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1. Characterization of DLBCL with a PMBL gene expression signature

2. TMEM30A loss-of-function mutations drive lymphomagenesis and confer therapeutically exploitable vulnerability in B-cell lymphoma

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4. Supplementary Table S11 and 15 from Molecular and Genetic Characterization of MHC Deficiency Identifies EZH2 as Therapeutic Target for Enhancing Immune Recognition

5. Supplementary Table S1-3 from Molecular and Genetic Characterization of MHC Deficiency Identifies EZH2 as Therapeutic Target for Enhancing Immune Recognition

6. Supplementary Data from Single-Cell Transcriptome Analysis Reveals Disease-Defining T-cell Subsets in the Tumor Microenvironment of Classic Hodgkin Lymphoma

7. Supplementary Table S8-9 from Molecular and Genetic Characterization of MHC Deficiency Identifies EZH2 as Therapeutic Target for Enhancing Immune Recognition

8. Supplementary Table S12-14 from Molecular and Genetic Characterization of MHC Deficiency Identifies EZH2 as Therapeutic Target for Enhancing Immune Recognition

9. Data from Single-Cell Transcriptome Analysis Reveals Disease-Defining T-cell Subsets in the Tumor Microenvironment of Classic Hodgkin Lymphoma

10. Supplementary Methods and Figures from Molecular and Genetic Characterization of MHC Deficiency Identifies EZH2 as Therapeutic Target for Enhancing Immune Recognition

11. Supplementary Table S10 from Molecular and Genetic Characterization of MHC Deficiency Identifies EZH2 as Therapeutic Target for Enhancing Immune Recognition

12. TRAF3 Loss-of-Function Reveals the Non-Canonical NF-Κb Pathway As a Therapeutic Target in Diffuse Large B-Cell Lymphoma

14. MHC class II transactivator CIITA is a recurrent gene fusion partner in lymphoid cancers

15. The Tumor Associated Antigen PRAME Exhibits Dualistic Functions That Are Targetable in Diffuse Large B-Cell Lymphoma

18. Single-Cell Transcriptome Analysis Reveals Disease-Defining T-cell Subsets in the Tumor Microenvironment of Classic Hodgkin Lymphoma

19. Abstract 3480:TMEM30Aloss-of-function mutations drive lymphomagenesis and confer therapeutically exploitable vulnerability in B-cell lymphoma

20. Molecular and Genetic Characterization of MHC Deficiency Identifies EZH2 as Therapeutic Target for Enhancing Immune Recognition

21. Molecular and Genetic Characterization of MHC Deficiency Identifies EZH2 As a Therapeutic Target for Restoring MHC Expression in Diffuse Large B-Cell Lymphoma

22. UBR5 Mutations in Mantle Cell Lymphoma Lead to Increased Proliferation through a Cyclin D1-Dependent Mechanism

23. TMEM30Aloss-of-function mutations drive lymphomagenesis and confer therapeutically exploitable vulnerability in B-cell lymphoma

25. Genetic Alterations of the MHC Class II Transactivator CIITA Are Frequent in Primary Mediastinal Large B-Cell Lymphoma and Associated with Diminished MHC Class II Expression

26. Protein Tyrosine Phosphatase Type-1 (PTPN1) Is Frequently Mutated In Primary Mediastinal B Cell Lymphoma and Hodgkin Lymphoma

27. Genomic Rearrangements Involving Programmed Death Ligands Are Recurrent In Primary Mediastinal Large B-Cell Lymphoma

28. Molecular and Functional Characterization Of The Novel Protein-Coding Gene Tihl (Translocated in Hodgkin’s Lymphoma) in Hematopoiesis

29. Gene Expression–Based Model Using Formalin-Fixed Paraffin-Embedded Biopsies Predicts Overall Survival in Advanced-Stage Classical Hodgkin Lymphoma

31. Somatic mutations altering EZH2 (Tyr641) in follicular and diffuse large B-cell lymphomas of germinal-center origin

32. TRAF3Loss Drives Alternative NF-κB Pathway Activation in Diffuse Large B-Cell Lymphoma

33. Genetic Alterations of the MHC Class II Transactivator CIITAAre Frequent in Primary Mediastinal Large B-Cell Lymphoma and Associated with Diminished MHC Class II Expression

34. Molecular and Functional Characterization Of The Novel Protein-Coding Gene Tihl (Translocated in Hodgkin's Lymphoma)in Hematopoiesis