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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.
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Submitted September 5, 2006
Accepted November 20, 2006
Temporal genetic program following B-cell receptor cross-linking: altered balance between proliferation and death in healthy and malignant B cells
Laurent D Vallat, Yuhyun Park, Cheng Li, and John G. Gribben*
Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, United States
Biostatistics, Harvard School of Public Health, Boston, MA, United States
* Corresponding author; email: john.gribben{at}cancer.org.uk.
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 early 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.
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