Abstract
Triple negative breast cancer (TNBC), a special subset of breast cancer, refers to negative expressions of estrogen receptors (ER), progesterone receptors (PR) and human epidermal growth receptor 2 (HER2). It is associated with extreme local recurrence and distant metastasis with highly invasive character. With advances in genomics, the bases of molecular classification of TNBC now include the heterogeneity of its expression at the molecular level and clinical pathology, apart from classical immunohistochemistry. Every subtype of TNBC has different individualized target drugs, which include epidermal growth factor receptor (EGFR) inhibitor, poly-AD-ribose polymerase (PARP) inhibitor, anthracycline or paclitaxel, immunotherapy and vascular endothelial growth factor receptor (VEGFR) inhibitor. Combinations of target drugs are also used. Thus, there are no widely recognized standards of genotype classification and individualized drug targeting in TNBC. In this review, relevant studies and latest developments on TNBC are presented. Keywords: Triple-negative breast cancer, Genotype classification, Individualized drug targeting, Breast cancer
Highlights
Evidence has shown that breast cancer is widely considered as a leading cause of death among women, and it has been associated with significantly increasing morbidity in recent years [1]
When poly-AD-ribose polymerase (PARP) inhibitor affected on cancer cells with BRCA1/2 mutations, the inhibition of PARP activity can prevent the formation, the dependent PARP of DNA damage repair recombination were not resolved, at last, the DNA single-strand break (SSB) without repair led to the DNA stalled replication forks to convert the DNA double-strand breaks (DSBs), causing the apoptosis because of the homologous recombination (HR) lacked of BRCA1/2, which was called the “PARP-BRCA synthetic lethality” [16]
The results showed objective RR of 21 %, complete response (CR) of 8 %, partial response of 13 %, and the data showed disease stability for at least 6 months in 19 % patients, a 40 % clinical benefit rate, while 74 % of the patients had aberrant PI3K pathway
Summary
Evidence has shown that breast cancer is widely considered as a leading cause of death among women, and it has been associated with significantly increasing morbidity in recent years [1]. Due to its poor prognosis, high local recurrence rate and distant metastasis, TNBC does not respond well to targeted therapies [4]. This disease is a highly heterogeneous tumor which has been classified into 6 subtypes according to histology and molecular biology characteristics; different molecular subtypes of TNBC have differences in clinical expressions, responses to treatment and prognosis [4,5,6]. It has been reported that the high BRCA1 rs80350973 mutation associated with Ki67 indices might be a predictor of prognosis of TNBC [10]. These important genic hereditary events may provide critical guide for prediction of genic targeted therapies in TNBC. The rapid developments in investigative technologies of tissue chip and tissue microarrays have facilitated studies on genotype classifications in TNBC, resulting in enhanced understanding and useful development of genic targeted therapies
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