis. More importantly, the knowledge of the mechanisms involved in the resistance of breast cancer cells to endocrine therapy offers potential for novel therapeutic strategies.


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