NDLI: Involvement of multiple signaling pathways in follicular lymphoma transformation: p38-mitogen-activated protein kinase as a target for therapy

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Involvement of multiple signaling pathways in follicular lymphoma transformation: p38-mitogen-activated protein kinase as a target for therapy

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Involvement of multiple signaling pathways in follicular lymphoma transformation: p38-mitogen-activated protein kinase as a target for therapy

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Palais, Robert A. Wang, Lai Y. Elenitoba-johnson, Kojo S. J. Bohling, Sandra D. Tripp, Sheryl Buckstein, Rena Perkins, Sherrie L. Perez-ordonez, Bayardo Lim, Megan S. Abbott, Robert T. Lin, Zhaosheng Shami, Paul J. Coupland, Robert W. Dube, Ian D. Jenson, Stephen D.
Description	Author Affiliation: Elenitoba-Johnson KS ( Department of Pathology, Associated Regional and University Pathologists Institute for Clinical and Experimental Pathology, University of Utah, Salt Lake City, UT 84132, USA. kojo.elenitobaj@path.utah.edu);
Abstract	Follicular lymphoma (FL) is the most common form of low-grade non-Hodgkin's lymphoma. Transformation to diffuse large B cell lymphoma (DLBCL) is an important cause of mortality. Using cDNA microarray analysis we identified 113 transformation-associated genes whose expression differed consistently between serial clonally related samples of FL and DLBCL occurring within the same individual. Quantitative RT-PCR validated the microarray results and assigned blinded independent group of 20 FLs, 20 DLBCLs, and five transformed lymphoma-derived cell lines with 100%, 70%, and 100% accuracy, respectively. Notably, growth factor cytokine receptors and p38beta-mitogen-activated protein kinase (MAPK) were differentially expressed in the DLBCLs. Immunohistochemistry of another blinded set of samples demonstrated expression of phosphorylated p38MAPK in 6/6 DLBCLs and 1/5 FLs, but not in benign germinal centers. SB203580 an inhibitor of p38MAPK specifically induced caspase-3-mediated apoptosis in t(14;18)+/p38MAPK+-transformed FL-derived cell lines. Lymphoma growth was also inhibited in SB203580-treated NOD-SCID mice. Our results implicate p38MAPK dysregulation in FL transformation and suggest that molecular targeting of specific elements within this pathway should be explored for transformed FL therapy.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	12
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Lymphoma, Follicular Drug Therapy Enzymology Mitogen-Activated Protein Kinases Metabolism Apoptosis Drug Effects Cell Transformation, Neoplastic Chromosomes, Human, Pair 14 Genetics Chromosomes, Human, Pair 18 Enzyme Inhibitors Pharmacology Gene Expression Profiling Imidazoles Lymphoma, B-Cell Lymphoma, Large B-Cell, Diffuse MAP Kinase Signaling System Antagonists & Inhibitors Oligonucleotide Array Sequence Analysis Pyridines Receptors, Cytokine Receptors, Growth Factor Translocation, Genetic Tumor Cells, Cultured P38 Mitogen-Activated Protein Kinases Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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