**1. Introduction**

Gliomas are associated with aggressive invasion of the surrounding brain parenchyma. The invasion is due to a combination of transformed cells phenotype changes, innate and acquired immunity and autocrine and paracrine release of growing and permeabilizing chemokines. This intricate scenario develops within the cerebral parenchyma, notoriously protected by an ultraspecialized system. Several experimental models of glioma, have been used in vivo to

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

monitor the infiltration of tumor cells in the parenchyma and/or perivascular spaces, even at a single cell level [1–3]. However, the relationship between glioma-induced BBB dysregulation and glioma invasion remains poorly understood. In this chapter we review the natural history of glioblastoma and, on the basis of the scientific evidence published to date, we try to give an explanation and meaning to biomarkers found in the peripheral blood. In particular, we focus our attention on cellular biomarkers, the circulating tumor cells and cellular endothelial progenitors. Our interest is aimed at giving an order in the context of human cell biology of human glioblastoma. This intracranial tumor remains today one of the big killers and represents a major challenge in the field of oncology because it is unresponsive to treatment and able to progress in a way difficult to monitor.
