Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The growth of B-cell lymphoma, LSCC-RP9, in culture was inhibited by spleen cells from bursa-immunized agammaglobulinemic (A-gamma) chickens. This inhibition was mediated by suppressor T-cells. The growth of transplantable LSCT-RP6 B-cell lymphoma was suppressed in A-gamma chickens, while that of the control SPCT-RP11 T-cell tumor was not affected. Furthermore, the incidence and growth of the LSCT-RP6 tumor in normal recipients were decreased when it was co-transplanted with spleen cells from bursa immunized A-gamma chickens. The results suggest that suppressor T-cells inhibit the growth of B-cell lymphoma.
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PMID:Inhibition of a chicken B-cell lymphoma by suppressor T-cells from agammaglobulinemic chickens. 214 19

Genetic amplification at chromosome 8p23.1 has been reported in some solid tumors. Translocation of 8p23.1 has also been reported in hematological malignancies and head and neck squamous cell cancer. In an attempt to clarify whether this translocation is implicated in lymphomagenesis, we performed FISH analysis of the immunoblastic B-cell lymphoma cell line OCI-LY8, which has chromosome translocation at 8p23.1, with various BAC clones. We found split signals on BAC, RP11-18L2 where the MASL1 gene is located. This translocation was found to produce a chimeric transcript of MASL1 exon 1 with a cryptic exon from the genome region at 14q21. Our study indicates that MASL1 is not only a target gene for genomic amplification but also for chromosomal translocation. Since tumorigenic activity of the MASL1 has not been proven, its in vitro transforming activity was studied and in vivo nude mice assay were performed. Although no in vitro transforming activity was detected by focus formation, the in vivo tumorigenesis assay with nude mice showed that both MASL1 and chimeric MASL1 possess tumorigenic activity. This suggests that MASL1 is an important oncogene not only for solid tumors but also for hematologic malignancies.
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PMID:MASL1, a candidate oncogene found in amplification at 8p23.1, is translocated in immunoblastic B-cell lymphoma cell line OCI-LY8. 1469 50

Deletions of chromosome 8p are a recurrent event in B-cell non-Hodgkin lymphoma (B-NHL), suggesting the presence of a tumor suppressor gene. We have characterized these deletions using comparative genomic hybridization to microarrays, fluorescence in situ hybridization (FISH) mapping, DNA sequencing, and functional studies. A minimal deleted region (MDR) of 600 kb was defined in chromosome 8p21.3, with one mantle cell lymphoma cell line (Z138) exhibiting monoallelic deletion of 650 kb. The MDR extended from bacterial artificial chromosome (BAC) clones RP11-382J24 and RP11-109B10 and included the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor gene loci. Sequence analysis of the individual expressed genes within the MDR and DNA sequencing of the entire MDR in Z138 did not reveal any mutation. Gene expression analysis and quantitative reverse transcriptase-polymerase chain reaction (QRT-PCR) showed down-regulation of TRAIL-R1 and TRAIL-R2 receptor genes as a consistent event in B-NHL with 8p21.3 loss. Epigenetic inactivation was excluded via promoter methylation analysis. In vitro studies showed that TRAIL-induced apoptosis was dependent on TRAIL-R1 and/or -R2 dosage in most tumors. Resistance to apoptosis of cell lines with 8p21.3 deletion was reversed by restoration of TRAIL-R1 or TRAIL-R2 expression by gene transfection. Our data suggest that TRAIL-R1 and TRAIL-R2 act as dosage-dependent tumor suppressor genes whose monoallelic deletion can impair TRAIL-induced apoptosis in B-cell lymphoma.
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PMID:Characterization of 8p21.3 chromosomal deletions in B-cell lymphoma: TRAIL-R1 and TRAIL-R2 as candidate dosage-dependent tumor suppressor genes. 1605 35