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)

Translocations of the c-myc, bcl-2 and the putative bcl-1 oncogene are recurrent events in B-cell lymphoma. Since it is likely that the rearranged genes contribute to the malignant phenotype of the tumor cells, such oncogene translocation is of major interest. The molecular detection of translocations using conventional Southern hybridization analysis is complicated by the fact that translocation breakpoints are dispersed over large chromosomal regions. In order to overcome this problem we used pulsed-field gel electrophoresis (PFGE) to detect c-myc, bcl-2 and bcl-1 translocations in 29 lymph node biopsies. C-myc translocation could not be detected in this group, either with standard Southern analysis of PFGE. Translocations of the bcl-2 gene were detected by PFGE in 5 samples and the breakpoints were mapped in all cases to the third exon of bcl-2 by standard Southern analysis. Furthermore, we also found rearrangements of the bcl-1 locus in 3 samples. Mapping of the breakpoint failed in one of these cases, which strongly indicates the existence of a breakpoint outside the bcl-1 major breakpoint region. Thus, PFGE allows the rapid detection of translocations in human lymphomas within large stretches of DNA.
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PMID:Analysis of c-myc, bcl-1 and bcl-2 translocations in human lymphoma by pulsed-field gel electrophoresis. 149 47

We have isolated a 2228 bp cDNA clone encoding a chicken homologue of the human Bcl-2 oncoprotein by low-stringency hybridization screening of a lambda gt10 cDNA library derived from a chicken B-cell lymphoma. DNA sequence analysis of this cDNA revealed an open reading frame predicting a polypeptide of 232 amino acids and an M(r) of 25,839. The predicted protein is highly homologous to the human (73%) and mouse (70%) Bcl-2 proteins, and contains a hydrophobic stretch of amino acids within its carboxyl-end (213-229) consistent with an integral membrane protein. Areas of very high sequence homology shared by all three Bcl-2 proteins at the NH2-terminus (amino acids 1-33) and within the last 150 amino acids of these proteins suggest the presence of at least two evolutionarily conserved domains within the family of Bcl-2 proteins that may be important either for their targeting to mitochondria or their ability to block programmed cell death.
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PMID:Molecular cloning and DNA sequence analysis of cDNA encoding chicken homologue of the Bcl-2 oncoprotein. 151 Oct 8

The purpose of this research was to determine whether prostaglandin E2 (PGE2), a major product of macrophages which can kill certain murine B cell lymphomas, induces death by a necrotic mechanism or by an alternate pathway called apoptosis. CH31 is a phenotypically "immature" B cell lymphoma which resembles immature neonatal B cells in its susceptibility to killing by reagents which cross-link surface immunoglobulin (sIg). In the present study we first show that PGE2, but not the closely related prostanoid, PGF2 alpha, kills CH31 lymphoma cells. In contrast, CH12, a phenotypically "mature" lymphoma which is not negatively affected by sIg cross-linking, is not induced to die after exposure to PGE2. Agarose gel electrophoresis demonstrated that the DNA of PGE2-treated CH31, but not CH12 cells, is cleaved into characteristic 200 base pair oligonucleosomal fragments indicative of an apoptotic mechanism of death. However, a necrotic form of death, indicated by random DNA cleavage which produces a smear following electrophoresis, could be induced by treatment of CH12 or CH31 with anti-class II MHC antibodies and complement. The apoptotic mechanism of CH31 cell killing by PGE2 was confirmed using scanning electron microscopy which demonstrated the unique membrane blebbing and bubbling pathognomonic of this form of death. Finally, using a recently devised flow cytometric method to study apoptosis in heterogeneous cell populations, we compared the ability of anti-IgM, PGE2, or PGF2 alpha to induce apoptosis in B lymphocytes from neonatal or adult mice. Anti-IgM, and to a lesser extent PGE2, but not PGF2 alpha, induces apoptosis in a fraction of neonatal B cells. None of these treatments induced cell death in B lymphocytes from mature mice. Overall, these observations suggest that PGE-secreting cells such as macrophages, which inhabit the B cell microenvironments of lymphoid organs, may eliminate a subset of immature B lymphocytes and may be important in controlling the spread of PGE-sensitive malignant B lymphoma cells.
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PMID:Prostaglandin E2 induces apoptosis in immature normal and malignant B lymphocytes. 162 42

B-cell associated antigens are frequently expressed by the Reed-Sternberg (RS) cells of lymphocyte predominance (LP) Hodgkin's disease (HD) and are sometimes expressed by those of nodular sclerosis (NS) and mixed cellularity (MC) HD. Clonal immunoglobulin gene rearrangements have been detected in some HD cases as well. These findings suggest that at least some cases of HD may be of B-cell derivation. Rearrangements of the bcl-2 gene, associated with the t(14;18)(q32;q21) are present in more than 75% of follicular and 30% of diffuse lymphomas of B-cell origin, suggesting that this translocation plays an important role in B-cell lymphomagenesis. In this study, we investigated 34 cases of HD (10 LP, 14 NS, and 10 MC) for bcl-2 gene rearrangements to determine if this B-cell lymphoma-associated translocation also plays a role in the pathogenesis of HD. The cases of HD were analyzed by Southern blot hybridization, using DNA probes that detect the major and minor breakpoint cluster regions and a 5'bcl-2 breakpoint region recently cloned and found to be involved in B-cell chronic lymphocytic leukemia, and by the polymerase chain reaction (PCR), using oligonucleotides capable of amplifying and detecting the major breakpoint region (mbr) and minor cluster region (mcr) breakpoint regions in t(14;18). bcl-2 translocations were not detected in any of the 34 cases of HD by Southern blot hybridization or by PCR. This is in spite of the fact that RS cells expressing B-cell-associated antigen CD20 were detectable in 7/8 cases of LP HD and 6/24 cases of NS and MC HD with monoclonal antibody L26. Therefore, these results indicate that the bcl-2 gene translocation does not play an important role in the pathogenesis of HD and did not provide evidence for the B-cell origin of HD.
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PMID:The bcl-2 gene translocation is undetectable in Hodgkin's disease by Southern blot hybridization and polymerase chain reaction. 163 63

The presence of neoplastic (light chain restricted) B-cell follicles in low-grade B-cell gastrointestinal (GI) lymphoma of mucosa-associated lymphoid tissue (MALT) has been explained on the basis of specific colonization of reactive follicles by centrocyte-like (CCL) cells. Low-grade B-cell thyroid lymphomas have been included in the category of MALT lymphoma, but the frequent presence of a follicular pattern in these tumors has contributed to the view that they are follicle center cell (FCC) tumors. We have reviewed the histology and investigated the phenotype and genotype of nine cases of primary low-grade B-cell lymphoma of the thyroid, all of which were distinguished by a predominantly follicular pattern. All cases also demonstrated features of MALT lymphoma, including CCL cells and lymphoepithelial lesions. The appearances and immunohistology of the follicles were those of follicular colonization as described in GI MALT lymphoma rather than FCC follicular lymphoma. The predominant pattern of follicular colonization was replacement of the follicle center by slightly enlarged CCL cells that showed a strikingly high proliferation rate. No evidence of the t(14;18) translocation was found in any case, using the polymerase chain reaction (PCR) on DNA extracted from fresh (n = 1) or paraffin-embedded (n = 9) tissue. These findings argue against a FCC lineage for primary thyroid lymphomas and support their inclusion in the MALT category.
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PMID:Follicular colonization in thyroid lymphoma. 163 70

Head and neck tumors include nasopharyngeal carcinoma (NPC) and lymphoma. The differential diagnosis of these tumors is based on histology, immunocytochemical staining, and EBV serology. In rare cases it might be difficult to distinguish between NPC and lymphoma in HE section or biopsies. DNA hybridization with cloned EBV and human immunoglobulin gene fragments allows the detection of EBV-related sequences and immunoglobulin gene rearrangements. The presence of EBV genome supports the diagnosis of NPC or EBV related BL, while rearrangement of immunoglobulin genes points to B-cell lymphoma. The diagnosis in 11 patients suspected of head and neck tumors was carried out by hybridization of DNA extracted from the tumors and assayed with cloned EBV and IgHCJ DNA probes. One patient proved to have EBV-associated BL based on positive hybridization with EBV probes and immunoglobulin rearrangement, presenting a unique hybridization with cloned EBV DNA BamHI W fragment, with bands of 3.2 and 3.9 kb. BL was confirmed in this patient by demonstration of c-myc rearrangement. A second patient was negative in hybridization with EBV, and positive for immunoglobulin rearrangement, and therefore was diagnosed as having B-cell lymphoma. In seven patients NPC was confirmed by hybridization with EBV-DNA probes. In two patients, both NPC and B-cell lymphomas were excluded.
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PMID:EBV genome and immunoglobulin gene rearrangement in the differential diagnosis of nasopharyngeal carcinoma and lymphoma. 164 89

Aggressive B-cell lymphomas are occurring with increasing incidence among individuals infected with human immunodeficiency virus (HIV). Several lines of evidence implicate both Epstein-Barr virus (EBV) and c-myc activation in the pathogenesis of a major subset of these tumors. These observations prompted our investigation of interactions among EBV, c-myc, and HIV in primary B cells. We show that nonimmortalized peripheral B lymphocytes from EBV-seropositive, HIV-seronegative donors can be infected by HIV and that a subset of these lymphocytes become transformed. Malignant transformation was documented by several criteria. These cells displayed altered growth properties, propagating in 1% serum and cloning in soft agar, and formed invasive tumors of Burkitt lymphoma phenotype after subcutaneous injection into severe combined immunodeficiency mice. Such cells revealed marked enhancement of EBV DNA and RNA and of endogenous c-myc transcripts and protein. HIV-1 infection of already immortalized B-cell lines led to a similar upregulation of EBV and c-myc transcripts. These data indicate that HIV has properties of a transforming retrovirus, as it mediates two events linked to B-cell neoplasia: deregulation of c-myc and activation of EBV. They also raise the possibility of a role for HIV, apart from induction of immune suppression, in the pathogenesis of B-cell lymphoma in the acquired immune deficiency syndrome.
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PMID:Human immunodeficiency virus induction of malignant transformation in human B lymphocytes. 165 56

The results of DNA or RNA study in EBV-associated lymphoproliferative diseases were shown. For detecting EBV DNA, Southern blot analysis with Bam HIW probe (Internal Repeat) and non-repeat (least often deleted) probe are used. Probes close to (ex. LMP) or within terminal repeat can indicate clonality in terms of junctional structure. Several such examples were shown, in which benign polyclonal EBV (+) CD3 + 8+ lymphocytes, EBV (+) CD3 + 4 - 8- granulay lymphocytosis, EBV (+) t(14, 22) B-cell lymphoma and EBV (-) follicular lymphoma with reactivation type serology were included. The detectability of EBV DNA was tested in consecutively sampled acute IM peripheral cells by Southern blot analysis with Bam HIW, PCR with Bam HIK (EBNA1) and its Southern re-estimation. The results indicated that EBV DNA was detectable rarely in the earliest samples, and that PCR can increase the sensitivity, as expected. The gene expression of IL-2R alpha (-) IL-2R beta (+) and perforin (-) by IM cells were assessed with Northern blot analysis. The abundant gamma IFN gene expression by IM cells was revealed by reversed PCR.
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PMID:[Epstein-Barr virus (EBV) in lymphoproliferative diseases]. 165 62

Rearrangement of the BCL1 (B-cell lymphoma 1) region on chromosome 11q13 appears to be highly characteristic of centrocytic lymphoma and also is found infrequently in other B-cell neoplasms. Rearrangement is thought to deregulate a nearby protooncogene, but transcribed sequences in the immediate vicinity of BCL1 breakpoints had not been identified. PRAD1, previously designated D11S287E, was identified on 11q13 as a chromosomal breakpoint region rearranged with the parathyroid hormone gene in a subset of parathyroid adenomas; this highly conserved putative oncogene, which encodes a novel cyclin, has been linked to BCL1 and implicated also in subsets of breast and squamous cell neoplasms with 11q13 amplification. We report pulsed-field gel electrophoresis data showing BCL1 and PRAD1 to be no more than 130 kilobases apart. PRAD1 mRNA is abundantly expressed in seven of seven centrocytic lymphomas (Kiel classification), in contrast to 13 closely related but noncentrocytic lymphomas. Three of the seven centrocytic lymphomas had detectable BCL1 DNA rearrangement. Also, two unusual cases of CLL with BCL1 rearrangement overexpressed PRAD1, in contrast to five CLL controls. Thus, PRAD1 is an excellent candidate "BCL1 oncogene." Its overexpression may be a key consequence of rearrangement of the BCL1 vicinity in B-cell neoplasms and a unifying pathogenetic feature in centrocytic lymphoma.
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PMID:PRAD1, a candidate BCL1 oncogene: mapping and expression in centrocytic lymphoma. 168 19

A newly described herpes virus, human herpes virus 6, (HHV-6), has been linked to exanthema subitum but beyond this its pathogenetic impact remains to be determined. A large body of evidence links it to various lymphoproliferative disorders and this study was conducted to identify forms of lymphoproliferation linked to HHV-6. We studied biopsy samples from 32 patients with disorders of the lymphatic system for the presence of HHV-6, both by polymerase chain reaction (PCR) and in-situ hybridization (ISH) methods, as well as Epstein-Barr virus (EBV) viral DNA, clonal rearrangements of the antigen receptor genes and bcl-2 genes. All the specimens were studied morphologically and a clinical follow-up of up to 4 years was obtained. Seven of the 32 patients were positive for HHV-6 DNA and the remainder were negative. Two of these HHV-6 positive specimens, both from elderly persons, showed a similar distinct histological pattern diagnosed as malignant B-cell lymphoma of high grade malignancy. Two other HHV-6-positive specimens were reactive lymphadenopathies occurring in younger adults. In addition, one further specimen with evidence of EBV-involvement was from a patient who died 3 months after biopsy with fatal infectious mononucleosis (IM). These five samples had HHV-6 DNA by PCR and ISH. Two specimens without specific histologic abnormalities showed evidence of HHV-6 only by PCR but not by ISH. Both high grade malignant lymphomas showed clonal proliferations, one of monoclonal B-cells and the other of clonal T-cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lymphadenitis and lymphoproliferative lesions associated with the human herpes virus-6 (HHV-6). 168 79


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