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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have used an in situ hybridization method for analysis of expression of BCL2 and MYC on cytospun preparations of normal and malignant lymphoid cell lines and tissue sections of normal and malignant lymph nodes. The probes comprised 50-mer antisense oligonucleotides starting at the ATG codons of exon 3 of BCL2 and exon 2 of MYC. We studied the expression of these two genes in frozen tissue sections of biopsy specimens derived from normal and hyperplastic lymph nodes, B-cell lymphomas carrying the t(14;18)(q32;q21) and t(8;14)(q24;q32) translocations, and T-cell lymphomas with clonal chromosome abnormalities. While all proliferating cells expressed both genes, BCL2 expression was increased two- to threefold in follicular lymphomas with t(14;18) and MYC expression was increased two- to four-fold in high-grade lymphomas with t(8;14). These results are consistent with previous data on deregulated expression of these genes obtained from study of lymphoma cell lines carrying the relevant translocations.
Diagn Mol Pathol 1992 Dec
PMID:Analysis of BCL2 and MYC expression in non-Hodgkin's lymphomas by in situ hybridization: correlation with chromosome translocations. 134 69

109 malignant lymphomas were surveyed by Southern blot analysis and polymerase chain reaction (PCR) for Epstein-Barr virus (EBV) DNA and compared with 16 examples of non-neoplastic lymphadenopathy and 4 normal thymuses. In specimens positive by the method of Southern and PCR, in situ hybridization studies were performed on formalin-fixed, paraffin-embedded sections. By Southern blot analysis, two of seven Hodgkin's disease samples (29%) (one of mixed cellularity and the other of lymphocyte predominance type), three of 56 B-cell lymphomas (5.6%) and five of 46 T-cell lymphomas (11%) demonstrated EBV DNA. However, the 16 examples of lymphadenitis and the 4 normal thymuses showed no EBV DNA. With PCR, EBV DNA was identified in one B-cell lymphoma, nine T-cell lymphomas, ten lymphadenitis specimens and two of the normal thymus, in addition to the positive specimens determined by the Southern blotting method. These results indicate that the presence of EBV DNA is not related to lymphoid malignancy, but enhancement of the DNA is demonstrated in some neoplastic conditions. By in situ hybridization, EBV genomes were not detected in all PCR-positive cases, but only in those positive by Southern blot analysis.
Virchows Arch B Cell Pathol Incl Mol Pathol 1990
PMID:Analysis of Epstein-Barr viral genomes in lymphoid malignancy using Southern blotting, polymerase chain reaction and in situ hybridization. 198 7

Previously, it has been shown that E mu-pim-1 transgenic mice are predisposed to T-cell lymphomas, whereas E mu-myc transgenic mice are predisposed to pre-B-cell lymphomas. Here we show that double-transgenic E mu-myc E mu-pim-1 mice exhibit pre-B-cell leukemia in utero. Upon transplantation into recipient mice, embryo-derived double-transgenic leukemic cells frequently progressed to highly malignant monoclonal tumors, indicating that additional (epi)genetic events had occurred during the progression of the disease.
Mol Cell Biol 1991 Feb
PMID:Mice bearing the E mu-myc and E mu-pim-1 transgenes develop pre-B-cell leukemia prenatally. 199 Feb 73

We have examined avian leukosis virus-induced B-cell lymphomas for multiple, stage-specific oncogene activations. Three targets for viral integration were identified: c-myb, c-myc, and a newly identified locus termed c-bic. The c-myb and c-myc genes were associated with different lymphoma phenotypes. The c-bic locus was a target for integration in one class of lymphomas, usually in conjunction with c-myc activation. The data indicate that c-myc and c-bic may act synergistically during lymphomagenesis and that c-bic is involved in late stages of tumor progression.
Mol Cell Biol 1989 Jun
PMID:Multiple proto-oncogene activations in avian leukosis virus-induced lymphomas: evidence for stage-specific events. 254 84

B cells can be activated by T-independent antigens or mitogens such as lipopolysaccharide (LPS) which will induce proliferation and differentiation of the B cells into Ig-secreting cells, without the intervention of T cells. The precise mechanism of T-independent proliferation and differentiation of B cells is still unclear. It is possible however that antigen-stimulated B cells may produce some factors which play a role in T-independent B-cell responses. In addition, since it has now been established that B cells can function as antigen-presenting cells, it is possible that they too secrete a molecule which is involved in the activation of T cells, analogous to IL-1 production by antigen-presenting macrophages. A number of human B-cell lines, as well as human normal B cells activated appropriately, have been shown to produce various cytokines, and similar studies are now being undertaken in the mouse. In the present study, six cloned murine B-cell lymphomas of different origin were analyzed for the presence of mRNA encoding a number of lymphokines by hybridization of specific cDNA probes to poly-A RNA, followed by the sensitive S1 nuclease digestion technique. The lymphokines included (IL-) 1, 2, 3, 4, 5, and neuroleukin. Whereas none of the lines expressed detectable levels of IL-2, IL-3, or IL-5 mRNA, all the lines expressed high levels of neuroleukin mRNA. Three of the lymphomas (CH12, CH31, and NBL) expressed low levels of IL-1 mRNA. The most striking finding was that one lymphoma, CH12, constitutively expressed IL-4 mRNA. This mRNA appeared to be functional, as IL-4 activity measured by the HT-2 T cell proliferation assay could be detected in supernatants collected from CH12 cells. The growth-inducing activity of CH12 supernatant on HT-2 cells could be completely blocked by an anti-IL-4 monoclonal (11B11), but not by an anti-IL-2 antibody (S4B6), consistent with our observations that CH12 cells produce IL-4 but not IL-2. CH12 cells were also found to express high affinity receptors for IL-4. Proliferation of CH12 cells was not affected by the addition of exogenous IL-4. Addition of anti-IL-4 antibodies to CH12 cells in culture caused a slight but reproducible increase in their proliferation at low cell numbers, which is probably not highly significant. These findings open the possibilities that murine B lymphocytes are capable of lymphokine production or alternatively that aberrant lymphokine production underlies B-lymphocyte transformation.
J Mol Cell Immunol 1989
PMID:Constitutive production of lymphokines by cloned murine B-cell lymphomas--CH12 B lymphoma produces interleukin-4. 278 29

AKXD-23 recombinant inbred mice develop myeloid tumors at a high frequency, unlike other AKXD recombinant inbred strains which develop B-cell lymphomas, T-cell lymphomas, or both. AKXD-23 myeloid tumors are monoclonal, and their DNA contains somatically acquired proviruses, suggesting that they are retrovirally induced. We identified a common site of ecotropic proviral integration that is present in the DNA of all AKXD-23 myeloid tumors that were analyzed and in the DNA of all myeloid tumors that occur in AKXD strains other than AKXD-23. We designated this locus Evi-1 (ecotropic viral integration site 1). Rearrangements in the Evi-1 locus were also detected in the DNA of a number of myeloid tumors and myeloid cell lines isolated from strains other than AKXD. In contrast, few Evi-1 rearrangements were detected in the DNA of T- or B-cell tumors. Evi-1 may thus identify a new proto-oncogene locus that is involved in myeloid disease.
Mol Cell Biol 1988 Jan
PMID:Identification of a common ecotropic viral integration site, Evi-1, in the DNA of AKXD murine myeloid tumors. 282 4

We have determined the nucleotide sequences of two independent DNA clones which contained the activated c-myc genes from avian leukosis virus-induced B-cell lymphomas. Neither of these c-myc genes contained missense mutations. This strongly supports the notion that the c-myc proto-oncogene in avian leukosis virus-induced B-cell lymphomas can be oncogenically activated by altered expression of the gene without a change in the primary structure of the gene product.
Mol Cell Biol 1988 Jun
PMID:Absence of missense mutations in activated c-myc genes in avian leukosis virus-induced B-cell lymphomas. 284 85

The infection of newly hatched chickens with reticuloendotheliosis virus strain T (REV-T) and a nonimmunosuppressive helper virus, chicken syncytial virus, induces rapidly metastatic B-cell lymphomas. In vivo analysis of these tumors with monoclonal antibodies detected the expression of the B-cell surface markers immunoglobulin M (IgM), CIa, Bu2, and CLA-1, but not IgG, Bu1, or a T-cell surface marker, CT-1. Cell lines derived from tumors exhibited the same pattern of staining, suggesting that expression of cell surface markers does not change during in vitro cell line development. All cell lines examined synthesized IgM in varying amounts. Northern (RNA blot) analysis confirmed abundant expression of v-rel mRNA, and Southern analysis revealed rearrangement of both heavy- and light-chain immunoglobulin loci. Analysis of the light-chain locus demonstrated that 20 of 22 lines contained a single rearranged allele. With respect to specific restriction enzyme sites within the V lambda 1 gene, the active allele in any given clone was either diversified or nondiversified. In contrast, examination of the heavy-chain loci within these lines demonstrated that 16 of the 22 had both alleles rearranged. Further diversification of the V lambda 1 locus did not occur after prolonged in vitro passage of the cell lines. We propose that v-rel expression arrests diversification of the light-chain locus in these lymphoid cells, allowing the production of stable, clonal B-cell populations. The development of these and similar cell lines will make it possible to identify specific stages of avian lymphoid ontogeny and to study the mechanism of rearrangement and diversification in the avian B lymphocyte.
Mol Cell Biol 1988 Dec
PMID:Expression of v-rel induces mature B-cell lines that reflect the diversity of avian immunoglobulin heavy- and light-chain rearrangements. 285 97

Subcellular localization of immunoglobulin (Ig) by immunoelectron microscopy was performed on 20 B-cell lymphomas of low- and high-grade malignancy. The efficiency in demonstrating Ig by pre-embedding technique depends on the antibodies used. F(ab')2 fragments of antibodies were more sensitive than both intact polyclonal and monoclonal antibodies in detecting cytoplasmic Ig. With immunoelectron microscopy Ig could be demonstrated in all cell types of B-CLL and LP-immunocytoma, even in some of the small lymphocytes in B-CLL. Thus, the presence of intracytoplasmic Ig has no diagnostic relevance in differentiating B-CLL from LP-immunocytoma. However, the amount of Ig in the tumor cells of LP-immunocytoma seemed to be greater than in B-CLL. Centrocytic lymphoma and centroblastic/centrocytic lymphoma could be differentiated by their different localization of Ig. In centrocytic lymphoma Ig was localized mainly on the surface membrane, whereas in centroblastic/centrocytic lymphoma moderate amounts of Ig could be detected in the rough endoplasmic reticulum and perinuclear space of the centroblasts and in roughly one third of the centrocytes. In malignant lymphomas of high-grade malignancy (ML centroblastic, ML immunoblastic, and ML lymphoblastic) Ig was localized mainly in the rough endoplasmic reticulum and sometimes in the perinuclear space.
Virchows Arch B Cell Pathol Incl Mol Pathol 1986
PMID:Immunoelectron microscopic localization of immunoglobulin in B-cell lymphomas. 287 78

We analyzed the lymphoma susceptibility of 13 AKXD recombinant inbred mouse strains derived from AKR/J, a highly lymphomatous strain, and DBA/2J, a weakly lymphomatous strain. Of the 13 strains used, 12 showed a high incidence of lymphoma development. However, the average age at onset of lymphoma varied considerably among the different AKXD strains, suggesting that they have segregated several loci that affect lymphoma susceptibility. A relatively unambiguous classification of lymphomas was made possible by using histopathology in addition to detailed molecular characterization of rearrangements in immunoglobulin heavy and kappa light genes and in T-cell receptor beta-chain genes. Among the 12 highly lymphomatous strains, only 2 were identified that, like the parental AKR/J strain, died primarily of T-cell lymphomas. Three strains died primarily of B-cell lymphomas, and one strain primarily of myeloid lymphomas. Six strains were susceptible to both T-cell and B-cell lymphomas. Thus, these strains have segregated genes that affect both lymphoma susceptibility and lymphoma type and should prove to be useful models for studying the molecular genetic basis of murine lymphomas.
Mol Cell Biol 1986 Dec
PMID:AKXD recombinant inbred strains: models for studying the molecular genetic basis of murine lymphomas. 302 47


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