. In our experience, it is very difficult to derive a conclusion about PTEN status using immunohistochemistry due to the heterogeneity of PTEN expression in the tumor tissue. The challenge of studying PTEN and any other marker of solid tumors is the need for direct access to the tumor through biopsies. This problem is especially 
challenging in clinical trials involving potential cancer therapies, as enrolled patients need to be exposed to multiple biopsies. At this point, the only way to assess the expression of PTEN and other molecules in PC patients is by direct access to tumor tissue, through biopsies or after radical prostatectomy. In this study, we propose a new noninvasive tool to profile PC tumors through blood exosomes. The expression of PSA in Scopoletin exosomes has been reported in exosomes from the urine of PC patients. The expression of PSA in exosomes from the blood of PC patients is an indicator that exosomes are derived from the diseased prostate gland. However, at this stage, we cannot rule out the possibility that PSA is incorporated into exosomal cargo after PSA secretion to the blood stream, as it has been suggested that PSA binds other blood proteins in the circulation and only a small fraction of PSA is not bound. The incorporation of PSA in exosomal cargo should be addressed in future studies. In this context, exosomes may provide a new tool to overcome the lack of specificity and prognostic value of PSA reported by Tosoian & Loeb, by correlating 20444863 PSA expression to other proteins expressed in exosomes, such as PTEN or other molecules. From our data, PTEN appears to be a better indicator than PSA in characterizing PC and can discriminate between PC patients and normal subjects, although this finding still needs validation and confirmation. The existence of tumor derived exosomes in the circulation of PC patients may be due to the fact that tumor vasculature is poorly organized and highly permeable Exosomal-PTEN in Prostate Cancer . This 7528253 may prevent tumor cells from re-uptaking shed exosomal-PTEN, by eliminating the accumulation of these exosomes within the tumor microenvironment and surrounding tissues. Epidermolysis bullosa is a genetically heterogeneous disease affecting the skin and mucous membranes. EB is characterized by the formation of blisters and erosions after minor traumatization, thereby significantly compromising life quality. EB is divided into four major groups: the simplex type, the dystrophic type, the junctional type and Kindler syndrome. The genes underlying the different subtypes of EB have major functions in mechanical stabilization of the basement membrane zone. Depending on the gene which is affected, EB can be either a relatively mild disease or a life-threatening disease due to secondary complications like squamous cell carcinomas in dystrophic EB, in which the collagen VII gene is mutated. In the EBS subtype, mutations in the keratin-5, keratin-14 and plectin genes are causative, with many being inherited as autosomal dominants and therefore presenting a challenge to gene therapy. EBS type Dowling-Meara is caused by such dominant mutations in the K5 and K14 genes and belongs to the more severe subtypes within the EBS group. The type-II keratin K5 and the type-I keratin K14 are the major components of the intermediate filament network in basal cells of epithelia, forming heterodimers that are bundled as tonofilaments. These IFs are attached to desmosomes and hemidesmosomes and provide mechanical stabi