Breast Cancer - Current and Alternative Therapeutic by Esra Gunduz and Mehmet Gunduz

By Esra Gunduz and Mehmet Gunduz

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1996; Minegishi et al. 1996), Efs/Sin (CASS3) (Alexandropoulos & Baltimore 1996; Ishino et al. 1995), and CASS4 (HEPL) (Singh et al. 2008). p130Cas is the founding member and was first identified as a major tyrosinephosphorylated 130 kDa protein in cells transformed by the v-crk and v-src oncogenes (Sakai et al. 1994a). HEF1 (human enhancer of filamentation)/NEDD9 (neural precursor cell expressed, developmentally downregulated 9) was isolated in a screen for human proteins that confer morphoregulatory changes leading to filamentous budding in yeast Saccharomyces cerevisiae (Law et al.

Inhibition of the PI3K pathway: Hope we can believe in? Clin Cancer Res, Vol. 16, No. 12 (June 2010), pp. 3094-9 Vermeulen K, Van Bockstaele DR, & Berneman ZN. (2003). The cell cycle: a review of regulation, deregulation and therapeutic targets in cancer. Cell Prolif. Vol. 36, No. 3, (June 2003), pp. 131-49 Wu Y, Amonkar MM, Sherrill BH, O'Shaughnessy J, Ellis C, Baselga J, Blackwell KL, & Burstein HJ. (2011). Impact of lapatinib plus trastuzumab versus single-agent lapatinib on quality of life of patients with trastuzumab-refractory HER2+ metastatic breast cancer.

OPN is involved in maintaining calcium homeostasis via its calcium binding site. OPN upon binding with integrins or CD44 regulates breast cancer cell proliferation, migration, invasion and chemotaxis. OPN plays an important role in regulation of tumor progression, angiogenesis and metastasis in breast cancer. OPN is detected in many biological fluids like plasma of metastatic breast cancer patients, urine, milk and seminal fluids. The ligation of OPN to its receptors stimulates a cascade of signalling pathways which cross talk and foster neoplastic growth in breast cancer (Rangaswami et al, 2006).

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