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1. Higher-order connections between stereotyped subsets: implications for improved patient classification in CLL

2. Safety and Efficacy of a-319 (a CD3xCD19 T cell engager) in Patients with Relapsed or Refractory B-Cell Non-Hodgkin Lymphoma

3. Integrin Signaling Pathway Is Crucial for the Recently Divided Fraction of CLL Cells and Facilitates Cell Migration in a Disease Progressive Manner

4. CLECL1+ CLL Cells: A Key Subset That Drives CLL Survival and Proliferation and Shapes a Th2-Biased Tumor Microenvironment

6. IGHV-unmutated and IGHV-mutated chronic lymphocytic leukemia cells produce activation-induced deaminase protein with a full range of biologic functions

7. Stereotyped B-cell receptors in one-third of chronic lymphocytic leukemia: a molecular classification with implications for targeted therapies

9. A novel adoptive transfer model of chronic lymphocytic leukemia suggests a key role for T lymphocytes in the disease

10. Efficacy of Ibrutinib Monotherapy in Pre-Clinical Mouse Models of Richter Transformation: Ibrutinib Effectively Reduces the Incidence of Richter Transformation but Fails in Treating Transformed Lymphoma, Especially in Primary Lymphoid Tissue

14. AID overexpression leads to aggressive murine CLL and nonimmunoglobulin mutations that mirror human neoplasms

15. Epidermal growth factor receptor–dependent DNA repair promotes murine and human hematopoietic regeneration

16. Socioeconomic Disparities in Diagnostic Testing Among Patients with Diffuse Large B-Cell Lymphoma in the US

17. Identification and Reporting of Cell of Origin, Double-/Triple-Hit and Double Expressor Lymphoma in a Real-World Cohort of Diffuse Large B-Cell Lymphoma Patients

18. B-cell chronic lymphocytic leukemia cells express a surface membrane phenotype of activated, antigen-experienced B lymphocytes: Presented in part at the 42nd Annual Meeting of the American Society of Hematology, December 1-5, 2000, San Francisco, CA.

20. CLL Intraclonal Fractions Defined By Time Since Cell Birth/Division Promote a Leukemia-Supportive, Immune-Tolerant Microenvironment By Distinct Mechanisms

22. Ibrutinib Treatment Reduces Myeloid Derived Suppressor Cell Numbers and Function in Chronic Lymphocytic Leukemia

24. Serum IgM/Fcmr Interactions Inhibit BCR Signaling and Influence the Cinical Course of CLL

25. Not all IGHV3-21 chronic lymphocytic leukemias are equal: prognostic considerations

27. Reappraising Immunoglobulin Repertoire Restrictions in Chronic Lymphocytic Leukemia: Focus on Major Stereotyped Subsets and Closely Related Satellites

29. Comparative Density Analyses of B Cell Receptor-Complex Components (Membrane IgM, Membrane IgD, and Stimulatory/Inhibitory Co-Receptors) on Intraclonal Subpopulations of CLL B Cells, before and during Ibrutinib Therapy

30. Automated Clustering Analysis of Immunoglobulin Sequences in Chronic Lymphocytic Leukemia Based on 3D Structural Descriptors

31. B Cells of the Proliferative Fraction of CLL Clones Exhibit Activated B-Cell and Myeloid-Cell Signatures Suggesting Enhanced Antigen-Presentation, Integrin Responsiveness, and IL-4 Receptiveness: Additional Targets for CLL Therapy

33. In CLL, Myeloid-Derived Suppressor Cells and Their Monocytic and Granulocytic Varieties Differ in T-Cell Subset Association and Polarization Induction

34. A validated gene expression model of high-risk multiple myeloma is defined by deregulated expression of genes mapping to chromosome 1

35. Reappraising Immunoglobulin Repertoire Restrictions in Chronic Lymphocytic Leukemia: Focus on Major Stereotyped Subsets and Closely Related Satellites

36. CLL with Mutated IGHV4-34 Antigen Receptors Is Clinically Heterogeneous: Antigen Receptor Stereotypy Makes the Difference

38. The Correlation of APOBEC Gene Family Member Expression with Worse CLL Patient Outcome Suggests a Role in CLL Mutational Evolution

41. Upregulation of Interferon-Inducible and Damage Response Receptors in Chronic Graft-Versus-Host Disease

42. CLL with Mutated IGHV4-34 Antigen Receptors Is Clinically Heterogeneous: Antigen Receptor Stereotypy Makes the Difference

48. Recurrent Mutations within the Nfkbie gene: A Novel Mechanism for NF-κB Deregulation in Aggressive Chronic Lymphocytic Leukemia

49. Chronic Lymphocytic Leukemia Patients Exhibit Expanded Functional Granulocyte-like Myeloid Derived Suppressor Cells

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