Mostrando 2,941 - 2,960 Resultados de 4,168 Para Buscar '"IDH"', tiempo de consulta: 0.56s Limitar resultados
  1. 2941
  2. 2942
    “…Better seizure outcome was observed in IDH1/2 mutated and 1p/19q codeleted subgroup. At multivariate analysis, age (p = 0.014), EOR (p = 0.030), ΔT2T1 MRI index (p = 0.016) resulted as independent predictors of postoperative seizure control. …”
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  3. 2943
    “…The median OS and DFS were similar in patients with or without TET2, DNMT3A, IDH2, TP53 and FLT3 mutations. Multivariate analysis showed that patient age above 75 years, high-risk status, and genetic anomalies, like deletions in chromosomes 5 and/or 7, were significant variables in predicting OS. …”
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  4. 2944
  5. 2945
    por Ichimura, Koichi
    Publicado 2019
    “…Since WHO2016 incorporated the status of IDH mutation and 1p/19q codeletion as a part of the definition for oligodendrogliomas, astrocytomas and glioblastomas, molecular tests have become an essential part of the clinical management of adult gliomas. …”
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  6. 2946
    “…Elevated levels of the metabolites, 2-hydroxyglutarate (2HG), succinate, and fumarate, occur in human malignancies due to somatic mutations in the isocitrate dehydrogenase-1/2 (IDH1/2) genes or germline mutations in the fumarate hydratase (FH) and succinate dehydrogenase (SDH) genes, respectively(2–4). …”
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  7. 2947
    “…Tumor-associated epilepsy and the IDH-1 mutation did not affect hippocampal volume in glioma patients. …”
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  8. 2948
    “…Astrocytoma progression groups were further distinguished by signaling pathway expression signatures affecting cell division, interaction and differentiation. As expected, IDH1 was most frequently mutated closely followed by TP53, but also MUC4 involved in the regulation of apoptosis and proliferation was frequently mutated. …”
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  9. 2949
  10. 2950
    “…No association was detected between methylation of MGMT promoter and molecular markers such as ATRX, IDH, p53 and Ki67. These results indicate that MGMT methylation did not influence in patient survival in our cohort.…”
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  11. 2951
  12. 2952
    “…Furthermore, TP-0903 demonstrated preclinical activity in AML models with FLT3-ITD and common co-occurring mutations in IDH2 and NRAS genes. We also showed that TP-0903 had ex vivo activity in primary AML cells with recurrent mutations including MLL-PTD, ASXL1, SRSF2, and WT1, which are associated with poor prognosis or promote clinical resistance to AML-directed therapies. …”
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  13. 2953
    “…Additionally, upregulated HMGA1 and vimentin were found in isocitrate dehydrogenase (IDH) wild-type and 1p/19q non-codeletion diffusely infiltrating glioma. …”
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  14. 2954
    “…Thirty-five (69%) patients had IDH-mutated tumors, of which 17 were 1p/19q codeleted (i.e., oligodendroglioma) and 18 non-1p/19q codeleted (i.e., IDHmut astrocytoma). …”
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  15. 2955
  16. 2956
  17. 2957
    “…Histology suggested many foam cell accumulations and the tumor was positive for CD34, CD99, Vimentin, β-Catenin and CD68, but negative for EMA, GFAP, IDH-1, Oliga-2, PR, S-100, and CD1a. Three months after surgery, MRI showed the midline structure was back to normal. …”
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  18. 2958
    “…The introduction of radiomics as a high throughput quantitative imaging technique that allows for improved diagnostic, prognostic and predictive indices has created more interest for such techniques in cancer research and especially in neurooncology (MRI-based classification of LGGs, predicting Isocitrate dehydrogenase (IDH) and Telomerase reverse transcriptase (TERT) promoter mutations and predicting LGG associated seizures). …”
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  19. 2959
    “…A Barrett’s cell line model treated with either lithocholic acid (LCA) or X-ray had 21 (e.g., ASNS, RALY, FAM120A, UBE2M, IDH1, ESD) and 32 (e.g., GLUL, CALU, SH3BGRL3, S100A9, FKBP3, AGR2) overexpressed proteins, respectively, compared to the untreated set. …”
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  20. 2960
    “…A unique distribution of somatic mutations was found for the young and adult population, particularly for genes related to DNA repair and chromatin remodelling, highlighting ATRX, MGMT and IDH1. Our results also revealed that highly lesioned genes undergo differential regulation with particular biological pathways for young patients. …”
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