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Genes up-regulated in lymph nodes from patients with mantle cell lymphoma (MCL) compared to the non-malignant hyperplastic lymph nodes.

PAG Title Genes up-regulated in lymph nodes from patients with mantle cell lymphoma (MCL) compared to the non-malignant hyperplastic lymph nodes.
PAG ID MAX001116
Type A
Source Link MSigDB
Publication Reference NA
PAG Description An imbalance between cellular apoptosis and survival may be critical for the pathogenesis of lymphoma. Therefore, the gene expression pattern in lymph node preparations from patients with mantle cell lymphoma (MCL) was compared to the pattern in nonmalignant hyperplastic lymph nodes (HLs). Oligonucleotide microarray analysis was performed comparing 5 MCLs to 4 HLs using high-density microarrays. The expression data were analyzed using Genespring software. For confirmation, the expression of selected genes was analyzed by real-time polymerase chain reaction using the RNA extracted from 16 MCL and 12 HL samples. The focus was on 42 genes that were at least 3-fold down-regulated in MCL; in addition to the B-cell leukemia 2 (BCL2) system other apoptotic pathways were altered in MCL. The FAS-associated via death domain (FADD) gene that acts downstream of the FAS cascade as a key gene to induce apoptosis was more than 10-fold down-regulated in MCL. Furthermore, the death-associated protein 6 (DAXX) gene, the caspase 2 (CASP2) gene, and the RIPK1 domain containing adapter with death domain (RAIDD) gene, which are key genes in other proapoptotic pathways, were also decreased in the MCL samples. The suggestion is made that in addition to the known overexpression of cyclin D1, which drives entry into the cell cycle, disturbances of pathways associated with apoptosis contribute to the development of MCL. (Blood. 2001;98:787-794)
Species Homo sapiens
nCoCo Score 223
Base PAG ID MAX001116
Human Phenotyte Annotation
Curator PAGER curation team
Curator Contact PAGER-contact@googlegroups.com
Gene ID Gene symbol Gene name RP_score
Gene A Gene B Source SCORE

Gene A Gene B Mechanism Source
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