In addition, they show that the 1N Tau is enriched in the nucleus while 2N Tau is expressed mainly in cytoplasmic and axonal compartments. To conclude, we demonstrated for the first time, in vitro and in vivo in a rat model of sporadic tauopathy, that Tau protein is present in the extracellular fluid in a new type of vesicles, i.e., ectosomes. Under basal conditions, in addition to major free forms, Tau is actively secreted through Enzalutamide secretory pathways – rather in ectosomes than in exosomes. Extracellular vesicles have emerged as important mediators of intercellular communication, being involved in the transmission of biological signals between cells in both prokaryotes and higher eukaryotes to regulate a diverse range of biological processes but also in pathological process. Moreover, it appears that cancer cell-derived extracellular vesicles containing many proteins, RNA and lipids participate to the cancer progression, which involves invasion, immune modulation, neovascularization, and metastasis. Tau secretion from primary/iPS cells has been documented, and this mechanism may be regulated by neuronal activity. Here, we provide evidence that an ectosomal pathway at least partly mediates this secretion. These specific vesicles, directly emerging from the PM, enabled cytosolic Tau to be shuttled to the extracellular medium. Over-accumulation of intra-cellular Tau results in targeting to MVBs, leading to release in exosomes. This deregulation of Tau secretion could participate in the pathological spreading of Tau, as we also detected Tau in vesicles in our rat model of sporadic tauopathy. Endometrial cancer is the fourth most common cancer and the most common gynecologic cancer in American women, with approximately 8200 deaths and 49500 new cases in the United States in 2013. While women with EMCA generally have a good prognosis with 81.5% 5-year survival, the incidence and death rate of EMCA have continued to rise on average 1.1% and 0.4% respectively each year over the last 10 years. Recent increases in the incidence of endometrial cancer rates have been considered largely attributed to the obesity epidemic. Women diagnosed with advanced or recurrent disease have much worse survival rates and limited adjuvant treatment options. In the clinical setting, however, few molecules have been assayed as therapeutic and/or diagnostic biomarkers. Therefore, identification of biologic markers and their downstream targets is essential for personalizing therapies and improving the outcome and quality of life in patients with EMCA. EMCA has been categorized into two types. Type 1 cancer accounts for approximately 80% of EMCA and is characterized as estrogen dependent, estrogen receptor and progesterone receptor positive with endometrioid morphology and generally a favorable prognosis. Conversely, type 2 cancer is estrogen-independent, ER/PR negative, poorly differentiated and associated with a much poorer prognosis. Standard therapy for both types includes a surgical removal of the uterus, cervix, bilateral fallopian tubes and ovaries.