Human Osteosarcomas
Mostrando 1-12 de 16 artigos, teses e dissertações.
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1. Vascular growth endothelial factor (VEGF) and microvessel density in human osteosarcomas. / Estudo do fator de crescimento endotelial vascular VEGF e da densidade de microvasos em osteossarcomas humanos.
INTRODUCTION: The role of angiogenesis as a prognostic indicator in cancer has been extensively studied in recent times with several studies demonstrating a positive correlation for various malignant tumours. However, the role of angiogenesis in osteosarcoma remains a topic of debate. AIM : evaluate the significance of intratumoral microvessel density (MVD)
Publicado em: 2010
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2. Imunoexpressão do c-kit em Osteossarcomas Humanos: Correlação com parâmetros anátomo-patológicos, clínicos e testes in vitro. / Immunoexpression of ckit in Human Osteosarcomas: clinicopathologic analysis and in vitro assays.
Objetivo: Investigar a imuno-expressão do c-kit e sua correlação com o prognóstico em pacientes portadores de Osteossarcoma e o efeito do Mesilato de Imatinibe (STI571) na proliferação e invasão de linhagens de células humanas de osteossarcoma. Material e Método Estudo retrospectivo com realização de imunohistoquímica dos blocos de parafina de 52
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 27/05/2009
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3. Osteosarcomas appearing in Syrian hamsters after treatment with extracts of human osteosarcomas.
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4. The presence of p53 mutations in human osteosarcomas correlates with high levels of genomic instability
The p53 gene is a critical tumor suppressor that is inactivated in a majority of cancers. The central role of p53 in response to stresses such as DNA damage, hypoxia, and oncogene activation underlies this high frequency of negative selection during tumorigenic transformation. Mutations in p53 disrupt checkpoint responses to DNA damage and result in the pote
National Academy of Sciences.
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5. Some retinoblastomas, osteosarcomas, and soft tissue sarcomas may share a common etiology.
DNA and RNA were extracted from primary human osteosarcomas and soft tissue sarcomas obtained from patients without retinoblastoma and were analyzed by hybridization with a cDNA probe for RB mRNA; absence or alterations of the RB gene are associated with development of retinoblastoma. Most of the osteosarcomas or soft tissue sarcomas examined by us did not e
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6. Modulation of the E2F1-Driven Cancer Cell Fate by the DNA Damage Response Machinery and Potential Novel E2F1 Targets in Osteosarcomas
Osteosarcoma is the most common primary bone cancer. Mutations of the RB gene represent the most frequent molecular defect in this malignancy. A major consequence of this alteration is that the activity of the key cell cycle regulator E2F1 is unleashed from the inhibitory effects of pRb. Studies in animal models and in human cancers have shown that deregulat
American Society for Investigative Pathology.
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7. Mechanisms of p53 loss in human sarcomas.
An important role for the p53 gene in neoplastic transformation in vitro and in vivo has been imputed by functional studies and identification of tumor-acquired gene defects or alterations in its expression. To study the generality and mechanisms of p53 alteration in human cancer, we examined 241 tumors of several types for structural aberrations of the locu
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8. p53 functions as a cell cycle control protein in osteosarcomas.
Mutations in the p53 gene have been associated with a wide range of human tumors, including osteosarcomas. Although it has been shown that wild-type p53 can block the ability of E1a and ras to cotransform primary rodent cells, it is poorly understood why inactivation of the p53 gene is important for tumor formation. We show that overexpression of the gene en
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9. High metastatic potential in mice inheriting a targeted p53 missense mutation
To understand the relevance of p53 missense mutations in vivo, we generated a mouse containing an arg-to-his substitution at p53 amino acid 172, which corresponds to the R175H hot-spot mutation in human tumors by homologous recombination. Inadvertently, this mouse contains the additional deletion of a G nucleotide at a splice junction that attenuates levels
The National Academy of Sciences.
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10. Telomere dysfunction triggers extensive DNA fragmentation and evolution of complex chromosome abnormalities in human malignant tumors
Although mechanisms for chromosomal instability in tumors have been described in animal and in vitro models, little is known about these processes in man. To explore cytogenetic evolution in human tumors, chromosomal breakpoint profiles were constructed for 102 pancreatic carcinomas and 140 osteosarcomas, two tumor types characterized by extensive genomic in
The National Academy of Sciences.
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11. Viable deletion mutant of human papovavirus BK that induces insulinomas in hamsters.
A plaque morphology mutant (pm-522) of human papovavirus BK, which was rescued from a human papovavirus BK-induced hamster pineocytoma, was characterized and compared with a cloned wild-type virus (wt-501). Mutant pm-522 formed turbid plaques and grew more slowly than wt-501 in human embryonic kidney (HEK) cells. The immunofluorescence assay revealed that mo
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12. Conditional biallelic Nf2 mutation in the mouse promotes manifestations of human neurofibromatosis type 2
Hemizygosity for the NF2 gene in humans causes a syndromic susceptibility to schwannoma development. However, Nf2 hemizygous mice do not develop schwannomas but mainly osteosarcomas. In the tumors of both species, the second Nf2 allele is inactivated. We report that conditional homozygous Nf2 knockout mice with Cre-mediated excision of Nf2 exon 2 in Schwann
Cold Spring Harbor Laboratory Press.