PATHOGENESIS OF MENINGIOMAS (LITERATURE REVIEW)

Abstract

Meningiomas are common tumors of the central nervous system, originating from the meningeal membrane of the brain or spinal cord. Most meningiomas are benign tumors characterized by slow growth and histologically correspond to Grade I according to the World Health Organization (WHO) classification. However, some rare histological variants (clear cell, chordoid , papillary and rhabdoid ), as well as atypical ( WHO Grade II) and anaplastic ( WHO Grade III) meningiomas exhibit more aggressive biological behavior and are clinically associated with a high risk of recurrence and less favorable outcome. forecast. This review summarizes the most important pathophysiological characteristics of meningiomas and also presents data on the molecular mechanisms involved in the initiation and progression of meningiomas . Current research suggests that the initiation of meningioma growth is closely related to the inactivation of one or more proteins from the highly conserved protein 4.1 family, including the neurofibromatosis type 2 gene product merlin / schwannomin , protein 4.1B (DAL-1) and protein 4.1R. The genetic changes in atypical meningiomas are complex and include losses in regions 1p, 6q, 10, 14q, and 18q, as well as additions of genetic material on different chromosomes. The significant genes are still unknown. Anaplastic meningiomas exhibit even more complex genetic changes, including frequent alteration of the tumor suppressor genes CDKN2A, p14ARF, and CDKN2B at 9p21, as well as gene amplification at 17q23. A better understanding of the molecular mechanisms involved in the pathogenesis of meningioma may not only lead to the identification of a new marker for diagnosis and prognosis assessment, but also facilitate the development of new pathogenetic therapeutic treatments.