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 Blood, 1 February 2006, Vol. 107, No. 3, pp. 1101-1107.
Prepublished online as a Blood First Edition Paper on October 20, 2005; DOI 10.1182/blood-2005-04-1510.

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NEOPLASIA

Loss of major histocompatibility class II expression in non-immune-privileged site diffuse large B-cell lymphoma is highly coordinated and not due to chromosomal deletions

Lisa M. Rimsza, Robin A. Roberts, Elias Campo, Thomas M. Grogan, Silvia Bea, Itziar Salaverria, Andreas Zettl, Andreas Rosenwald, German Ott, H. Konrad Muller-Hermelink, Jan Delabie, Richard I. Fisher, Joseph M. Unger, Michael LeBlanc, Louis M. Staudt, Elaine S. Jaffe, Randy D. Gascoyne, Wing C. Chan, Dennis D. Weisenburger, Timothy Greiner, Rita M. Braziel, and Thomas P. Miller

From the Department of Pathology, University of Arizona, Tucson, AZ; Hospital Clinic, University of Barcelona, Barcelona, Spain; Department of Pathology, University of Wuerzburg, Wuerzburg, Germany; Norwegian Radium Hospital, Oslo, Norway; James P. Wilmot Cancer Center, University of Rochester Medical Center, Rochester, NY; Statistical Center, Fred Hutchinson Cancer Research Center, Seattle, WA; Metabolism Branch, National Cancer Institute, Bethesda, MD; British Columbia Cancer Agency, Vancouver, British Columbia, Canada; Department of Pathology and Microbiology, University of Nebraska, Omaha, NE; Department of Pathology, Oregon Health Sciences Center, Portland, OR; and Arizona Cancer Center, Tucson, AZ.

Decreased major histocompatibility class II (MHCII) expression is associated with poor survival in diffuse large B-cell lymphoma (DLBCL). Immune-privileged site DLBCL (IP-DLBCL) patients reportedly have frequent large deletions at the MHCII locus whereas the mechanism of decreased expression in non-IP-DLBCL is unknown. Gene expression profiling data were used for correlation analyses between expression levels of MHCII genes with each other and their transcriptional regulator, CIITA. Comparative genomic hybridization (CGH) assessed chromosomal alterations at MHCII-related loci. Finally, a map was created of expression of genes that are telomeric, within, or centromeric to the MHCII locus. Correlation coefficients among MHCII genes ranged from 0.73 to 0.92, whereas those between adjacent and intervening genes were lower (-0.12 to 0.49). Correlations between MHCII and CIITA expression were higher (0.53 to 0.60) than between CIITA and neighboring genes (-0.05 to 0.22). In 23 MHCII- cases, CGH detected 2 losses and 2 gains at MHCII loci. Expression of genes telomeric, within, and centromeric to MHCII loci were near normal in most MHCII- cases. Large deletions of the MHCII locus are uncommon in non-IP-DLBCL, implicating altered transcription as the operative mechanism for decreased expression.


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