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1. Initial surgical resection and long time to occurrence from initial diagnosis are independent prognostic factors in resected recurrent IDH wild-type glioblastoma

2. Mechanisms and therapeutic implications of hypermutation in gliomas

4. A threshold for mitotic activity and post‐surgical residual volume defines distinct prognostic groups for astrocytoma IDH‐mutant

5. Hypersomnia in anti‐glutamic acid decarboxylase 65 (GAD65) associated neurological syndromes: A pilot study.

7. Spatial and Ecological Factors Modulate the Incidence of Anti-NMDAR Encephalitis—A Systematic Review

8. Supplementary Figure 5 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

9. Supplementary Figure 2 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

10. Supplementary Figure 1 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

11. Supplementary Figure 6 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

12. Supplementary Figure Legends from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

13. Supplementary Figure 3 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

14. Supplementary Figure 4 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

15. Supplementary Table 1 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

16. Revisiting anti-Hu paraneoplastic autoimmunity: phenotypic characterization and cancer diagnosis.

17. In Vivo 2-Hydroxyglutarate Monitoring With Edited MR Spectroscopy for the Follow-up of IDH-Mutant Diffuse Gliomas

19. Tumor cells with neuronal intermediate progenitor features define a subgroup of 1p/19q co‐deleted anaplastic gliomas

23. IDH-wildtype lower-grade diffuse gliomas: the importance of histological grade and molecular assessment for prognostic stratification

26. PATH-16. MOLECULAR PATHOLOGY AND CLINICAL CHARACTERISTICS OF MMR DEFICIENCY (MMRd) IN DIFFUSE GLIOMAS

27. A recurrent point mutation in PRKCA is a hallmark of chordoid gliomas

28. De novo and secondary anaplastic meningiomas: a study of clinical and histomolecular prognostic factors

29. Tumor cells with neuronal intermediate progenitor features define a subgroup of 1p/19q co-deleted anaplastic gliomas

30. Diffuse gliomas with FGFR3‐TACC3 fusion have characteristic histopathological and molecular features

31. GENE-54. A NOVEL MUTATION IN PRKCA IS THE MAJOR DRIVER OF CHORDOID GLIOMAS

32. EGFRAmplification andIDHMutations in Glioblastoma Patients of the Northeast of Morocco

33. Chromosome 17p Homodisomy Is Associated With Better Outcome in 1p19q Non-Codeleted and IDH-Mutated Gliomas

34. Diffuse gliomas with FGFR3‐TACC3 fusion have characteristic histopathological and molecular features.

36. TERT promoter mutations and rs2853669 polymorphism: prognostic impact and interactions with common alterations in glioblastomas

37. Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

38. Chordoid Gliomas of the Third Ventricle Share TTF-1 Expression With Organum Vasculosum of the Lamina Terminalis

39. EGFR Amplification and IDH Mutations in Glioblastoma Patients of the Northeast of Morocco.

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