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1. Clinical Efficacy of ONC201 in H3K27M-Mutant Diffuse Midline Gliomas Is Driven by Disruption of Integrated Metabolic and Epigenetic Pathways.

2. Therapeutic targeting of prenatal pontine ID1 signaling in diffuse midline glioma.

3. Clinical, genomic, and epigenomic analyses of H3K27M-mutant diffuse midline glioma long-term survivors reveal a distinct group of tumors with MAPK pathway alterations

5. An ERK5-PFKFB3 axis regulates glycolysis and represents a therapeutic vulnerability in pediatric diffuse midline glioma

6. Targeting integrated epigenetic and metabolic pathways in lethal childhood PFA ependymomas

7. Combined cytotoxic and immune-stimulatory gene therapy for primary adult high-grade glioma: a phase 1, first-in-human trial

8. Recurrent ACVR1 mutations in posterior fossa ependymoma

9. Purine salvage promotes treatment resistance in H3K27M-mutant diffuse midline glioma

10. Immunohistochemical analysis of H3K27me3 demonstrates global reduction in group-A childhood posterior fossa ependymoma and is a powerful predictor of outcome

11. The oncolytic adenovirus Delta-24-RGD in combination with ONC201 induces a potent antitumor response in pediatric high-grade and diffuse midline glioma models

12. Abstract B045: Adaptive purine metabolism drives radiation therapy resistance in H3K27M-diffuse midline glioma

13. Abstract PR-007: H3.3K27M diffuse midline gliomas are sensitive to SWI/SNF chromatin remodeler degradation

14. Lowered H3K27me3 and DNA hypomethylation define poorly prognostic pediatric posterior fossa ependymomas

15. Everolimus improves the efficacy of dasatinib in PDGFR[alpha]-driven glioma

16. Single-molecule systems for detection and monitoring of plasma circulating nucleosomes and oncoproteins in Diffuse Midline Glioma

17. Table S4 from Clinical Efficacy of ONC201 in H3K27M-Mutant Diffuse Midline Gliomas Is Driven by Disruption of Integrated Metabolic and Epigenetic Pathways

18. Supplementary Figures 1-15 from Clinical Efficacy of ONC201 in H3K27M-Mutant Diffuse Midline Gliomas Is Driven by Disruption of Integrated Metabolic and Epigenetic Pathways

19. Supplementary Data S2 from Clinical Efficacy of ONC201 in H3K27M-Mutant Diffuse Midline Gliomas Is Driven by Disruption of Integrated Metabolic and Epigenetic Pathways

20. TMET-02. CLINICAL EFFICACY OF ONC201 IN H3K27M-MUTANT DIFFUSE MIDLINE GLIOMAS IS DRIVEN BY DISRUPTION OF INTEGRATED METABOLIC AND EPIGENETIC PATHWAYS

21. Metabolomic Profiles of Human Glioma Inform Patient Survival

23. TMET-13. DNA DAMAGE SIGNALING ACTIVATES GTP SYNTHESIS TO PROMOTE GLIOBLASTOMA TREATMENT RESISTANCE

24. Data from Clinical Efficacy of ONC201 in H3K27M-Mutant Diffuse Midline Gliomas Is Driven by Disruption of Integrated Metabolic and Epigenetic Pathways

25. Rewiring of cortical glucose metabolism fuels human brain cancer growth

28. Adaptive rewiring of purine metabolism promotes treatment resistance in H3K27M-mutant diffuse midline glioma

29. Clinical Efficacy of ONC201 in H3K27M-Mutant Diffuse Midline Gliomas Is Driven by Disruption of Integrated Metabolic and Epigenetic Pathways

30. Supplementary Data from β-Catenin–Driven Differentiation Is a Tissue-Specific Epigenetic Vulnerability in Adrenal Cancer

31. Data from β-Catenin–Driven Differentiation Is a Tissue-Specific Epigenetic Vulnerability in Adrenal Cancer

34. Supplementary Information from β-Catenin–Driven Differentiation Is a Tissue-Specific Epigenetic Vulnerability in Adrenal Cancer

35. β-Catenin–Driven Differentiation Is a Tissue-Specific Epigenetic Vulnerability in Adrenal Cancer

36. Targeting SWI/SNF ATPases in H3.3K27M diffuse intrinsic pontine gliomas

37. Abstract 6047: ZFTA-RELA fusion aberrantly drives glutamine metabolism in lethal pediatric ependymomas

39. Abstract 1501: Epigenetic dedifferentiation as a therapeutic strategy in adrenal cancer

40. Abstract 3523: A systematic comparison of molecular features shared by H3K27-altered diffuse midline gliomas and posterior fossa A ependymomas

41. Abstract 3677: DNA damage signaling activates de novo GTP synthesis to promote chemoradiation resistance in glioblastoma

42. Data from Serine Catabolism Regulates Mitochondrial Redox Control during Hypoxia

43. Supplementary Table 1 from Serine Catabolism Regulates Mitochondrial Redox Control during Hypoxia

44. Data from Expression of the Androgen Receptor Governs Radiation Resistance in a Subset of Glioblastomas Vulnerable to Antiandrogen Therapy

45. Supplementary Figure 5 from Serine Catabolism Regulates Mitochondrial Redox Control during Hypoxia

46. Supplementary Figure 2 from Serine Catabolism Regulates Mitochondrial Redox Control during Hypoxia

47. Supplementary Figure 4 from Serine Catabolism Regulates Mitochondrial Redox Control during Hypoxia

48. Supplementary Figure 1B from Serine Catabolism Regulates Mitochondrial Redox Control during Hypoxia

49. Supplementary Data and Methods from Expression of the Androgen Receptor Governs Radiation Resistance in a Subset of Glioblastomas Vulnerable to Antiandrogen Therapy

50. Supplementary Figure 3 from Serine Catabolism Regulates Mitochondrial Redox Control during Hypoxia

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