At high levels in neuroblasts of the developing larval brain suggesting that Insb may have a broader role as a Notch antagonist. Breast cancer is one of the leading causes of death in the United States and worldwide. Early diagnosis and effective use of adjuvant therapies are required to improve patient survival. Prognostic factors that are frequently used for making clinical decisions in breast cancer are age, tumor size, status of lymph nodes, histological types of the tumor, pathological grade, and hormone receptor status. However, more biomarkers are needed for therapy and prediction of outcome because human breast cancers are diverse in their genetic nature and their response to therapy. Recently, many groups have tried to identify gene signatures of breast cancer patients. These gene signatures can lead to more accurate clinical decisions for cancer patients. Breast cancer can be classified into several groups depending on their expressions of biomarkers and pathology of breast cancer specimens. The most common molecular markers for breast cancers include estrogen receptor, progesterone receptor, HER2/neu, EGFR, Ki-67 and others. The subgroups of breast cancer include Luminal A, Luminal B, Basal, HER2-enriched subtypes. Triple negative breast cancer subtypes, which have deficient expression of ER, PR and HER2/neu, usually have poor prognosis and do not respond to hormone therapy. However, triple negative breast cancer is also a heterogeneous group, which shows different gene signatures. For example, some triple negative breast cancers have defective BRCA1 genes, whereas other triple negative breast cancer patient groups have 1800401-93-7 functional BRCA1. BRCA1 is one of the most frequently mutated genes in breast cancer patients. Women with germline mutations in BRCA1 have high risk of breast cancer, ovarian cancer and other cancers. BRCA1 is involved in maintaining genomic integrity by functioning in pathways involved in DNA repair, cell cycle checkpoint control, apoptosis, chromosome segregation and others. One of the main roles of BRCA1 is to promote homologous recombination repair and G2/M cell cycle arrest during DNA damage response. Thus, the loss of BRCA1 is frequently associated with a dramatic increase of genomic instability and tumorigenesis. While germline BRCA1 mutations are rarely found in Eleutheroside E patients with sporadic breast cancers, the functions of BRCA1 may be inactivated by other mechanisms, which are often referred to as BRCAness. One of the possible mechanisms of BRCAness is the inactivation of BRCA1 function at the epigenetic level by DNA methylation of the BRCA1 promoter. BRCA status is also important for cancer therapy. The genomic instability of BRCA1- and BRCA2-defective cells can be exploited for cancer therapy. Clinicall
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