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Blood, 15 January 2005, Vol. 105, No. 2, pp. 794-803.
Prepublished online as a Blood First Edition Paper on September 23, 2004; DOI 10.1182/blood-2004-04-1424.
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Submitted April 15, 2004
Accepted August 30, 2004
Functional gene expression analysis of clonal plasma cells identifies unique molecular profile for light chain (AL) amyloidosis
Roshini S Abraham*, Karla V Ballman, Angela Dispenzieri, Diane E Grill, Michelle K Manske, Tammy L Price-Troska, Natalia Gonzalez-Paz, Morie A Gertz, and Rafael Fonseca
Division of Hematology, Mayo Clinic College of Medicine, Rochester, MN, USA
Division of Biostatistics, Mayo Clinic Cancer Center, Rochester, MN, USA
Division of Hematology, Mayo Cancer Center, Mayo Clinic, Scottsdale, AZ, USA
* Corresponding author; email: abraham.roshini{at}mayo.edu.
Immunoglobulin light chain amyloidosis (AL) is characterized by a clonal expansion of plasma cells within the bone marrow. Gene expression analysis was used to identify a unique molecular profile for AL using enriched plasma cells (CD138+) from the bone marrow of 24 AL and 28 MM patients and 6 normal controls. Class prediction analysis (PAM) revealed a subset of 12 genes, which included TNFRSF7 (CD27), SDF-1 and PSMA2 that distinguished between these 2 groups with an estimated and observed accuracy of classification of 92%. This model was validated with an independent dataset of 11 AL and 12 MM patients with 87% accuracy. Differential expression for the most discriminant genes in the 12-gene subset was validated using qPCR and protein expression analysis, which upheld the observations from the microarray expression data. Functional analyses using a novel network mapping software revealed a number of potentially significant pathways that were dysregulated in AL patients, with those regulating proliferation, apoptosis, cell signaling, chemotaxis and migration being substantially represented. This study provides new insight into the molecular profile of clonal plasma cells and its functional relevance in the pathogenesis of light chain amyloidosis.
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