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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

bcl-2 is a marker for the translocation t(14;18)(q32;q21) indicative of follicular B-cell lymphoma. We studied 115 cases of lymphoproliferative disease with the polymerase chain reaction for bcl-2 oncogene using biotin and radiolabeled probes to the major breakpoint and minor cluster regions. Twenty-three percent of B-cell lymphomas were positive for bcl-2. These included 12 of 20 cases of nodular follicular center cell lymphoma (nine small cleaved cell, one mixed small and large cell, and two large cell types). bcl-2 translocation was detected in only three of 45 cases of diffuse B-cell lymphoma, and cases of AIDS-related malignant lymphoma, monocytoid B-cell lymphoma, and mantle zone lymphoma were all negative. Nonneoplastic lymphoid proliferations were negative for bcl-2 including nine cases of abnormal follicular hyperplasia from patients with acquired immunodeficiency syndrome (AIDS) and AIDS-related complex. Cases of T-cell lymphoma and five cases of Hodgkin's disease were also negative. The polymerase chain reaction for bcl-2 is a rapid, sensitive technique in the evaluation of follicular B-cell proliferations, and the use of biotinylated probes and the alkaline phosphatase reaction eliminates the requirement for radioactive reagents.
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PMID:Polymerase chain reaction for bcl-2 in diagnostic lymph node biopsies. 226 90

Consecutive 431 patients with B-cell lymphoma seen in Aichi Cancer Center Hospital from 1964 to 1988 were analysed. Median age was 56 yr (range 8-86). There were 76 patients (17.6%) with follicular lymphoma and 355 with diffuse lymphoma. Among the 30 patients with follicular lymphoma, 10 (33%) were found to have a bcl-2 rearrangement. The incidence was lower than those reported in the United States. This might contribute to the lower incidence of follicular lymphoma cases in Japan. There were 168 patients (39.0%) with nodal lymphoma and 263 with extranodal lymphoma. Eight-four cases arose from the stomach, 84 from Waldeyer's ring, 21 small intestine and 13 thyroid. The distributions of extranodal B-cell lymphoma differed from those of T-cell lymphoma. Patients with gastric lymphomas in stage I were treated with resection alone. In the same manner, patients with Waldeyer's ring lymphoma in stage I were treated with radiotherapy alone. More than 90% of these patients were expected to survive without relapse. On the other hand, only 55% of patients with nodal lymphoma in stage I were expected to survive for more than 10 years. These findings suggest the site of localized lymphoma is an important determinant of outcome of clinical behavior.
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PMID:[Characteristics of B-cell lymphoma in Japan]. 239 5

The rearrangement of bcl-2 gene was studied in 56 Japanese B cell lymphoma cases to investigate the contribution of bcl-2 gene to lymphomagenesis in Japan. Ten out of 56 cases showed bcl-2 gene rearrangement; it was detected in only 5 out of 16 follicular lymphoma cases (31%) and in 5 out of 40 diffuse B cell lymphoma cases (13%). The incidence of bcl-2 gene involvement in Japanese follicular lymphomas was lower than those reported in the United States. This might contribute to the lower incidence of follicular lymphoma cases in Japan. Novel recombination between bcl-2 and Ig kappa genes at the 5' region of bcl-2 and J kappa 4 segment was observed in one follicular lymphoma case, suggesting that bcl-2 gene is transcriptionally activated by Ig kappa enhancer. It was also suggested that this case had originated from a more differentiated B cell than most follicular lymphomas with bcl-2-Ig H recombination.
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PMID:bcl-2 gene rearrangement analysis in Japanese B cell lymphoma; novel bcl-2 recombination with immunoglobulin kappa chain gene. 251 Nov 76

The bcl-2 gene rearrangement representing t(14:18) chromosomal translocation is the most frequent karyotypic abnormality in non-Hodgkin's lymphomas of follicle center-cell lineage. By using three bcl-2 DNA probes, 21 cases of non-Hodgkin's B cell lymphoma arising from gastrointestinal mucosa and eight cases of follicular lymphomas were examined. No rearrangement of the gene could be detected in the group of gastrointestinal lymphomas, although it was identified in 75% of the follicular lymphomas. The findings suggest that these two groups of lymphomas are not a family at genetic level and support the earlier suggestion that B cell lymphomas arising from gastrointestinal mucosa-associated lymphoid tissue are not of follicle center-cell lineage.
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PMID:The bcl-2 gene in primary B cell lymphoma of mucosa-associated lymphoid tissue (MALT). 267 27

The bcl-2 (B cell lymphoma/leukemia-2) gene at band 18q21 is involved in t(14;18) chromosomal translocations in most follicular lymphomas and occasional other human B cell malignancies, where it becomes juxtaposed to the transcriptionally active immunoglobulin (Ig) locus at 14q32. Regulation of bcl-2 gene expression was investigated in neoplastic lymphoid cell lines containing normal #18 chromosomes or a t(14;18) translocation with regard to steady-state mRNA levels, RNA stability, transcription rates, and DNA methylation. High steady-state levels of bcl-2 mRNA, and proportionally high rates of bcl-2 transcription (measured in isolated nuclei), were found in B cell lines containing t(14;18) translocations. The half-life of bcl-2 mRNA (approximately 2-3 hr) was similar in all cell lines examined, including a t(14;18)-containing follicular lymphoma cell line, which has a translocated and rearranged bcl-2 gene that produces bcl-2/Ig fusion transcripts. However, in the presence of cycloheximide (inhibitor of protein synthesis), the half-life of some of the bcl-2/Ig mRNAs produced by these cells was prolonged, indicating that in some circumstances mRNA stability may contribute to deregulated bcl-2 expression. Despite stabilizing some bcl-2 mRNAs, the overall effect of treating cell lines with cycloheximide was a reduction in the levels of accumulated bcl-2 mRNAs through inhibition of bcl-2 gene transcription. These latter data provide indirect evidence that short-lived transacting factor(s) regulate transcription of the human bcl-2 gene in lymphoid cells with or without a t(14;18) translocation. No clear correlation was discovered between bcl-2 gene methylation and transcription.
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PMID:Regulation of bcl-2 gene expression in lymphoid cell lines containing normal #18 or t(14;18) chromosomes. 277 9

The t(14;18) chromosomal translocation of human follicular lymphoma recombines the candidate transforming gene bcl-2, located at 18q21, with the immunoglobulin (Ig) H-chain joining region (JH) at 14q32. To elucidate the consequences of this translocation, we cloned bcl-2 cDNAs from a pre-B cell line (Nall-1) and a t(14;18) lymphoma cell line (SU-DHL-6) and compared these sequences with their genomic counterparts. These studies revealed the complexity of bcl-2 gene expression in which six potential polyadenylation signals in exon 3 and two different 5' exons (exons 1 and 2) and promoters are alternatively used to generate different sized bcl-2 mRNAs. A single open reading frame (ORF), at the junction of exons 2 and 3, predicts a 239 amino acid, 26 kD protein. Most chromosome 18 breakpoints cluster within a 150 bp region of exon 3. In SU-DHL-6 the t(14;18) translocation juxtaposes a truncated bcl-2 gene with J6 in a tail-to-head configuration, resulting in the deregulated expression of chimeric bcl-2/Ig transcripts. Importantly, the SU-DHL-6 bcl-2 cDNA also contained several point mutations in the ORF, two of which altered the primary amino acid sequence. The deregulated expression of an altered bcl-2 gene may play a critical role in the disordered growth and differentiation of follicular B cell lymphoma.
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PMID:Consequences of the t(14;18) chromosomal translocation in follicular lymphoma: deregulated expression of a chimeric and mutated BCL-2 gene. 328 1

The phenotypically immature B cell lymphoma WEHI-231 undergoes apoptotic cell death when cultured with anti-immunoglobulin (Ig) antibodies, via a bcl-2-independent mechanism. We have therefore studied the role of the bcl-2-related protein bcl-x in controlling cell death in WEHI-231. We find that overexpression of the long form of bcl-x (bcl-XL) renders these cells refractory to anti-Ig-induced cell death. Stimulation of WEHI-231 via CD40 has similar protective effects. We show here that ligation of CD40 rapidly induces the appearance of the bcl-XL protein in WEHI-231, while stimulation via sIgM, sIgD, CD5 or CD45 receptors, or with phorbol esters plus ionomycin does not. WEHI-231 cells also rapidly undergo massive apoptosis following culture with thapsigargin, a specific inhibitor of the Ca(2+)-ATPase of the endoplasmic reticulum: this is also reversed by anti-CD40, or by overexpression of bcl-XL. We, therefore, conclude that bcl-XL plays a key role in the regulation of antigen receptor-mediated apoptosis via CD40 in WEHI-231. In addition, the fact that this protein is not induced in WEHI-231 in response to phorbol dibutyrate plus ionomycin points to a fundamental signaling defect in these cells, which could conceivably be a reflection of their immature, apoptosis-susceptible phenotype.
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PMID:The role of bcl-XL in CD40-mediated rescue from anti-mu-induced apoptosis in WEHI-231 B lymphoma cells. 753 57

In the present study we investigated the pathogenetic role of c-myc, bcl-2, and lyt-10 oncogenes, bcl-1 locus, and p53 suppressor gene in a representative panel of cutaneous lymphomas, including 25 cases of cutaneous B cell lymphoma (CBCL) and 29 cases of cutaneous T cell lymphoma (CTCL). In our analysis four cases of CBCL were found rearranged for bcl-2 and two for the bcl-1 locus. Two cases of CTCL and one case of CBCL were found rearranged for lyt-10. No rearrangements of c-myc oncogene were found in CBCL. Analysis of p53 gene showed mutation only in one case of mycosis fungoides in tumoral stage, at codon 163 of p53 gene (TAC-->CAC; Tyr--> Asp). Our data suggest that in primary CBCL bcl-2 oncogenes and bcl-1 locus are rarely involved. Furthermore, in primary CTCL p53 gene is not affected at significant frequency. The occurrence of p53 mutation in a patient affected by mycosis fungoides in tumoral stage may represent an involvement of p53 gene in tumor progression of CTCL, a finding observed in several types of human cancer.
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PMID:bcl-1, bcl-2, p53, c-myc, and lyt-10 analysis in cutaneous lymphomas. 759 96

t(14;18) is the most common translocation in human lymphoid malignancy and results in bcl-2 overexpression. Bcl-2 blocks apoptosis and constitutes the initial member of a new category of oncogenes, ie, regulators of cell death. Bcl-2-Ig transgenic mice develop follicular hyperplasia and progress to malignant B-cell lymphoma. To assess the oncogenic potential of bcl-2 in the T-cell lineage, a cohort of 68 lckpr-bcl-2 transgenic mice and 56 control littermates were monitored for signs of malignancy over a 24-month period. Eighteen (26%) lckpr-bcl-2 mice developed diffuse, predominantly large-cell lymphomas at a mean age of 18 months. In contrast, only one nontransgenic control mouse developed lymphoma. CD3 surface expression and clonal T-cell receptor beta rearrangements support the T-lineage classification of these neoplasms. lckpr-bcl-2-enforced lymphomas are predominantly CD4+CD8-, consistent with a mature peripheral T-cell phenotype. These data provide support for the thesis that violation of homeostasis through the repression of cell death can be a primary mechanism of tumorigenesis in multiple lineages.
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PMID:Peripheral T-cell lymphoma in lckpr-bcl-2 transgenic mice. 763 29

Recent studies have indicated that nodular lymphocyte predominance Hodgkin's disease (nLP-HD) is a B-cell lymphoma. Although molecular events in the neoplastic transformation of B-cells are not well understood, Epstein-Barr virus infection and bcl-2 protein overexpression have been postulated to have etiologic roles in some lymphomas. Epstein-Barr virus has been demonstrated in the Reed-Sternberg cells of Hodgkin's disease cases (other than nLP-HD) as well as in some B-cell lymphomas; bcl-2 overexpression is found in the majority of follicular lymphomas. The biologic role for bcl-2 in HD is controversial. Some reports have indicated the presence of bcl-2 gene rearrangements, associated with the t(14;18) (q32;q21), detected by the polymerase chain reaction in HD; recent studies have failed to confirm this finding. Reports in the literature describe only a few such analyses in the nLP-HD subtype. To address these conflicting issues, we examined 12 cases of nLP-HD to determine whether bcl-2 protein expression (by immunohistochemistry) and Epstein-Barr virus (by in situ hybridization) could be detected in the Reed-Sternberg variants. None of the cases showed expression of bcl-2 protein or Epstein-Barr virus RNA in the neoplastic cells. Epstein-Barr virus does not appear to play an important role in the pathogenesis of nLP-HD. Similarly, we cannot substantiate a role for bcl-2 in the development of this type of Hodgkin's disease.
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PMID:Epstein-Barr virus and bcl-2 protein overexpression are not detected in the neoplastic cells of nodular lymphocyte predominance Hodgkin's disease. 767 75


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