Depending of the origin of the initiating cell, different affliction types may occur. Serous cancers may initiate from a tubal origin and endometrioid cancers from an endometrial origin. These two types of cancers represent the most prevalent ones and bear very different morphologic properties. It would be very relevant to discriminate

whether PC implications are constant between these two types of EOC. Finally, the determination of PACE4-specific substrates in ovarian cancer progression would pave the way to a better understanding of molecular and cellular pathways in tumorigenesis but also potentially reveal biomarkers regulated by this enzyme. Nowadays, N-terminomics methods based on mass spectrometry allow one to decipher the action of an enzyme by the characterization Selleck BAY 73-4506 of its generated N-terminal fragments [38]. Evaluation of the general action of an

enzyme is the crucial learn more step to describe biologic mechanistics, and it may be of great relevance to reveal the key position of PACE4 among molecular events of ovarian cancer progression. Other mass spectrometry–based approaches for the analysis of tissues regarding the anatomic context [39], [40], [41] and [42] may also be useful for the exploration of molecular events occurring in xenografts. Indeed, it would be interesting to compare the molecular events occurring between the developed tissue and the surrounding environment or within the tissue itself between the different interacting cell types, for example, between blood vessels and the cancerous cells. In conclusion, the present

study provides a new outlook for the use of PACE4 inhibitors in neoplastic afflictions. The authors thank Alain Piché for kindly providing the OVCAR3 and CAOV3 cell lines and Leonid Volkov and Vanessa Couture for their helpful discussions and technical assistance FAD with IHC analyses. “
“It has been shown that transplantation of neural stem/progenitor cells (NSPCs) has potential as a therapy for various disorders of the central nervous system, such as stroke [1], multiple sclerosis [2], Parkinson disease [3], Huntington disease [4], amyotrophic lateral sclerosis [5], and gliomas [6], [7], [8] and [9]. NSPCs tend to migrate toward injured regions in these various brain pathologies [1], [2], [4], [7], [8] and [9]; this migration is regulated mainly by the signaling axis of C-X-C motif chemokine 12 (CXCL12) and its receptor C-X-C chemokine receptor type 4 (CXCR4) [10]. NSPCs move along the CXCL12 concentration gradient formed by the increased levels at sites of injuries [11], [12] and [13], resulting in targeted migration [10], [13], [14] and [15]. Targeted migration of NSPCs to lesion sites is essential for the direct repair of damaged tissues.