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1. GABAergic neuronal lineage development determines clinically actionable targets in diffuse hemispheric glioma, H3G34-mutant

2. Gliomatosis cerebri in children: A poor prognostic phenotype of diffuse gliomas with a distinct molecular profile

3. Gliomatosis cerebri in children:A poor prognostic phenotype of diffuse gliomas with a distinct molecul profile

4. Integrated Molecular Meta-Analysis of 1,000 Pediatric High-Grade and Diffuse Intrinsic Pontine Glioma

5. HGG-17. SINGLE-CELL AND SPATIAL ANALYSES DECIPHER THE UNIQUE INVASIVE GROWTH PATTERN OF GLIOMATOSIS CEREBRI

6. Data from DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition

7. Supplementary Data from DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition

8. Data from Infant High-Grade Gliomas Comprise Multiple Subgroups Characterized by Novel Targetable Gene Fusions and Favorable Outcomes

9. Supplementary Data from Infant High-Grade Gliomas Comprise Multiple Subgroups Characterized by Novel Targetable Gene Fusions and Favorable Outcomes

10. Supplementary Table S3 from Infant High-Grade Gliomas Comprise Multiple Subgroups Characterized by Novel Targetable Gene Fusions and Favorable Outcomes

11. Supplementary Figures S1-S3 from Repurposing Vandetanib plus Everolimus for the Treatment of ACVR1-Mutant Diffuse Intrinsic Pontine Glioma

12. Data from Repurposing Vandetanib plus Everolimus for the Treatment of ACVR1-Mutant Diffuse Intrinsic Pontine Glioma

13. EPCO-24. MULTI-OMIC PROFILING OF PATIENT-DERIVED SUBCLONES IDENTIFIES AGGRESSIVE CELLULAR SUBPOPULATIONS IN PAEDIATRIC DIFFUSE HIGH GRADE GLIOMAS (PDHGGS)

14. DIPG-41. Multi-omic profiling of patient-derived subclones identifies aggressive cellular subpopulations in paediatric diffuse high-grade gliomas (PDHGGs)

15. HGG-49. Gliomatosis cerebri in children: A collaborative report from the European Society for Pediatric Oncology (SIOPE)

16. HGG-42. Evolutionary selection of key oncogenic alterations in patient-derived models of paediatric diffuse high grade glioma (PDHGG) subtypesin vitro andin vivo

17. DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition

18. sj-docx-1-tam-10.1177_17588359221113693 – Supplemental material for Targeted therapy for pediatric diffuse intrinsic pontine glioma: a single-center experience

19. sj-docx-2-tam-10.1177_17588359221113693 – Supplemental material for Targeted therapy for pediatric diffuse intrinsic pontine glioma: a single-center experience

20. Targeted therapy for pediatric diffuse intrinsic pontine glioma: a single-center experience

21. Repurposing Vandetanib plus Everolimus for the Treatment of ACVR1-Mutant Diffuse Intrinsic Pontine Glioma

22. EARLY GABAERGIC NEURONAL LINEAGE DEFINES DEPENDENCIES IN HISTONE H3 G34R/V GLIOMA

23. Loss of the H4 lysine methyltransferase KMT5B drives tumorigenic phenotypes by depleting H3K27me3 at loci otherwise retained in H3K27M mutant DIPG cells

24. HGG-06. EARLY GABAERGIC NEURONAL LINEAGE DEFINES DEPENDENCIES IN HISTONE H3 G34R/V GLIOMA

25. Droplet digital PCR-based detection of circulating tumor DNA from pediatric high grade and diffuse midline glioma patients

26. Drug screening linked to molecular profiling identifies novel dependencies in patient-derived primary cultures of paediatric high grade glioma and DIPG

27. HGG-37. PAEDIATRIC GLIOBLASTOMA CELLS SHOW CRITICAL DEPENDENCIES ON EPIGENOMIC AND EPITRANSCRIPTOMIC CONTROL OF GENE EXPRESSION BY H3.3G34R/V MUTATIONS

28. MODL-19. DIPG HARBOUR ALTERATIONS TARGETABLE BY MEK INHIBITORS, WITH ACQUIRED RESISTANCE MECHANISMS OVERCOME BY COMBINATORIAL UP- OR DOWN-STREAM INHIBITION

29. MODL-20. A BIOBANK OF ~100 PATIENT-DERIVED MODELS REPRESENTING BIOLOGICAL HETEROGENEITY AND DISTINCT THERAPEUTIC DEPENDENCIES IN PAEDIATRIC HIGH GRADE GLIOMA AND DIPG

31. IMG-12. CHARACTERISATION OF MODELS OF H3F3A_G34R/V MUTANT PAEDIATRIC GLIOBLASTOMA IN VIVO USING MAGNETIC RESONANCE IMAGING

32. DDRE-07. DIPG HARBOUR ALTERATIONS TARGETABLE BY MEK INHIBITORS, WITH ACQUIRED RESISTANCE MECHANISMS OVERCOME BY COMBINATORIAL INHIBITION

33. Infant High-Grade Gliomas Comprise Multiple Subgroups Characterized by Novel Targetable Gene Fusions and Favorable Outcomes

34. DIPG-25. GENETIC ALTERATIONS TARGETING THE MAPK PATHWAY CONFERS PRECLINICAL SENSITIVITY TO TRAMETINIB IN A CO-CLINICAL TRIAL IN DIPG

36. PDTM-31. DRUG SCREENING LINKED TO MOLECULAR PROFILING IDENTIFIES NOVEL DEPENDENCIES IN PATIENT-DERIVED PRIMARY CULTURES OF PAEDIATRIC HIGH GRADE GLIOMA AND DIPG

37. HGG-23. DRUG SCREENING LINKED TO MOLECULAR PROFILING IDENTIFIES NOVEL DEPENDENCIES IN PATIENT-DERIVED PRIMARY CULTURES OF PAEDIATRIC HIGH GRADE GLIOMA AND DIPG

38. HGG-25. INFANT GLIOMAS COMPRISE MULTIPLE BIOLOGICAL AND CLINICOPATHOLOGICAL SUBGROUPS

39. Simultaneous DNA amplification and detection using a pH-sensing semiconductor system

40. Repurposing Vandetanib plus Everolimus for the Treatment of ACVR1 -Mutant Diffuse Intrinsic Pontine Glioma.

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