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

Molecular diagnostics in low grade B cell lymphoma is currently based on polymerase chain reaction (PCR) detection of lymphoid clonality or of molecular (onco)genetic markers that result from chromosomal translocations. The former is based on detection of clonal immunoglobulin (Ig) and/or T cell receptor (TCR) rearrangements, which can be used for distinguishing between malignant and reactive lymphoproliferation, for staging, for comparison of diagnostic and relapse material and for minimal residual disease assessment. Informativity has risen with the development of improved, standardised DNA-based Ig/TCR strategies but remains dependent on tumour subtype, largely as a function of the rate of IgH somatic mutation. PCR-based detection of molecular genetic markers can aid diagnosis, although genetic breakpoint heterogeneity and low level molecular informativity means that alternative techniques, such as fluorescent in situ hybridisation or immunohistochemistry of the deregulated genes, can be preferable. Appropriate molecular diagnostic practise is entirely dependent on the conservation of appropriate material, with the increasing tendency for RNA based diagnostics, particularly for transcriptional profiling, rendering tissue banking of unfixed material extremely important. Therapeutic stratification of patients with low grade lymphoma is likely to be increasingly based on multiparameter genetic and/or immunological analysis, with monoparameter targets being reserved for follow-up. Appropriate use of the increasing number of analytical techniques available is best applied in specialised diagnostic platforms with a complementary, interdisciplinary approach that can be adapted to the clinical situation.
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PMID:Clinical impact of molecular diagnostics in low-grade lymphoma. 1569 87

Clonal diversity of the immunoglobulin (Ig) gene rearrangement represents the oligoclonality of B-cell neoplasm, and has been shown to be a marker for poor prognosis in acute lymphoblastic leukemia. However, no previous report has addressed its prognostic impact in diffuse large B-cell lymphoma (DLBCL). We investigated the clinical significance of clonal diversity in DLBCL patients. Lymph node samples from 98 DLBCL patients were examined for Ig heavy and light chain gene rearrangements using Southern blot analysis. Clonal diversity was defined as oligoclonality detected on Southern blotting as previously described, and PCR analysis for IgH oligoclonality was performed on parts of DLBCL samples with clonal diversity for confirming the Southern blot analysis results. We found that clonal diversity could be detected in 36 (36.7%) of DLBCL patients, and PCR analysis showed concordant results. Regarding the clinical relevance, clonal diversity was significantly associated with relapse or refractory disease. Survival analysis showed that clonal diversity is an independent prognostic factor in DLBCL (p=0.05, Cox's proportional hazard method), and stratified analyses found the most significant subgroup is the high-intermediate risk category (p=0.01, log-rank test). We conclude that clonal diversity of Ig gene rearrangements is associated with a high risk of relapse or refractory disease in DLBCL patients. It is also a factor of poor prognosis in DLBCL, especially for high-intermediate risk category.
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PMID:Prognostic significance of clonal diversity of immunoglobulin gene rearrangements in patients with diffuse large B-cell lymphoma. 1570 25

T-cell/histiocyte-rich large B-cell lymphoma (THRLBCL), a proliferating peripheral B-cell neoplasm, is a morphologic variant of diffuse large B-cell lymphoma (DLBCL), which may be confused with Hodgkin's lymphoma, non-Hodgkin's lymphoma, and reactive lymphadenopathies. Though more recent studies suggested that it might be a distinct clinicopathologic entity and/or a heterogeneous entity with derivation from germinal center B cells, its histogenetic derivation remains controversial. The authors analyzed 30 cases of THRLBCL to further characterize the origin of the neoplastic cells using immunohistochemical and molecular studies for expression of Bcl-6, CD10, and CD138, as well as rearrangements of IgH/bcl-2 genes on paraffin-embedded tissue. Half of the cases (15/30) showed Bcl-6 expression and five cases (19%) showed CD10 expression, but none had CD138 expression (0/20). Only three cases showed coexpression of both Bcl-6 and CD10. Molecular studies performed in 21 cases detected rearrangement of immunoglobulin heavy gene in 18 cases, with none having detectable Bcl-2 gene rearrangement. These data indicate that similar to DLBCL, the cell origin of neoplastic cells in THRLBCL is composed of a heterogeneous group of proliferating peripheral B cells, with only some cases originating from germinal center B cells and others derived from heterogeneous origins. Lack of Bcl-2 gene rearrangements seems to argue against a possible progression from preexisting follicular lymphoma. Thus, the normal counterpart of the neoplastic cells cannot at this time be the sole basis for the subclassification of THRLBCL.
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PMID:T-cell/histiocyte-rich large B-cell lymphoma displays a heterogeneity similar to diffuse large B-cell lymphoma: a clinicopathologic, immunohistochemical, and molecular study of 30 cases. 1589 21

We report an instructive case of diffuse large B-cell lymphoma presenting as acute heart failure. A 69-year-old human immunodeficiency virus-negative man was admitted to our hospital for general fatigue. A computed tomographic scan of the chest and abdomen showed pericardial effusion, but there was no evidence of tumor masses, lymph node enlargement, or hepatosplenomegaly. During the chemotherapy, increased lactate dehydrogenase and pleural effusion appeared. The tumor cells in the effusion showed positivity for CD5, CD19, CD20, kappa chain, and Bcl-2 and negativity for CD10 and CD23. The chromosomes showed t(8;14)(q24;q32) with c-myc/immunoglobulin (Ig)H rearrangement, and the MIB-1 index was not high (60%). Neither human herpes virus 8 nor Epstein-Barr virus DNA was detected in the cells by polymerase chain reaction. The response to chemotherapy was very poor, and the patient died 4 months after the diagnosis. A spectrum of the symptoms of CD5+ lymphoma encompasses pericardial effusion and also can accompany c-myc/IgH rearrangement.
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PMID:CD5+ diffuse large B-cell lymphoma with c-myc/IgH rearrangement presenting as primary effusion lymphoma. 1591 62

Clonally related composite lymphomas of Hodgkin's lymphoma (HL) and Non-Hodgkin's lymphoma (NHL) represent models to study the multistep transformation process in tumorigenesis and the development of two distinct tumors from a shared precursor. We analyzed six such lymphomas for transforming events. The HLs were combined in two cases with follicular lymphoma (FL), and in one case each with B-cell chronic lymphocytic leukemia, splenic marginal zone lymphoma, mantle cell lymphoma (MCL) and diffuse large B-cell lymphoma (DLBCL). In the HL/FL and HL/MCL combinations, BCL2/IGH and CCND1/IGH translocations, respectively, were detected in both the HL and NHL. No mutations were found in the tumor suppressor genes FAS, NFKBIA and ATM. The HL/DLBCL case harbored clonal replacement mutations of the TP53 gene on both alleles exclusively in the DLBCL. In conclusion, we present the first examples of molecularly verified IgH-associated translocations in HL, which also show that BCL2/IGH or CCND1/IGH translocations can represent early steps in the pathogenesis of composite HL/FL or HL/MCL. The restriction of the TP53 mutations to the DLBCL in the HL/DLBCL case exemplifies a late transforming event that presumably happened in the germinal center and affected the fate of a common lymphoma precursor cell towards development of a DLBCL.
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PMID:Insights into the multistep transformation process of lymphomas: IgH-associated translocations and tumor suppressor gene mutations in clonally related composite Hodgkin's and non-Hodgkin's lymphomas. 1597 55

Several patterns of association between Hodgkin and non-Hodgkin lymphomas are recognized, some of which support a common cellular origin or shared transformation events for both malignancies. We describe the U-2940 cell line derived from a diffuse large B-cell lymphoma with some features consistent with mediastinal large B-cell lymphoma, clinically apparent 1 month after the initial course of chemotherapy for Hodgkin's disease, fulfilling the criteria for composite malignancies. U-2940 cells display a mature B phenotype with hypermutated IgH rearrangement typical of germinal/postgerminal center origin. The cell line is negative for Epstein-Barr virus and no evidence of t(14;18) was found. U-2940 cells display multiple chromosomal rearrangements similar to recurrent aberrations described in both Hodgkin and non-Hodgkin lymphomas, also partially shared by U-2932 derived from a B-cell lymphoma sequential to Hodgkin's disease. The original large B-cell lymphoma and the U-2940 cell line bear microsatellite instability, an abnormality associated with particular subtypes of non-Hodgkin lymphomas and found in tissues involved by Hodgkin lymphoma. Therefore, U-2940 cells bear several features known to occur in Hodgkin and in non-Hodgkin lymphomas, leading to the assumption that this cell line may constitute a useful tool to address elective pathways of lymphomagenesis and eventually the Hodgkin and non-Hodgkin lymphoma association.
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PMID:U-2940, a human B-cell line derived from a diffuse large cell lymphoma sequential to Hodgkin lymphoma. 1610 19

Rituximab is a chimeric anti-CD20 monoclonal antibody. It has shown efficacy in patients with B-cell non-Hodgkin lymphoma and also in CD20-positive Hodgkin lymphoma. Recently, CD20-negative tumors have been described after Rituximab therapy. We report a 34-year-old man with a history of nodular lymphocyte-predominant Hodgkin lymphoma (NLPHL), treated with different chemotherapy regimens, including anthracyclines and Rituximab. After 4 years in complete remission, he developed a CD20-negative T-cell-rich B-cell lymphoma (TCRBCL) presenting as multiple lung lesions. This case shows the difficulties in the diagnosis of CD20-negative lymphomas when the number of tumor cells is low and when they are found in a predominant T-cell context. Using anti-CD79a as a B-cell marker is mandatory to overcome the difficulties in identifying these tumors. Moreover, this case illustrates the usefulness of laser capture microdissection to obtain purified cell populations for molecular studies in lymphomas with relative paucity of tumor cells, as well as the need to analyze different IgH gene regions to decrease the rate of false-negative results in PCR clonality studies.
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PMID:CD20-negative T-cell-rich B-cell lymphoma as a progression of a nodular lymphocyte-predominant Hodgkin's lymphoma treated with rituximab: a molecular analysis using laser capture microdissection. 1616 Apr 85

The translocation t(1 ; 14)(p22 ; q32) has been reported only in cases of mucosa-associated lymphoid tissue (MALT) lymphomas. Moreover, bcl-10 is a novel apoptotic signaling gene located at 1p22 and t(1 ; 14)(p22 ; q32) may directly expose bcl-10 to Ig somatic hypermutation. A recent report indicates a pathogenic role of bcl-10 mutation in the progression of MALT lymphomas. In this report, we describe the first case of multiple extranodal diffuse large B-cell lymphoma (DLBCL) with t(1 ; 14)(p22 ; q32). A 70-year-old woman was diagnosed as having DLBCL of multiple extranodal sites (lung, duodenum, colon and kidney). Cytogenetic analysis of a renal lesion revealed the chromosome translocations t(1 ; 14)(p22 ; q32) and both IgH and bcl-10 gene rearrangements were confirmed by Southern blot hybridization. The patient received a regimen of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP). She achieved complete remission after six cycles of chemotherapy and has been free of disease for more than five years. This is the first case of bcl-10 gene rearrangement in DLBCL with t(1 ; 14)(p22 ; q32) and this gene may be involved in the pathogenesis of aggressive lymphomas such as MALT lymphomas or in the progression of MALT lymphomas.
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PMID:[Long-term remission after CHOP therapy in a case of multifocal extranodal diffuse large B-cell lymphoma with t(1 ; 14) (p22 ; q32) and rearrangement of bcl-10]. 1644 Jul 71

A 71-year-old man with high fever and enlargement of the bilateral submandibular, cervical and inguinal lymph nodes was hospitalized at Hiroshima University Hospital. The immunohistochemical and pathologic findings from the biopsy specimens led to the diagnosis of angioimmunoblastic T-cell lymphoma (AILT) with a cluster of CD20-positive cells. Flow cytometry analysis by two-color staining did not reveal any neoplastic B cells. Southern blot analysis showed rearrangement of both the IgH gene and the TCR gene. Furthermore, PCR of the IgH gene using DNA extracted from purified CD19-positive cells from the lymph nodes showed a monoclonal band, and it was different from that of purified CD138-positive cells from the bone marrow. Furthermore, monoclonal Epstein-Barr virus (EBV) infection was detected with PCR using the SL18 and SL19 primers of the LMP-1 gene. Numerous EBER-positive cells were detected diffusely in the lymph nodes. These findings indicated a diagnosis of angioimmunoblastic T-cell lymphoma complicated with EBV-associated B-cell lymphoma, and that immunodeficiency in AILT led to an expansion of EBV infected B-cells.
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PMID:[Angioimmunoblastic T-cell lymphoma complicated with EBV-associated B-cell lymphoma]. 1644 6

Four cases of central nervous system (CNS) lymphoma are reported which presented obstacles in diagnosis due to steroid treatment prior to biopsy. Reliable diagnoses were provided by molecular analysis. Malignant lymphoma of the CNS may be indistinguishable from other conditions, even in view of the gravity of the diagnosis. All patients had a previous history of glucocorticoid injection, for 2-18 days prior to stereotactic brain biopsy. The pathologic examination revealed in all cases axonal destruction and reactive gliosis with a variable infiltration of B- or T lymphocytes and macrophages. Characteristically, scattered degenerating small round cells with pyknotic or fragmented nuclei were also observed. However, the molecular assessment of paraffin-embedded tissues revealed the monoclonal IgH gene rearrangement, which allowed the confident diagnosis of B cell lymphoma. The histopathological findings of the present cases suggest that the tumor cells might be selectively destroyed by steroid treatment, which may render diagnosis impossible. Thus, molecular genetic investigation constitutes an important tool for establishing a diagnosis of CNS lymphoma obscured by steroid administration. This is especially true in cases where a paucity of tumor cells is observed or when monoclonality fails to be demonstrated by immunohistochemical tests.
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PMID:Malignant lymphoma of the central nervous system: difficult histologic diagnosis after glucocorticoid therapy prior to biopsy. 1646 72


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