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

Primary T-cell lymphoma within the central nervous system is extremely rare. Imaging characteristics appear indistinguishable from the more common B-cell lymphoma. A case of such a primary tumor is discussed and the MRI and CT findings presented.
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PMID:Cerebellar T-cell lymphoma: an unusual primary intracranial neoplasm. 128 44

We have previously reported that infection of 9- to 13-day-old chicken embryos with RAV-1 results in rapid development of a novel B-cell lymphoma in which proviral insertion has activated expression of the c-myb gene (E. Pizer and E. H. Humphries, J. Virol. 63:1630-1640, 1989). The biological properties of these B-cell lymphomas are distinct from those associated with the B-cell lymphomas that develop following avian leukosis virus proviral insertion within the c-myc locus. In an extension of this study, more than 200 chickens, infected as 10- to 11-day-old embryos, were examined for development of lymphomas that possess disrupted c-myb loci. Fourteen percent developed disseminated B-cell lymphoma. In the majority of these tumors, the RAV-1 provirus had inserted between the first and second exons that code for p75c-myb. However, insertions between the second and third exons and between the third and fourth exons were also detected. In situ analysis of myb protein expression in tumor tissue revealed morphological features suggesting that the tumor originates in the bursa. Within the bursa, the lymphoma appeared to spread from follicle to follicle without compromising the structural integrity of the organ. Tumor masses in liver demonstrated heterogeneous levels of myb protein suggestive of biologically distinct subpopulations. In contrast to the morbidity data, immunohistological analysis of bursae from 4- to 6-week-old chickens at risk of developing lymphomas bearing altered c-myb loci revealed lesions expressing elevated levels of myb in 16 of 19 birds. The activated myb lymphoma displayed very poor capacity to proliferate outside its original host. Only 1 of 33 in vivo transfers of tumor to recipient hosts established a transplantable tumor. None of the primary tumor tissue nor the transplantable tumor exhibited the capacity for in vitro proliferation. Similar experimental manipulation has yielded in vitro lines established from avian B-cell lymphomas expressing elevated levels of c-myc or v-rel. The dependence on embryonic infection for development of activated-myb lymphoma suggests a requirement for a specific target cell in which c-myb is activated by proviral insertion. It is likely, moreover, that continued tumor development requires elevated expression of myb proteins within a specific cell population in a restricted stage of differentiation.
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PMID:Activation of the c-myb locus is insufficient for the rapid induction of disseminated avian B-cell lymphoma. 130 60

We have previously identified Id- tumor vaiants that emerge after anti-Id mAb therapy of the murine B cell lymphoma 38C13. This report characterizes the molecular basis for these variants. By using a modification of the polymerase chain reaction (PCR), mu and kappa Ig loci were sequenced from nine Id- variants derived directly by anti-Id immunoselection in vivo. Ig kappa loci sequence analysis was also performed from 10 additional variants amplified directly from tumor cells in vitro without immunoselection. We demonstrate that the molecular mechanism underlying tumor cell escape in this model is the spontaneous emergence of variants that have undergone kappa L chain gene "re-rearrangement" before positive selection by the anti-Id antibody. A second round of re-rearrangement was also demonstrated to occur within primary tumor variants. Re-rearrangement of the 38C13 tumor cell Ig kappa locus is strongly biased toward use of variable kappa genes within the conserved V kappa-Ox1 gene family, although their use is not exclusive. With the use of RNA PCR re-rearrangement was documented to occur in vitro at a frequency of approximately 1.0 x 10(-5)/cell. These findings may have important implications for the application of anti-Id antibodies as a therapeutic approach for human lymphomas and for understanding of the Ig gene rearrangement process.
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PMID:Molecular characterization of anti-idiotype antibody-resistant variants of a murine B cell lymphoma. 211 49

We report the molecular analysis of primary cells from four cases of human B-cell malignancies each with an 8;14 chromosomal translocation involving the c-myc proto-oncogene and the immunoglobulin (Ig) gene cluster. In two cases of B-cell acute lymphocytic leukemia (B-ALL) the c-myc is truncated, rearranged into the Ig C alpha 1 locus and over-expressed in two abnormal mRNAs of approximately 2.0 and 2.8 kb. Conversely, in two cases of B-cell lymphoma progressed into leukemia the c-myc locus was translocated intact in its coding and 5'-flanking region into an Ig region different from C alpha 1, and over-expressed in two normal mRNA species. Cloning and sequencing of the breakpoint region on chromosome 14q+ from one of the two B-ALL cases showed that the myc gene is truncated 1077 nucleotides upstream from the translation start site, and rearranged in the opposite transcriptional orientation into an Ig class-switch segment approximately 4.8 kb upstream from the C alpha 1 gene. The c-myc anti-sense strand contains two class-switch recombination consensus sequences in the immediate boundaries of the breakpoint on chromosome 8: this allows us to postulate that an erroneous, class-switch-like recombination between Ig and myc sequences gave rise to the chromosomal translocation. Furthermore, we report 13 point mutations clustered in a region spanning from the first intron to the second exon of the translocated c-myc gene, five of which cause amino acid changes leading to an abnormal myc protein. This is the first evidence of mutations in a translocated c-myc in primary tumor cells.
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PMID:Translocation of c-myc into the immunoglobulin heavy-chain locus in human acute B-cell leukemia. A molecular analysis. 301 23

Synthetic peptide ligands specific for the surface immunoglobulin receptor of the human Burkitt's lymphoma cell line SUP-B8, previously identified using phage display libraries, induced apoptosis of the SUP-B8 cells in vitro when administered as dimers or tetramers. The use of synthetic peptide ligands is being explored for immunotherapy of B-cell lymphoma. It will be critical to identify which of the peptide ligands identified are the most active functionally. Using the Cytosensor microphysiometer, SUP-B8 cells and B-lymphoma cells obtained from patients were found to acidify their extracellular environment within minutes of specific activation by surrogate peptide ligands or by anti-idiotype antibodies. This signal was blocked by pretreatment of the lymphoma cells with the tyrosine kinase inhibitor genistein. Treatment of SUP-B8 cells with dimeric and tetrameric specific peptide ligands caused a rapid increase in extracellular acidification rate, which peaked after 10 min at approximately 15 and 20% above basal rates, respectively. These responses were blocked by excess monomeric peptide. To evaluate the ability of different peptide ligands to induce a signal directly on lymphoma cells, thereby establishing their relative affinity to the surface immunoglobulin receptor, acidification rate changes were measured at varying peptide concentrations. The microphysiometer signal correlated with the known relative affinities and antiproliferative potencies of the peptides. This approach is particularly useful for primary tumor cells that cannot be cultured. The signal may be predictive of the efficacy of treatment with synthetic peptide ligands and may be useful in the evaluation of ligands for other cell surface receptors with biological effects on B-lymphoma cells.
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PMID:B-lymphoma cells are activated by peptide ligands of the antigen binding receptor or by anti-idiotypic antibody to induce extracellular acidification. 758 48

Interleukin-10 (IL-10) is an acid-sensitive protein of 35 kD that has pleiotropic effects including inhibition of cytotoxic T-cell response, induction of major histocompatibility complex type II in B lymphocytes, induction of B-cell growth and differentiation, and autocrine growth factor activity in monocytes. We and others have shown that IL-10 is produced spontaneously by blood mononuclear cells from human immunodeficiency virus-seropositive patients. In an attempt to ascertain the potential role of IL-10 in acquired immunodeficiency syndrome (AIDS)-related B-cell lymphoma, we evaluated the expression of human IL-10 in both tumor-derived B-cell lines and primary tumor cells. Expression of human IL-10 (hIL-10) mRNA and protein was detected in four of five cell lines examined. An IL-10 antisense oligonucleotide inhibited IL-10 mRNA expression and IL-10 protein production. The proliferation of all B-cell lines was inhibited by an antisense oligonucleotide in a dose-dependent manner that was abrogated by the addition of recombinant hIL-10 protein. No effect of antisense oligonucleotide was observed in the B-cell line not producing hIL-10. Evaluation of primary tumor cells from patients with AIDS-lymphoma cells showed similar production and response to IL-10. These data suggest an autocrine growth mechanism for IL-10 in AIDS-related lymphoma cells and that IL-10 may be important in its pathogenesis.
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PMID:Interleukin-10 is an autocrine growth factor for acquired immunodeficiency syndrome-related B-cell lymphoma. 749 1

The product of the retinoblastoma tumor-suppressor gene (pRB), a nuclear phosphoprotein that regulates transcription factors such as E2F, is involved in cell cycle control and differentiation. Its activity is regulated by phosphorylation; the underphosphorylated form inhibits transcription whereas the highly phosphorylated form is inactive. Cyclin D1 and its associated kinase (CDK 4/6) phosphorylate pRB in vitro, and therefore are thought to contribute to the regulation of pRB function. To examine the effect of cyclin D1 overexpression on pRB in primary tumor tissue, we studied pRB expression in low-grade B-cell neoplasms, with particular regard to mantle cell lymphoma, which is characterized by cyclin D1 (bcl-1) overexpression. pRB expression was studied by immunostaining with a well-characterized anti-pRB antibody; the phosphorylation status of pRB was examined by immunoblots; and the functional binding capacity of pRB was examined by in vitro binding to adenovirus E1A protein. We studied 3 reactive lymph nodes, 28 low grade B-cell lymphomas, 4 cases of hairy cell leukemia (HCL) and 3 plasmacytomas. Reactive lymph nodes showed intense pRB staining of germinal centers, with strongest (2+) staining in the large cells (centroblasts) of the proliferating (dark) zone and weak or no staining of small lymphocytes, including those of the mantle zone. In B-chronic lymphocytic leukemia (B-CLL) (4 cases), follicular lymphoma (3 cases) and mucosa-associated (MALT) lymphoma (3 cases) strong (2+) pRB staining was limited to centroblasts in reactive and neoplastic follicles and occasional proliferation centers, with only faint staining of small lymphoid cells. In contrast, 15 of 16 cases of mantle cell lymphoma showed strong (1-2+) staining of most cells; one blastoid mantle cell lymphoma showed only faint pRB staining. All cases of (HCL) and plasmacytoma showed strong pRB staining. Although most lymphomas with strong pRB expression were cyclin D1(+), three cyclin D1(+) cases showed only weak pRB expression (1 B-CLL, 1 blastoid mantle cell, 1 unclassifiable low grade B-cell lymphoma). Conversely, of the 4 pRB(+) HCLs and 3 pRB(+) plasmacytomas, only 1 of each was cyclin D1(+). pRB appeared to exist primarily in the underphosphorylated (fastest migrating) form on Western blot, despite the fact that cyclin D1 was complexed to CDK4, a form in which it normally phosphorylates pRB. In addition, pRB appeared to be unmutated, because it bound normally to the adenovirus E1A protein and showed nuclear localization by immunostaining. We conclude that most cases of mantle cell lymphoma, HCL, and plasmacytoma show high levels of pRB in contrast to follicle center lymphoma and small lymphocytic lymphoma; however, pRB expression does not appear to be consistently related to cyclin D1 overexpression. The pRB appears to be unmutated and underphosphorylated, and therefore should be in its active form. Our data from primary lymphoma tissue suggests that overexpression of cyclin D1, whereas tumorigenic, does not lead to pRB loss or hyperphosporylation. Thus, the mechanism by which cyclin D1 contributes to tumorigenesis and the significance of the restricted expression of pRB in low-grade lymphoid neoplasms remain to be determined.
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PMID:Expression of the retinoblastoma protein in low-grade B-cell lymphoma: relationship to cyclin D1. 870 83

B-cell lymphoma frequently shows simultaneous dissemination to multiple organs. It also occasionally involves bone and causes osteolytic lesions. To study the mechanisms responsible for this capacity of lymphoma cells to grow in different tissue microenvironments and search for effective therapeutic interventions for this hematological malignancy, we established a new murine B-cell lymphoma cell line named MH-95. The tumor disseminated to multiple organs including the lung, liver, kidney, spleen and lymph nodes within 2 weeks after subcutaneous inoculation in nude mice. In addition, the tumor also grew in bone and caused osteoclastic osteolytic lesions. Thus, this tumor model mimics the behavior in many ways of B-cell lymphoma in humans. We studied the role of laminin, a major component of the basement membrane, in this model, since although it has been implicated in solid tumor metastasis, little is known about the involvement of laminin in the growth of B-cell lymphoma in bone and other organs. Immunohistochemical examination showed strong laminin expression in the stroma of the primary subcutaneous tumor and tumors in the bone and other organs. Systemic administration of the antagonistic laminin peptide YIGSR decreased primary tumor growth and tumor cell deposit in the bone, liver and kidney. In addition, the peptide also decreased apparent neovascularization in the tumor, suggesting that the peptide suppressed angiogenesis presumably due to inhibition of laminin binding to its receptors. These results demonstrate that the MH-95 B-cell lymphoma cells express laminin and suggest that laminin plays a critical role in the growth and simultaneous dissemination of tumor cells to multiple organs, similar to what has been described in solid tumors. The results also suggest that suppression of angiogenesis through interfering with laminin actions may be a useful adjuvant therapy for B-cell lymphoma.
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PMID:Growth and dissemination of a newly-established murine B-cell lymphoma cell line is inhibited by multimeric YIGSR peptide. 993 11

Primary-effusion lymphoma (PEL) is a rare form of non-Hodgkin's lymphoma which predominantly occurs in patients with acquired immunodeficiency syndrome and is characterized by the presence of a malignant effusion in one or more of the body cavities, generally in the absence of a primary tumor mass. Recently, we encountered two cases of PEL presenting as cardiac tamponade. In both cases, a diagnosis of diffuse large B-cell lymphoma was made by examination of the pericardial fluid. Because human herpes virus-8 (HHV-8) antibodies were positive and human immunodeficiency virus antibodies were negative, HHV-8 seemed likely to be an etiologic agent for the PEL. One of the two patients (case 1) was not treated for religion reasons and died. The other (case 2) achieved complete remission after treatment using the CHOP regimen and is alive at present. The prognosis of this disease is believed to be poor, therefore more cases should be collected to establish reliable therapy for PEL.
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PMID:Human herpes virus-8 associated with two cases of primary-effusion lymphoma. 1090 15

Mucosa-associated lymphoid tissue (MALT) lymphomas are low-grade B-cell neoplasms that occur in a variety of extranodal sites. Only rarely has this entity been discovered as a primary tumor involving the dura of the cavernous sinus. We report the case of a 46 year old woman who presented with a mass involving the cavernous sinus that was originally diagnosed as a meningioma by MRI. However, at surgery the mass was found to be an extranodal marginal zone B-cell lymphoma of the MALT type. The patient underwent partial excision of the lesion followed by radiation. There are only seven other cases of marginal zone B-cell lymphoma involving the intracranial dura reported in the literature. These patients were females who presented with intracranial lesions thought to be consistent with meningioma by preoperative radiographic imaging. MALT lymphomas of the dura, as their counterparts in other organs, appear to have favorable clinical outcomes and excellent long-term prognoses with local therapy alone.
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PMID:Extranodal marginal zone B-cell lymphoma of malt type involving the cavernous sinus. 1169 33


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