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1. Author Correction: Compartments in medulloblastoma with extensive nodularity are connected through differentiation along the granular precursor lineage

2. Developmental basis of SHH medulloblastoma heterogeneity

3. Compartments in medulloblastoma with extensive nodularity are connected through differentiation along the granular precursor lineage

4. Comparison of spatial transcriptomics technologies using tumor cryosections

5. Clinically aggressive pediatric spinal ependymoma with novel MYC amplification demonstrates molecular and histopathologic similarity to newly described MYCN-amplified spinal ependymomas

6. Transcriptional profiling of medulloblastoma with extensive nodularity (MBEN) reveals two clinically relevant tumor subsets with VSNL1 as potent prognostic marker

7. MYCN amplification drives an aggressive form of spinal ependymoma

8. Data from Cross-Species Genomics Reveals Oncogenic Dependencies in ZFTA/C11orf95 Fusion–Positive Supratentorial Ependymomas

9. Supplementary Table S4 from Cross-Species Genomics Reveals Oncogenic Dependencies in ZFTA/C11orf95 Fusion–Positive Supratentorial Ependymomas

10. Supplementary Data from Cross-Species Genomics Reveals Oncogenic Dependencies in ZFTA/C11orf95 Fusion–Positive Supratentorial Ependymomas

11. Optimizing biomarkers for accurate ependymoma diagnosis, prognostication, and stratification within International Clinical Trials: A BIOMECA study

12. Optimising biomarkers for accurate ependymoma diagnosis, prognostication and stratification within International Clinical Trials: A BIOMECA study

13. Compartments in medulloblastoma with extensive nodularity are connected through differentiation along the granular precursor lineage

15. EPEN-24. Biological markers of ependymoma in children and adolescents (BIOMECA): Systematic comparison of methods for the precise evaluation of biomarkers for ependymoma diagnosis and prognostication

17. Cross-Species Genomics Reveals Oncogenic Dependencies in ZFTA/C11orf95 Fusion-Positive Supratentorial Ependymomas

18. Recurrent fusions in PLAGL1 define a distinct subset of pediatric-type supratentorial neuroepithelial tumors

19. Single cell multi-omics analysis of chromothriptic medulloblastoma highlights genomic and transcriptomic consequences of genome instability

20. EPEN-03. ZFTA/C11ORF95 FUSIONS DRIVE SUPRATENTORIAL EPENDYMOMA VIA SHARED ONCOGENIC MECHANISMS

21. Additional file 1 of Clinically aggressive pediatric spinal ependymoma with novel MYC amplification demonstrates molecular and histopathologic similarity to newly described MYCN-amplified spinal ependymomas

22. Recurrent fusions in PLAGL1 define a distinct subset of pediatric-type supratentorial neuroepithelial tumors

23. Cross-Species Genomics Reveals Oncogenic Dependencies in ZFTA/C11orf95 Fusion–Positive Supratentorial Ependymomas

24. EPEN-18. CROSS-SPECIES GENOMICS IDENTIFIES GLI2 AS AN ONCOGENE OF C11orf95 FUSION-POSITIVE SUPRATENTORIAL EPENDYMOMA

25. MYCN amplification drives an aggressive form of spinal ependymoma

26. Transcriptional profiling of medulloblastoma with extensive nodularity (MBEN) reveals two clinically relevant tumor subsets with VSNL1 as potent prognostic marker

27. CROSS-SPECIES GENOMICS IDENTIFIES GLI2 AS AN ONCOGENE OF C11ORF95 FUSION-POSITIVE SUPRATENTORIAL EPENDYMOMA

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