110 results on '"Tracy T. Batchelor"'
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2. Supplementary Table S3 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets
3. Supplementary Methods, Figures S1 - S20 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets
4. Supplementary Figure 5 from Brain Tumor Cells in Circulation Are Enriched for Mesenchymal Gene Expression
5. Supplementary File 1 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets
6. Supplementary Methods, Figure Legends from Brain Tumor Cells in Circulation Are Enriched for Mesenchymal Gene Expression
7. Supplementary Figure 2 from Brain Tumor Cells in Circulation Are Enriched for Mesenchymal Gene Expression
8. Supplementary Table 1 from Brain Tumor Cells in Circulation Are Enriched for Mesenchymal Gene Expression
9. Supplementary Table S2 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets
10. Supplementary Figure 4 from Brain Tumor Cells in Circulation Are Enriched for Mesenchymal Gene Expression
11. Supplementary Figure 1 from Brain Tumor Cells in Circulation Are Enriched for Mesenchymal Gene Expression
12. Supplementary Table 2 from Brain Tumor Cells in Circulation Are Enriched for Mesenchymal Gene Expression
13. Supplementary File 3 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets
14. Supplementary Table S1 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets
15. Supplementary File 2 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets
16. Supplementary Figure 6 from Targetable Signaling Pathway Mutations Are Associated with Malignant Phenotype in IDH-Mutant Gliomas
17. Figure S3 from Dopamine Receptor D5 is a Modulator of Tumor Response to Dopamine Receptor D2 Antagonism
18. Data from Vaccination with Irradiated Autologous Tumor Cells Mixed with Irradiated GM-K562 Cells Stimulates Antitumor Immunity and T Lymphocyte Activation in Patients with Recurrent Malignant Glioma
19. Supplementary Table S2 from Myc-Driven Glycolysis Is a Therapeutic Target in Glioblastoma
20. Supplementary Figure Legends from The Alkylating Chemotherapeutic Temozolomide Induces Metabolic Stress in IDH1-Mutant Cancers and Potentiates NAD+ Depletion–Mediated Cytotoxicity
21. Supplementary Figure 5 from Targetable Signaling Pathway Mutations Are Associated with Malignant Phenotype in IDH-Mutant Gliomas
22. Lymphocyte Immunophenotyping methods from Vaccination with Irradiated Autologous Tumor Cells Mixed with Irradiated GM-K562 Cells Stimulates Antitumor Immunity and T Lymphocyte Activation in Patients with Recurrent Malignant Glioma
23. Figure S1 from Dopamine Receptor D5 is a Modulator of Tumor Response to Dopamine Receptor D2 Antagonism
24. Figure S4 from Dopamine Receptor D5 is a Modulator of Tumor Response to Dopamine Receptor D2 Antagonism
25. ELISA for angiogenic cytokines from Vaccination with Irradiated Autologous Tumor Cells Mixed with Irradiated GM-K562 Cells Stimulates Antitumor Immunity and T Lymphocyte Activation in Patients with Recurrent Malignant Glioma
26. Supplementary Figures 1-6 from The Alkylating Chemotherapeutic Temozolomide Induces Metabolic Stress in IDH1-Mutant Cancers and Potentiates NAD+ Depletion–Mediated Cytotoxicity
27. Supplementary Figures from Myc-Driven Glycolysis Is a Therapeutic Target in Glioblastoma
28. Supplementary Figure 2 from Targetable Signaling Pathway Mutations Are Associated with Malignant Phenotype in IDH-Mutant Gliomas
29. Data from Loss of the Mismatch Repair Protein MSH6 in Human Glioblastomas Is Associated with Tumor Progression during Temozolomide Treatment
30. Supplementary Figure 3 from Targetable Signaling Pathway Mutations Are Associated with Malignant Phenotype in IDH-Mutant Gliomas
31. Supplementary Table 2 from Targetable Signaling Pathway Mutations Are Associated with Malignant Phenotype in IDH-Mutant Gliomas
32. Supplementary Table S1 from Myc-Driven Glycolysis Is a Therapeutic Target in Glioblastoma
33. Data from Treatment Response Assessment in IDH-Mutant Glioma Patients by Noninvasive 3D Functional Spectroscopic Mapping of 2-Hydroxyglutarate
34. Supplementary Figure 1 from Targetable Signaling Pathway Mutations Are Associated with Malignant Phenotype in IDH-Mutant Gliomas
35. Supplementary Data from A Hyperactive RelA/p65-Hexokinase 2 Signaling Axis Drives Primary Central Nervous System Lymphoma
36. Figure S2 from Dopamine Receptor D5 is a Modulator of Tumor Response to Dopamine Receptor D2 Antagonism
37. Data from Dopamine Receptor D5 is a Modulator of Tumor Response to Dopamine Receptor D2 Antagonism
38. Supplementary Table from PI3K/AKT/mTOR Pathway Alterations Promote Malignant Progression and Xenograft Formation in Oligodendroglial Tumors
39. Table S1 from Dopamine Receptor D5 is a Modulator of Tumor Response to Dopamine Receptor D2 Antagonism
40. Supplementary Figure from A Hyperactive RelA/p65-Hexokinase 2 Signaling Axis Drives Primary Central Nervous System Lymphoma
41. Supplemental Figure from A Multicenter, Phase II, Randomized, Noncomparative Clinical Trial of Radiation and Temozolomide with or without Vandetanib in Newly Diagnosed Glioblastoma Patients
42. Supplementary Data clean from Treatment Response Assessment in IDH-Mutant Glioma Patients by Noninvasive 3D Functional Spectroscopic Mapping of 2-Hydroxyglutarate
43. Supplemental Tables 1-3 from A Multicenter, Phase II, Randomized, Noncomparative Clinical Trial of Radiation and Temozolomide with or without Vandetanib in Newly Diagnosed Glioblastoma Patients
44. Supplementary Figure 4 from Targetable Signaling Pathway Mutations Are Associated with Malignant Phenotype in IDH-Mutant Gliomas
45. Data from Targetable Signaling Pathway Mutations Are Associated with Malignant Phenotype in IDH-Mutant Gliomas
46. Data from Myc-Driven Glycolysis Is a Therapeutic Target in Glioblastoma
47. Figure S5 from Dopamine Receptor D5 is a Modulator of Tumor Response to Dopamine Receptor D2 Antagonism
48. Supplementary Figure from PI3K/AKT/mTOR Pathway Alterations Promote Malignant Progression and Xenograft Formation in Oligodendroglial Tumors
49. Data from A Hyperactive RelA/p65-Hexokinase 2 Signaling Axis Drives Primary Central Nervous System Lymphoma
50. Supplementary Figure 7 from Targetable Signaling Pathway Mutations Are Associated with Malignant Phenotype in IDH-Mutant Gliomas
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