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Pathology

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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The same germline mutation has subsequently been identified in patients with Turcot syndrome (polyposis coli together with malignant gliomas or medulloblastomas) but, surprisingly, APe mutation was not found in 91 patients with sporadic neuroepithelial tumors [2320]. However, in a recent study [1231], germline mutation of APe gene and loss of the remaining normal allele on the homologue 5q chromosome have been demonstrated in a medulloblastoma in a Turcot patient. Moreover, in other Turcot families the germline mutation was identified in the genes hMLHI or hPMS2, which are normally involved in the repair of DNA mismatches [1231].

At the beginning, 100% of cells of this layer become labeled with [3H]thymidine, while subsequently an area devoid of mitoses is formed adjacent to the molecular layer. 4 Radial Glia and Ependyma 11 their immunoreactivity with class III J3-tubulin isotype (J3III) and calbindin-D28K. J3III, which is one of the earliest-appearing markers of neuronal differentiation [799], is expressed early by EGL and stellate neurons, basket cells, and granules; while calbindin-D28K is expressed early by cells of the VM at the roof of the fourth ventricle and by Purkinje and Golgi II neurons [1607].

An autocrine loop involving PDGF B chain and PDGF-~ receptor has also been demonstrated in meningiomas [1626, 2183, 265, 3608, 895, 2180]. The use of suramin, an inhibitor of different growth factors including PDGF, has been proposed as a treatment for controlling meningioma proliferation in patients with inoperable meningiomas [3089]. 3 Congenital Tumors 29 Other growth factors have been investigated in relation to brain tumors. Transforming growth factor-~ 1 (TGF~-l) and TGF~-2 are expressed in gliomas [2939, 1539, 928, 1391, 2373] and meningiomas [2441, 1547], and have been implicated in control of different aspects of glioma pathogenesis, including control of cell growth, invasiveness and migration, angiogenesis, and immunomodulation [2854, 2184, 1484, 2248].

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