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)

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.
 ...
PMID:Analysis of Epstein-Barr viral genomes in lymphoid malignancy using Southern blotting, polymerase chain reaction and in situ hybridization. 198 7

We describe a case of massively necrotizing B-cell lymphoma, involving both axillary and cervical lymph nodes. Histologically, no vascular lesions were noted, and the necrosis was manifested by death of the tumor cells themselves. These cells were surrounded by macrophages, simulating the features of tuberculous lymphadenitis. Immunostaining was a useful method of defining the origin not only of viable cells, but also of necrotic cells in the lymphoma.
 ...
PMID:Necrotizing B-cell lymphoma. A case report with a review of the literature. 229 7

Frozen lymph node biopsy specimens from 38 patients with B cell tumors, including 5 with childhood non-T-ALL and 3 with reactive lymphadenitis, were investigated using a direct immunohistochemical method to detect alpha-, beta- and gamma-enolases. alpha-Enolase-positive cells were not observed in reactive lymphadenitis. On the contrary, almost all the lymphocytes including germinal center cells were positive for beta-enolase. Small lymphocytes in the mantle zones were negative, centrocytes were negative or weakly positive, the majority of centroblasts were strongly positive and the remaining were weakly positive for gamma-enolase. In all 5 patients with childhood non-T-ALL, leukemic lymphocytes were strongly positive only for alpha-enolase. In all 33 patients with B cell lymphoma, lymphoma cells were positive for beta-enolase. In many patients with follicular lymphoma, lymphoma cells were positive only for beta-enolase. Four of five patients with malignant lymphoma, diffuse, small cleaved cell, showed the reactivity of alpha-, beta+, gamma+-enolases in lymphoma cells. Our results suggest the possibility of the two isoenzyme switches from alpha- to beta-enolase and from alpha- to gamma-enolase in the B lymphocyte lineage accompanying differentiation, similar to those of skeletal muscles and neurons.
 ...
PMID:Expression of enolases in B cell tumors. 264 88

T lymphomas are classified into two types from surface phenotype, thymic T (T1) and Peripheral T (T2) lymphoma, and T2 lymphomas, are furthermore subdivided to inducer/helper (Ti/h or T4) and cytotoxic/suppressor (Tc/s or T8) type. But even in ATLL (adult T cell leukemia/lymphoma) believed to be a model of Ti/h type, the heterogeneities of surface phenotype are reported frequently. All of the pleomorphic and lymphoblastic and a part of small cell, medium-sized cell, mixed and large cell types have a T-cell phenotype. In addition to these histologies, AILD/IBL/IBL-like T lymphoma, T-zone lymphoma and So-called Lennert's lymphoma also hold T-cell nature. The heterogenecity and the existence of the borderline area between neoplasm and reactive lymphadenitis or hyperplasia often confused the clinicians and hematopathologists. From our experience, forty nine percent 5 year survival of T lymphoma other than lymphoblastic and pleomorphic type suggests the propriety of classifying T lymphoma into high grade and intermediate grade malignancies. Treatment of T lymphomas are basically distinguishable to two categories, for T1 and T2 lymphomas. The treatment of T1 lymphoma should be an aggressive one including CNS prophylaxis. At present, the recommendable treatment of T2 lymphoma is to apply the best regimens obtained from B cell lymphoma study. As aggressive treatment for ATL does not always yield favorable results, the concept of therapy will become clear near future. An intensive supportive therapy including T-S prophylaxis should be combined actively in the treatment program.
 ...
PMID:[Pathological features and treatment of T lymphoma]. 348 2

Cell suspensions obtained from 54 human lymph nodes involved by different pathological conditions were characterized by conventional markers and by the OKT-3, OKT-4, OKT-8, OKIa-1, and OKM-1 monoclonal antibodies. In 18 cases of reactive lymphoid hyperplasia, the majority of lymph node cells were mature T lymphocytes (E-RFC = 56 +/- 9%; OKT-3+ = 63 +/- 10%); among T-cell subsets, OKT-4+ cells were 49 +/- 8% whereas OKT-8+ cells were 21 +/- 8% (T4/T8 = 2.7 +/- 1.1). This distribution of T-cell phenotypes was not similar in the different histological types of reactive lymphoid hyperplasia. In fact, an increase in the percentage of OKT-8+ cells (25 +/- 9%; P less than 0.05) and a decrease in the values of the T4/T8 ratio (2.1 +/- 1.0; P less than 0.05) were observed in 9 cases of reactive lymphoid hyperplasia of follicular type when they were compared to the mixed and sinus types. In 13 lymph nodes involved by B-cell lymphoma, the percentage of T lymphocytes was markedly reduced (E-RFC = 21 +/- 12%; OKT-3+ = 27 +/- 18%) and the percentage of OKIa-1+ cells (51 +/- 15%) was significantly (P less than 0.01) increased as compared to reactive nodes; in addition, in these cell suspensions, an increase in the relative proportion of OKT-8+ cells (T4/T8 = 1.4 +/- 0.7; P less than 0.01) could also be demonstrated. Finally, a clear prevalence of OKT-4+ cells on OKT-8+ cells was demonstrated in 5 cases of tuberculous lymphadenitis (T4/T8 = 3.9 +/- 1.5; NS) and in 18 cases of Hodgkin's disease (T4/T8 = 4.2 +/- 2.0; P less than 0.01). In tuberculous lymphadenitis, a significant increase (P less than 0.01) in the percentage of OKM-1+ cells could also be demonstrated.
 ...
PMID:T-lymphocyte subsets in human lymph nodes: relative increase of OKT-8+ cells in neoplastic and reactive B-cell proliferation. 660 99

To distinguish reactive versus neoplastic monocytoid B-cell (MBC) proliferations, the clonality of MBC was examined in paraffin-embedded tissues by in situ hybridization (ISH) of immunoglobulin (Ig) light chain messenger RNA (mRNA) with sensitive oligonucleotide probes in 26 cases. They included 13 cases of lymphadenitis with MBC reaction and 13 cases of nodal (n = 8) and extranodal (n = 5) monocytoid B-cell lymphoma (MBCL). Two cases represented a composite lymphoma showing a centroblastic-centrocytic and MBCL component. The clonality of MBC infiltrates could be demonstrated in 16 of 26 (61.5%) cases by immunostaining for Ig light chains and in all (100%) cases by ISH. Neoplastic MBC usually expressed a faint-to-moderate light chain restriction of mRNA, whereas some MBC (10% to 30% of total MBCL population) showed a strong positivity irrespective of plasmacytoid differentiation as indicated by Ig immunostaining (present in 9 of 13 cases). Reactive MBC expressed a faint kappa and lambda light-chain mRNA positivity. Five percent to 20% of total reactive MBC showed also a strong positivity for both Ig light chain mRNA, although only a minor part of these cells (7 of 13 cases) expressed polyclonal Ig by immunohistochemistry. These results indicate that (1) both reactive and neoplastic MBC can differentiate into plasma cells; and (2) a relatively high percentage of reactive and neoplastic MBC show a detectable mRNA transcription, but not a corresponding Ig synthesis. Either the Ig detection is not sensitive enough or these cells might be in an early differentiation phase, where the Ig production has not yet started.
 ...
PMID:Reactive versus neoplastic monocytoid B-cell proliferations. In situ hybridization study of immunoglobulin light chain mRNA. 787 56

Benign monocytoid B cells are seen in lymph nodes in different types of lymphadenitis and they occur in the form of clusters within and around sinuses and in the interfollicular areas, but rarely completely surround benign follicles to produce a marginal-zone pattern. The cytologic hallmark of these cells is the presence of abundant pale to clear cytoplasm; these cells usually are of medium size, and they have a rather bland-appearing, irregular nuclei with inconspicuous nucleoli. Malignant monocytoid B-cell proliferations in a lymph node have been classified as monocytoid B-cell lymphomas (MBCL), which are now called nodal marginal-zone B-cell lymphoma (MZL) in the World Health Organization (WHO) classification. In the recently published clinical evaluation of the International Lymphoma Study Group classification of non-Hodgkin's lymphoma, 25 of 1,378 cases (1.8%) were classified as primary MZL, whereas four times as many cases (105 or 7.6%) were classified as low-grade mucosa-associated lymphoid tissue (MALT)-type lymphoma. Transformation to large-cell lymphoma at the time of diagnosis was seen in five of 25 (20%) cases of nodal MZL and in 32 of 105 (30%) cases of MALT-type lymphoma. Comparison of the clinical findings at presentation and the survival results indicate that nodal MZL is more aggressive clinically than low-grade MALT-type lymphoma. For example, patients with nodal MZL had a significantly higher incidence of advanced-stage disease, including peripheral and paraaortic lymphadenopathy, than those with MALT-type lymphoma. Moreover, patients with nodal MZL had lower 5-year overall survival and failure-free survival than patients with MALT type lymphoma. When analysis was restricted to those patients with zero to three adverse risk factors in the International Prognostic Index, patients with nodal MZL still had a significantly lower overall and failure-free survival at 5 years than patients with MALT-type lymphoma. We conclude that nodal MZL is a distinctive disease entity and is similar to other low-grade nodal lymphomas, such as the follicular or small lymphocytic lymphomas, but different than MALT-type lymphoma.
 ...
PMID:Nodal monocytoid B-cell lymphoma (nodal marginal-zone B-cell lymphoma). 1031 81

A definitive diagnosis of T-cell lymphoma may be contingent on the rearrangement profile of the T-cell receptor. This is most accurately done by molecular analysis of the beta-chain of the T-cell receptor (TCR beta) by Southern blotting hybridization that requires unfixed tissue. We describe a reverse transcriptase in situ PCR (RT in situ PCR) method that permits the target-specific direct incorporation of the reporter nucleotide into the different transcripts that comprise the TCR beta, using paraffin-embedded, formalin-fixed tissue. Each of the 25 possible V beta segment rearrangements was documented in three lymph nodes with nonspecific lymphadenitis, with clonal expansion evident in a case of metastatic melanoma. Monoclonal expression was documented in seven tissues diagnostic of a T-cell lymphoma. We analyzed five additional tissues for which a definitive diagnosis of T-cell vs B-cell lymphoma could not be rendered on the basis of histological, immunohistological, and flow cytometric analysis. RT in situ PCR for TCR beta expression with CD3 co-labeling demonstrated which of these lesions was a B-cell-rich T-cell lymphoma. We conclude that the RT in situ PCR methodology will allow the routine determination of monoclonal vs multiclonal expression patterns of the TCR beta using archival paraffin-embedded tissues.(J Histochem Cytochem 49:139-145, 2001)
 ...
PMID:In situ determination of T-cell receptor beta expression patterns. 1115 82

Sections of surgical lymph-node biopsies of four types of malignant non-Hodgkin's lymphoma of B-cell origin (B-NHL) classified according to the R.E.A.L. terminology or lymphadenitis were immunostained in order to demonstrate endothelial CD34 (QBEnd 10) and to determine the microvascular density and vessel-size distribution using an interactive image-analysis technique. Only microvessels displaying a cross-sectional area corresponding to a diameter of between 3.2 and 34.6 microm were included. The intratumoral microvascular density (iMVD) was found to be significantly higher in chronic lymphatic leukaemia (CLL, n = 13) compared with the clinically more aggressive mantle cell lymphoma (MCL, n = 9) and diffuse large B-cell lymphoma (DLBCL, n = 14). iMVD in CLL was also higher than in the follicular neoplastic parts (FL FOLL) of follicular lymphoma (FL, n = 16). In FL FOLL the microvessel density was, moreover, significantly lower than in the surrounding non-neoplastic FL tissue. In lymphadenitis (LA, n = 10) the iMVD was higher than in DLBCL, FL FOLL and MCL. The data suggest that future studies focusing on the relationship between iMVD and the clinical outcome within each particular NHL group should be carried out in order to verify whether iMVD is a prognostic factor in NHL, as it is in carcinomas.
 ...
PMID:Intratumoral microvascular density in malignant lymphomas of B-cell origin. 1129 95

The cyclin-dependent kinase inhibitor p57(KIP2) is thought to be a potential tumor suppressor gene (TSG). The present study examines this possibility. We found that the expression of p57(KIP2) gene is absent in various hematological cell lines. Exposing cell lines to the DNA demethylating agent 5-aza-2'-deoxycytidine restored p57(KIP2) gene expression. Bisulfite sequencing analysis of its promoter region showed that p57(KIP2) DNA was completely methylated in cell lines that did not express the p57(KIP2) gene. Thus, DNA methylation of its promoter might lead to inactivation of the p57(KIP2) gene. DNA methylation of this region is thought to be an aberrant alteration, since DNA was not methylated in normal peripheral blood mononuclear cells or in reactive lymphadenitis. Methylation-specific polymerase chain reaction analysis found frequent DNA methylation of the p57(KIP2) gene in primary diffuse large B-cell lymphoma (54.9%) and in follicular lymphoma (44.0%), but methylation was infrequent in myelodysplastic syndrome and adult T-cell leukemia (3.0% and 2.0%, respectively). These findings directly indicate that the profile of the p57(KIP2) gene corresponds to that of a TSG.
 ...
PMID:Aberrant DNA methylation of p57(KIP2) gene in the promoter region in lymphoid malignancies of B-cell phenotype. 1223 71


1 2 3 Next >>