الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 122 |  |  |
| | | from | 122 | | |
Abstract
Triple negative tumor is estrogen receptor-negative (ER-), progesterone receptor-negative (PR-) and HER2/neu-negative (HER2-).Most triple negative tumors are basal-like and most basal-like tumors are triple negative.
These tumors also tend to express HER1 and/or cytokeratin 5/6- proteins and many contain p53 mutations, in addition to “basal-like” cytokeratins (CK 5, 14, 17) and HER1 /EGFR EGFR expression appears in 30% to 45% of Breast cancer
Also, an association between the triple-negative phenotype and breast cancers harboring germline mutations in the BRCA1 gene has been well-described.
Patients with triple-negative breast cancer tend to be younger at diagnosis than their counterparts.
although around than 70% of TNBCare ductal (Lermaet al.,2007)(Pure lobular or mixed types account for less than 10% and only medullary tumors or those with medullary features have been clearly related with TNBC.
The benefits of cytotoxic chemotherapy for the treatment of TNBC are now well established with numerous studies demonstrating the effectiveness of chemotherapy in the neoadjuvant, adjuvant, and metastatic settings such as platinum agent/paclitaxel/adriamycine/capcitabine.
New agents in management of tnbc:
*Epitholones analogues:which maintain activity against taxane-sensitive and -resistant cell lines such as ixapapilone.
* antiangiogenic agents such as:sorafinib, sunitinib, axitinib, Pazopanib, Vatalanib.
* HER1 targeted treatment with cetuximab in breast cancer has produced superior however insignificant prolongation of disease free survival.
*PARP inhibitors:such as inaparip.
*Other targeted therapy includes :src inhibitors ,m-tor inhibitors ,histone deacetylase inhibitor