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Triple Negative Breast Cancer (TNBC) is an aggressive subtype of breast cancer (BC) that lacks the expression of estrogen receptor, pro.gesterone receptor and human epidermal growth factor receptor-2.Despite TNBC represents only 15 % of all types of BC, it accounts a disproportionate number of metastatic cases and deaths.Because of the poor prognosis and the high rate of metastasis, local and systemic recurrence associated with TNBC, researchers have been actively looking for target therapies and innovative therapeutic strategies to effectively treat this aggressive disease.Unfortunately, molecular targets and predictors for the treatment of TNBC do no currently exist.Accordingly,this study has been initiated to investigate the differential expression of biological markers in TNBC and Non-TNBC Saudi females that might be utilized as potential targeted-therapy and/or predict sensitivity to currently available therapeutic regimens.To achieve the ultimate goal of this study, a total of 200 formalin-fixed and paraffin-embeded (FFPE) breast cancer samples were selected and divided into 3 groups;control benign and normal breast tissues (20),TNBC (80) and Non-TNBC (100).Expression ofmRNA in FFPE tissues was performed using RT-PCR for the following genes;poly(ADP-ribose)polymerase (PARP-1), topoisomerase-2A (TOP-2A), vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), matrix metalloproteinases (MMP-2 and MMP-9), human epidermal growth factor-1 (HER-1) and multidrug resistance genes.In TNBC group, mRNA expression ofPARP-1, TOP-2A,HER-1, VEGF, bFGF and MMP-2 genes showed a highly significant and differential increase as compared to NonTNBC group.Data from this study suggest that inhibition of these target genes is emerging as one of the most exciting and promising targeted therapeutic strategies to treat TNBC in which the intended targets are DNA repair, tumour angiogenesis and metastasis.Accordingly, TNBC patients will be more benefited from PARP-1, TOP-2A and HER-1 inhibitors as well as antiangiogenic and antimetastatic therapies.