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 Blood, 15 July 2005, Vol. 106, No. 2, pp. 681-689.
Prepublished online as a Blood First Edition Paper on April 7, 2005; DOI 10.1182/blood-2004-10-4073.

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NEOPLASIA

Distinctive gene expression pattern in VH3-21 utilizing B-cell chronic lymphocytic leukemia

Susann Fält, Mats Merup, Gerard Tobin, Ulf Thunberg, Gösta Gahrton, Richard Rosenquist, and Anders Wennborg

From the Unit of Environmental Medicine, Center for Nutrition and Toxicology, Department of Biosciences at Novum, Karolinska Institutet, Huddinge, Sweden; Department of Hematology, Karolinska Institutet, Karolinska University Hospital, Huddinge, Stockholm, Sweden; Department of Genetics and Pathology, Uppsala University, Sweden; and Department of Oncology, Radiology and Clinical Immunology, Uppsala University, Sweden.

The usage of the immunoglobulin (Ig) VH3-21 gene is associated with poor prognosis in B-cell chronic lymphocytic leukemia (B-CLL) despite VH gene mutation status. Many VH3-21+ patients also display restricted heavy- and light-chain Ig gene rearrangements, implying a role of antigen selection in disease development. To explore the specific phenotypic/genotypic features among VH3-21+ B-CLLs, we compared gene expression patterns in 15 VH3-21+ and 24 non-VH3-21 patients (11 with unmutated and 13 with mutated VH genes) using Affymetrix microarray analysis (~12 500 genes). A distinct expression profile was identified for VH3-21+ patients in contrast to the Ig-unmutated and -mutated groups. By applying different algorithms, the data enabled an efficient class discrimination of the VH3-21+ subset based on 27 or 57 genes. A set of genes was sorted out which, using different analytical methods, consistently gave a distinction between VH3-21+ and non-VH3-21 samples. Several of these genes are involved in regulation of DNA replication/cell-cycle control, transcription and protein kinase activity, which may render the VH3-21+ cells with a higher proliferative drive. However, no clear evidence of increased B-cell receptor signaling was found in the VH3-21+ group. Altogether, our identification of a specific VH3-21 profile may provide insights into the pathogenesis of the VH3-21+ subgroup. (Blood. 2005;106:681-689)


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