Navegando por Assunto "Astrocitoma"
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Item Acesso aberto (Open Access) Análises moleculares da região controle do DNA mitocondrial de astrocitomas na população paraense(Universidade Federal do Pará, 2012-06-06) COSTA JÚNIOR, Carlos Antonio da; ANSELMO, Nilson Praia; http://lattes.cnpq.br/6518287721873199The central nervous system cancer represents 2% of all malignancies in the world population and 23% of cases of childhood cancer. In Brazil, an estimated 4,820 cases of cancer in men and women in 4450 to the year 2012. Gliomas are tumors of the central nervous system formed from glial cells, making up over 70% of brain tumors. The most important property of gliomas is the ability of immune evasion. Age, ethnicity, gender and occupation may be considered risk factors for the development of gliomas, and are twice as common in African-Americans. The astrocytoma is the most common glial tumor, constituting about 75% of cases of gliomas. These tumors are classified into four levels according to the World Health Organization. Mitochondrial DNA is related to the development and progression of various types of tumors. Mitochondrion is responsible for cellular energy balance and is involved in triggering apoptosis responding to oxidative stress. Mutations in DLOOP can change DNA replication rates and increase the developing cancer risk. We analyzed 29 samples astrocytoma classified according to the WHO. Our data suggest that low-grade astrocytomas may be related to genetic inheritance, making some patients with specific mutations or polymorphisms more susceptible to the risk of developing the disease, and high grade may be related to prolonged exposure to carcinogenics. Polymorphisms and mutations have been identified which correlate with some risk of developing astrocytomas and disease progression. The insertion of two or more nucleotides at microsatellite regions may cause instability and contribute to the cancer onset. Deletion at the site 16132 may be a high-grade astrocytoma marker, as well as insertion of two or more cytosines to the site 16190 can be an astrocytoma specific marker. Heteroplasmy may be decisive for the emergence and / or progression of high-grade astrocytomas.Item Acesso aberto (Open Access) Screening de polimorfismos e análise comparativa de alterações no número de copias do gene tp53 em gliomas(Universidade Federal do Pará, 2012-01-24) BRITO, José Reginaldo Nascimento; OLIVEIRA, Edivaldo Herculano Correa de; http://lattes.cnpq.br/0094007714707651Astrocytic neoplasms comprises around 60% of the Central Nervous System tumors, affecting mainly adults in a highly productive phase of life, and showing poor prognosis despite of the available treatments. A better knowledge of the molecular biology of this group of tumors is necessary to understand their evolution and to plan the treatment in a better way, as well as to develop new therapies. Hence, this study had the aim the analysis of modifications of gene TP53 related to changes in the number of copies and the presence of polimorphisms in exons 4 to 11, considered hotspots for mutations. A total of 14 samples of different malignant grades were analyzed by interphasic FISH using locus-specific probes for gene TP53 and centromeric for chromosome 17, and by SSCP for screening polymorphism in exons 4 to 11. The results were compared between tumors with grades I and II (benign) to those with grades III and IV (malign). The results concerning the locus specific probes (gene TP53 and centromere of chromosome 17) showed that the occurrence of deletions and amplifications were statistically important when compared to nuclei with normal copy number. However, these alterations were not related to the age, sex or malignancy. On the other hand, these alterations were found more frequently in patients with tumors with intermediate grades (III). SSCP experiments revealed polymorphisms in exons 5, 7 and 10, and although they were not realted to the malignancy of tumors, the samples with polymorphism corresponded to the patients with shorter survival after treatment, suggesting a relation between the mutations in these exons and higher aggressively tumors.