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  1. 1961
    “…METHODS: Using immunohistochemistry, the expression profile of metabolic proteins (hBCAT, IDH) was assessed between breast cancer subtypes, HER2 + , luminal A, luminal B and TNBC. …”
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  2. 1962
  3. 1963
  4. 1964
    “…Furthermore, the 5hmC biomarkers in cfDNA showed the potential as an independent indicator from IDH1 mutation status and worked in synergy with IDH1 mutation to distinguish GBM from WHO II-III gliomas. …”
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  5. 1965
  6. 1966
  7. 1967
    “…Meanwhile related to the pathological classification of gliomas. Oligodendroglioma, IDH-mutant and 1p/19q-codeleted was higher than Astrocytoma, IDH-mutant, higher than Glioblastoma, IDH-wildtype. …”
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  8. 1968
    “…Surgical tumor samples were analyzed by routine histopathology and immunohistochemistry for H3 K27M, IDH1 R132H, ATRX, p53, OLIG2, glial fibrillary acidic protein, and Ki-67; Sanger sequencing for hot mutation spots in genes including H3F3A, HIST1H3B, IDH1, IDH2, TERT, and BRAF; and methylation-specific polymerase chain reaction for O ( 6 ) -methylguanine DNA methyltransferase promoter methylation. …”
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  9. 1969
    “…It was observed that CBV, ktrans, Ve and Vp values were, in general, significantly higher in IDH wildtype compared to IDH mutated glioma. Meta-analysis comprising of five papers (totaling 316 patients) showed that the AUC of CBV, ktrans, Ve and Vp were 0.85 (95%-CI 0.75–0.93), 0.81 (95%-CI 0.74–0.89), 0.84 (95%-CI 0.71–0.97) and 0.76 (95%-CI 0.61–0.90), respectively. …”
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  10. 1970
    “…SIMPLE SUMMARY: The malignant growth and therapy resistance of isocitrate dehydrogenase (IDH)-wildtype glioblastoma is thought to be driven by a subpopulation of tumor cells with cancer stem-like cell (CSC) properties. …”
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  11. 1971
    por Li, Fengli, Li, Na, Wang, Anyou, Liu, Xin
    Publicado 2022
    “…DNMT3A, BCOR, U2AF1, and BCORL1 mutations were unevenly distributed among different FAB classifications (p < 0.05). DNMT3A, IDH2, NPM1, FLT3-ITD, ASXL1, IDH1, SRSF2, BCOR, NRAS, RUNX1, U2AF1, MPO, and WT1 mutations were distributed differently when an immunophenotype was expressed or not expressed (p<0.05). …”
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  12. 1972
    “…The first tumor recurrence had oligodendroglial morphology, IDH1 R132H and TERT promoter mutations, and 1p/19q codeletion detected by fluorescent in situ hybridization (FISH). …”
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  13. 1973
    “…Pathological diagnoses of all cases were glioblastomas, IDH-wildtype. All patients underwent chemoradiotherapy after surgery. …”
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  14. 1974
  15. 1975
    “…RESULTS: The combined model showed the better performance in some groups of genotype status among some models (IDH AUC = 0.93, MGMT AUC = 0.88, TERT AUC = 0.76). …”
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  16. 1976
    “…Genetically, CHS are heterogenous, but there is no characteristic mutation defining CHS, and yet, IDH1 and IDH2 mutations are frequent. Hypovascularization, extracellular matrix composition of collagen, proteoglycans, and hyaluronan create a mechanical barrier for tumor suppressive immune cells. …”
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  17. 1977
    “…Gene detection analysis revealed no mutations in isocitrate dehydrogenase (IDH)1 and IDH2, and neurotrophic tyrosine kinase receptor-1 (NTRK1), NTRK2 and NTRK3 genes. …”
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  18. 1978
    “…Using two important diagnostic questions, the non-invasive determination of IDH mutation status and ATRX status, we analyze whether it is possible to use AutoML to develop models that are comparable in performance to conventional machine learning models (ML) developed by experts. …”
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  19. 1979
    “…Many adult immature T-ALLs harbored mutations in myeloid-specific oncogenes and tumor suppressors including IDH1, IDH2, DNMT3A, FLT3, and NRAS. Moreover, we identified ETV6 mutations as a novel genetic lesion uniquely present in immature adult T-ALL. …”
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  20. 1980
    “…CEBPA, ETV6, RUNX1), epigenetic regulators (e.g. ASXL1, DNMT3A, EZH2, IDH1, IDH2, SUZ12, TET2, UTX), tumor suppressors (e.g. …”
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