Brain Tumors: Biology, Pathology and Clinical References by Professor Dr. Davide Schiffer, Professor Dr. Maria Teresa

By Professor Dr. Davide Schiffer, Professor Dr. Maria Teresa Giordana, Dr. Alessandro Mauro, Dr. Riccardo Soffietti (auth.)

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In both forms of the disease (hereditary and sporadic), a variety of different mutations have been described, ranging from subtle base changes to large deletions and mimicking of spontaneous mutagenesis mechanisms [1042]. The biochemical mechanism by which the product of the RB gene exerts its anti oncogenic effect is unknown, but its ability to bind DNA suggests that it participates in the control of the transcription or replication of DNA. In fact, the levels of phosphorylation of the RBI gene product are variable during the cell cycle, increasing in the Sand G2 phases [566, 488].

Transcripts of three different sizes are widely expressed in normal human tissues, including brain, as well as in fetal mouse nervous tissue [2858, 3459]. The protein encoded by NF2 gene, merlin, shares homology with a highly conserved family of proteins which are thought to create a link between integral proteins of the cell membrane and intracellular cytoskeletal components [3459]. It has been postulated that merlin is involved in pathways addressing growth inhibitory signals from the cell surface to intracellular structures [2022].

Following these observations, p53 has been described as a "guardian of the genome" [1859]. One possible outcome of the arrest of cell cycle induced by p53 is apoptosis [1859]; this is dependent on p53 in the case of DNA strand breakage caused either by ionizing radiation or chemical agents, but not in other cases [2027,529]. 1 Genetics and Molecular Biology 23 vivo, while this antitumor response is not produced by p53 mutants [1932]. Moreover, transgenic mice lacking p53 are significantly predisposed to spontaneous development of tumors at early age [750].

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