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DIAGNOSTIC "Run-on"
Paragraph Type
Proc
Natl Acad Sci U S A. 2003 Jun 10;100(12):7259-64. Epub 2003 May 19.
Involvement of multiple signaling pathways in follicular lymphoma
transformation: p38-mitogen-activated protein kinase as a target for
therapy.
Elenitoba-Johnson KS, Jenson SD, Abbott RT, Palais RA, Bohling SD, Lin
Z, Tripp S, Shami PJ, Wang LY, Coupland RW, Buckstein R, Perez-Ordonez
B, Perkins SL, Dube ID, Lim MS.
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
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.
PMID: 12756297
DIAGNOSTIC Structured
Type
Proc
Natl Acad Sci U S A. 2003 Jun 10;100(12):7259-64. Epub 2003 May 19
Title:
Involvement of multiple signaling pathways in follicular
lymphoma transformation: p38-mitogen-activated protein kinase as a
target for therapy. PMID: 12756297
Authors:
Elenitoba-Johnson KS, Jenson SD, Abbott RT, Palais RA,
Bohling SD, Lin Z, Tripp S, Shami PJ, Wang LY, Coupland RW, Buckstein
R, Perez-Ordonez B, Perkins SL, Dube ID, Lim MS.
Centers:
Department of Pathology, Associated Regional and University
Pathologists Institute for Clinical and Experimental Pathology,
University of Utah, Salt Lake City, UT 84132, USA.
Study
questions: 1) What genes are associated with
transformation from FL to DLBCL? 2)
Are identified genes potential targets for treatment?
Background: 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..
Methods:
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.
Sample:
20 FLs, 20 DLBCLs, and five transformed lymphoma-derived cell lines
Findings:
1) 113 transformation-associated genes whose expression
differed consistently between serial clonally related samples of FL
and DLBCL occurring within the same individual. 2)
Growth factor cytokine receptors and p38beta-mitogen-activated protein
kinase (MAPK) were differentially expressed in the DLBCLs
Conclusion:
1) Our results implicate p38MAPK dysregulation in FL
transformation. 2) Notably, growth
factor cytokine receptors and p38beta-mitogen-activated protein kinase
(MAPK) were differentially expressed in the DLBCLs.
Validation:
1) 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. 2)
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. 3)
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.
Statistical
significance: Not specified/calculated
Discussion:
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.
Disclosures: None
specified.
