Anti-CD45RB monoclonal antibody, clone B30

The presence of chromosome abnormalities promotes tumor progression in B-chronic lymphocytic leukemia (CLL). However, the molecular pathways that are relevant to tumor progression remain unclear. In this study, we screened for common chromosome abnormalities [13q14 del, 11q22.3 (ATM) del, 17p13 (p53) del and trisomy 12] by fluorescent in situ hybridization in 40 B-CLL patients. Each of the four chromosome abnormality groups was compared to several clinical factors related to lymphocyte behaviour in CLL. The 11q22.3 (ATM) deletion group was significantly associated with the presence of bulky abdominal/mediastinal lymphadenopathy ( P = 0.014). We hypothesized that this phenotype would be associated with an altered transcription pattern of genes. Class comparison analysis by significance analysis of microarrays on a subset of CLL samples ( n = 14) indicated that a number of cell surface receptor and adhesion related genes were under-expressed in the 11q22.3 deletion group (CD44, CD11a, PTPRC, CD79a, chemokine ligand 17 and chemokine receptor type 6). The presence of additional prognostic factors, such as CD38 and immunoglobulin heavy chain variable region mutational status, may also influence the transcriptional pathways between the two groups. Therefore, we employed a novel analysis technique for the correlation of log 2 gene expression ratios with the percentage of each tumor that carried the 11q22.3 deletion. Using Spearman's correlation, ZAP-70, chemokine ligand 17, BSAP (PAX5), CD7, LAG3 and PTPR6 were significantly correlated with the percentage of cells with the 11q22.3 deletion. However, the down-regulation of cell surface receptors and adhesion molecules observed by class comparison could not be confirmed to be specific for the 11q22.3 deletion by this method.

The CD45 77C>G transversion (rs17612648) in exon A of the CD45 gene has been reported to be associated with the development of various autoimmune diseases. Because Hashimoto's thyroiditis (HT) is a typical autoimmune disease, we performed a study to determine the association of the 77C>G transversion with susceptibility to HT. We enrolled 170 patients and 230 healthy individuals in the study. The 77C>G transversion was genotyped by polymerase chain reaction-allele specific restriction enzyme analysis (PCR-ASRA). We found four patients and six control individuals who carried the 77C>G transversion in a heterozygous form. No homozygous individual was detected in patients with HT or control population. The frequency of the 77G allele in patients was 1.2%, which did not significantly differ from 1.3% in controls (p = 0.871). Our data did not reveal any association between CD45 77C>G transversion and susceptibility to HT in a German population. (C) 2010 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.