**6. MicroRNAs and their relationship with cancer**

Calin et al. were the first ones to find evidence regarding the relation between miRNAs and cancer, demonstrating that miR-15 and miR-16 are located in a mutated region, in over half of chronic lymphocytic leukaemias in B-cells [30]. Several following studies have demonstrated that the expression profiles of several miRNAs are altered in different types of tumours such as glioblastoma, pituitary adenoma, prostate cancer, breast carcinoma, hepatocellular carcinoma, lung carcinoma, colorectal carcinoma, ovarian carcinoma, thyroid and cervical carcinoma, lymphoma and chronic lymphocytic leukaemia [31–35]. For this reason, some of them are considered tumour-suppressive genes or oncogenes [36–38]. Genetic events guiding the development of tumours in the brain are yet unknown; nevertheless, there is evidence which suggests that gliomas may surge starting from a subpopulation of cells within the tumoural mass; these cells have been called 'stem tumour cells', which maintain their ability for renewal and multi-potentiality. MiRNAs are important regulators of the process of differentiation and proliferation of stem cells (**Figure 4**) [39–41].

**Figure 4.** Mir-15b regulates the progression of the cell cycle because it has cyclin E as a target. The over-expression of miR-15b causes an arrest of the cell cycle in the G0/G1 phase, whereas the low expression causes a reduction in the population of cells in G0/G1 and an increase in phase S [51].
