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Blood, 1 November 2006, Vol. 108, No. 9, pp. 3135-3142. Prepublished online as a Blood First Edition Paper on July 11, 2006; DOI 10.1182/blood-2006-02-003921. This Article Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2006-02-003921v1 108/9/3135    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Irish, J. M. Articles by Levy, R. Search for Related Content PubMed PubMed Citation Articles by Irish, J. M. Articles by Levy, R. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted February 15, 2006 Accepted June 12, 2006 Altered B cell receptor signaling kinetics distinguish human follicular lymphoma B cells from tumor infiltrating non-malignant B cells Jonathan Michael Irish, Debra K Czerwinski, Garry P Nolan, and Ronald Levy* Department of Medicine, Oncology Division, Stanford University Department of Microbiology & Immunology, Stanford University * Corresponding author; email: levy{at}stanford.edu. The B cell receptor (BCR) transmits life and death signals throughout B cell development, and altered BCR signaling may be required for survival of B lymphoma cells. We used single-cell signaling profiles to compare follicular lymphoma (FL) B cells and nonmalignant host B cells within individual patient biopsies and identified BCR-mediated signaling events specific to lymphoma B cells. Expression of CD20, Bcl-2, and BCR light chain isotype ( or ) distinguished FL tumor B cell and non-tumor host B cell subsets within FL patient biopsies. BCR-mediated signaling via phosphorylation of Syk, Erk1/2, p38, and Btk occurred more rapidly in tumor B cells from FL samples than in infiltrating non-tumor B cells, achieved greater levels of per-cell signaling, and sustained this level of signaling for hours longer than non-tumor B cells. The timing and magnitude of BCR-mediated signaling in non-tumor B cells within a FL sample instead resembled that observed in mature B cells from the peripheral blood of healthy subjects. BCR signaling pathways that are potentiated specifically in lymphoma cells should provide new targets for therapeutic attention. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. W. Lee, E. R. Sharp, A. O'Mahony, M. G. Rosenberg, D. M. Israelski, G. P. Nolan, and D. F. Nixon Single-Cell, Phosphoepitope-Specific Analysis Demonstrates Cell Type- and Pathway-Specific Dysregulation of Jak/STAT and MAPK Signaling Associated with In Vivo Human Immunodeficiency Virus Type 1 Infection J. Virol., April 1, 2008; 82(7): 3702 - 3712. [Abstract] [Full Text] [PDF] L. Chen, S. Monti, P. Juszczynski, J. Daley, W. Chen, T. E. Witzig, T. M. Habermann, J. L. Kutok, and M. A. Shipp SYK-dependent tonic B-cell receptor signaling is a rational treatment target in diffuse large B-cell lymphoma Blood, February 15, 2008; 111(4): 2230 - 2237. [Abstract] [Full Text] [PDF] H. Oh, E. Ozkirimli, K. Shah, M. L. Harrison, and R. L. Geahlen Generation of an Analog-sensitive Syk Tyrosine Kinase for the Study of Signaling Dynamics from the B Cell Antigen Receptor J. Biol. Chem., November 16, 2007; 282(46): 33760 - 33768. [Abstract] [Full Text] [PDF]

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