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Blood, 1 May 2007, Vol. 109, No. 9, pp. 3989-3997. Prepublished online as a Blood First Edition Paper on January 18, 2007; DOI 10.1182/blood-2006-09-045377. This Article Full Text Full Text (PDF) Supplemental Figure All Versions of this Article: blood-2006-09-045377v1 109/9/3989    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 CrossRef Citing Articles via Google Scholar Google Scholar Articles by Vallat, L. D. Articles by Gribben, J. G. Search for Related Content PubMed PubMed Citation Articles by Vallat, L. D. Articles by Gribben, J. G. Related Collections Gene Expression Genomics Immunobiology Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Temporal genetic program following B-cell receptor cross-linking: altered balance between proliferation and death in healthy and malignant B cells Laurent D. Vallat1, Yuhyun Park2, Cheng Li2, and John G. Gribben1 1 Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA; 2 Biostatistics, Harvard School of Public Health, Boston, MA Gene expression in cells is a dynamic process but is usually examined at a single time point. We used gene expression profiling over time to build temporal models of gene transcription after B-cell receptor (BCR) signaling in healthy and malignant B cells and chose this as a model since BCR cross-linking induces both cell proliferation and apoptosis, with increased apoptosis in chronic lymphocytic leukemia (CLL) compared to healthy B cells. To determine the basis for this, we examined the global temporal gene expression profile for BCR stimulation and developed a linear combination method to summarize the effect of BCR simulation over all the time points for all patients. Functional learning identified common early events in healthy B cells and CLL cells. Although healthy and malignant B cells share a common genetic pattern early after BCR signaling, a specific genetic program is engaged by the malignant cells at later time points after BCR stimulation. These findings identify the molecular basis for the different functional consequences of BCR cross-linking in healthy and malignant B cells. Analysis of gene expression profiling over time may be used to identify genes that might be rational targets to perturb these pathways. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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