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)

Infectious etiology has been confirmed only in a few lymphoproliferative disorders such as human T-cell lymphotropic virus in adult T-cell leukemia lymphoma, Epstein-Barr virus in African-type Burkitt's lymphoma and Hodgkin's disease, and Helicobacter pylori infection in primary gastric B-cell lymphoma. In recent years, Ferri and colleagues have found hepatitis C virus (HCV) association with non-Hodgkin's lymphoma (NHL) in Italy. The aim of our study was to determine the HCV association in NHL patients in Antalya. Forty-eight patients (22 women and 26 men, with a median age of 52 years) with NHL were included in the study. The control group consisted of 28 patients with various hematological disorders (11 women and 17 men with a median age of 50 years). Anti-HCV antibodies were investigated in 48 patients, and HCV RNA was assessed in 35 of them. Anti-HCV antibodies were found to be negative in the NHL group, but HCV RNA was positive in the serum of three patients (8.6%), who were diagnosed with diffuse small cell lymphoma (19%). Anti-HCV antibodies and HCV RNA were negative in the control group. Since HCV association with NHL has previously been reported in Italy, it is likely that both genetic and environmental factors in the Mediterranean sea-region may be involved in the oncogenesis in HCV RNA-positive patients. Multicenter studies with large patient groups will disclose the true association of HCV with NHL in Turkey.
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PMID:Hepatitis C virus association with non-Hodgkin's lymphoma. 1043 70

We have used YAC (yeast artificial chromosome) technology to create large translocation regions where the c-myc proto-oncogene is coupled to the core region of the human immunoglobulin heavy chain (IgH) locus (from VH2-5 through to Cdelta). Chimeric mice were obtained from embryonic stem cells carrying a single copy of the 240-kb IgH/c-myc translocation region. B-cell tumorigenesis occurs in the translocus mice, even when the entire Emu intron enhancer region between the joining segments and switch mu is deleted. This demonstrates that as yet unidentified regulatory elements in the IgH locus, independent from the known enhancers, are sufficient to cause B-cell specific activation of c-myc after translocation. The phenotype of tumors from IgH/c-myc YAC transgenic mice with or without Emu (B220+, IgM+/IgD+) is reminiscent of Burkitt's lymphoma. A rapidly expanding abnormal B-cell population is present at birth and accumulates in bone marrow, periphery, and spleen, well before discrete tumor establishment. Molecular analysis identified a clonal origin, with rearrangement of one mouse heavy chain allele retained in tumor cells from different sites, whereas subsequent rearrangements of heavy or light chain loci can be diverse. These mice routinely develop mature B-cell tumors early in life and may provide an invaluable resource of a B-cell lymphoma model.
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PMID:B-cell tumorigenesis in mice carrying a yeast artificial chromosome-based immunoglobulin heavy/c-myc translocus is independent of the heavy chain intron enhancer (Emu). 1055 44

Few large series compare lymphomas of the nasal cavity with those of the paranasal sinuses. We studied the cases of 58 patients, 34 males and 24 females, aged 7 to 92 years (mean, 57 years), who had lymphoma involving the nasal cavity or paranasal sinuses. Thirty-three patients had diffuse large B-cell lymphoma (DLBCL). Twenty-three were male and 10 were female, with an age range of 7 to 91 years (mean, 63 years); two were HIV-positive. Only 2 of 11 cases tested (one in an HIV-positive patient and one of lymphomatoid granulomatosis type) were Epstein-Barr virus (EBV)-positive. Thirty (91%) involved paranasal sinuses, 10 with nasal involvement, whereas three cases had nasal, but not sinus, involvement. At last follow-up, 16 (67%) were free of disease 7 to 169 months later (mean, 65 months), and 8 (33%) had died of disease 2 to 166 months later (mean, 45 months). Seventeen patients had nasal-type natural killer (NK)/T-cell lymphoma. There were 10 women and 7 men, aged 27 to 78 years (mean, 48 years). Thirteen of 14 were EBV-positive. Sixteen patients had nasal involvement, eight with sinus involvement. Eleven (73%) of 15 were alive and well 6 to 321 months later (mean, 139 months), three (20%) died of lymphoma 1, 11, and 12 months later, and one (7%) is alive with disease. There was one case each of marginal zone B-cell lymphoma, Burkitt's lymphoma, Burkitt-like lymphoma, peripheral T-cell lymphoma of unspecified type, and adult T-cell lymphoma/leukemia. In an additional three cases, the lymphomas were composed predominantly of large cells, but no immunophenotyping could be performed for subclassification. In 19 cases (17 DLBCLs, 1 Burkitt-like lymphoma, and 1 lymphoma of uncertain lineage), presenting symptoms included complaints related to the eyes. In 16 cases (13 DLBCLs, 1 Burkitt-like lymphoma, 1 nasal NK/T-cell lymphoma, and 1 lymphoma of uncertain lineage), the orbit was invaded by lymphoma. In our series, the most common lymphoma to arise in the sinonasal area is DLBCL, followed by nasal NK/T-cell lymphoma. Comparison of these two types of lymphoma showed that lymphomas involving sinuses without nasal involvement were predominantly DLBCLs (20 of 21), whereas nasal cavity lymphomas without sinus involvement were usually NK/T-cell type (8 of 11) (p = 0.000125). Compared with patients with DLBCL, patients with nasal NK/T-cell lymphoma were overall younger, with a lower male-to-female ratio. Lymphomas of B-cell lineage were more likely to be associated with symptoms related to the eyes (p < 0.0005) and to have extension to the orbit (p < 0.01) than were lymphomas of T- or NK-cell lineage. In contrast to results of Asian studies in which nasal NK/T-cell lymphoma has a very poor prognosis, our nasal NK/T-cell lymphomas had an outcome similar to that of DLBCL.
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PMID:Sinonasal lymphoma: a clinicopathologic analysis of 58 cases from the Massachusetts General Hospital. 1055 4

Long-circulating submicron lipid emulsions, stabilized with poly(ethylene glycol)-modified phosphatidylethanolamine (PEG-PE), are promising drug carriers with substantial capacity for solubilization of lipophilic anticancer agents. This study describes the conjugation of the anti-B-cell lymphoma monoclonal antibody LL2 to the surface of lipid-emulsion globules by use of a novel poly(ethylene glycol)-based heterobifunctional coupling agent. The efficiency of coupling of LL2 to the lipid emulsion was 85% (approx.) and essentially independent of the LL2/emulsion particle ratio and amount of surface-bound PEG-PE. Results from sucrose-gradient centrifugation and Sepharose CL-4B gel filtration indicated stable binding of the antibody to the emulsion. The immunoreactivity of the emulsion-LL2 conjugates was tested with alkaline phosphatase-conjugated LL2 against a monoclonal anti-idiotype antibody, WN. The binding of the conjugates to WN increased with increasing surface density of LL2 up to 40 monoclonal antibodies/emulsion particle, and exceeded that for the free monoclonal antibody (approx. 20 molecules/particle). Results from competitive-binding ELISA were indicative of similar displacement curves for free LL2 and emulsion-LL2 conjugates. Direct cellular ELISA revealed similar binding of emulsion-LL2 complexes to three types of Burkitt's lymphoma cell lines, Raji, Ramos and Daudi. The results from this study indicate that emulsion-LL2 complexes might be a useful drug-carrier system for more specific delivery of anticancer drugs to B-cell malignancy.
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PMID:Conjugation of an anti-B-cell lymphoma monoclonal antibody, LL2, to long-circulating drug-carrier lipid emulsions. 1057 80

Besides the problems inherent in endoscopically obtained tissue and the low incidence of intestinal lymphomas, the major difficulties reside in the distinction to reactive processes and in the differential diagnosis among several lymphoma entities. Knowledge of the microanatomical and biological properties of the intestinal MALT, supplemented by sufficient clinical information, are important prerequisites for the diagnostic work-up which has to include immunohistochemical studies. Whereas the diagnosis of aggressive B-cell lymphomas (diffuse large B-cell lymphoma, Burkitt's lymphoma) is usually straightforward, lymphomatous polyposis (LP, the intestinal equivalent of mantle cell lymphoma) and low-grade B-cell lymphoma of MALT-type may be difficult to diagnose and to separate from reactive lymphoproliferations. The characteristic immunohistochemical profile of LP (cyclin D1 + CD5 + CD43 + CD23 - CD10 - IgM kappa or lambda, is very helpful in this regard and similarly useful to exclude intestinal involvement by B-CLL or follicular center lymphoma. In addition, the endoscopic appearance characterized by seeds of small polyps along the colorectum favors LP although MALT-type lymphoma may occasionally produce polypoid lesions. Focal lymphoid hyperplasia occurs in the terminal ileum and may present with a mass in the right iliac fossa. The diagnosis of intestinal T-cell lymphoma (ITL) represents the most challenging task for both clinicians and pathologists. This disease is often associated with and may closely mimick celiac disease of adult onset type, or can be misdiagnosed as inflammatory bowel disease. The presence of an abnormal activated T-cell phenotype, i.e. different from that of normal intraepithelial lymphocytes, strongly suggests ITL and is of particular importance in cases that lack overt cytological atypia.
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PMID:[Problems in biopsy differential diagnosis in lymphomas of the small and large intestines]. 1071 99

Primary brain lymphoma (PBL) is an uncommon extranodal lymphoma. Its incidence is rapidly increasing in both immunocompromised and immunocompetent patients in Western countries. Eighteen cases of PBL were identified during a 16-year period among HIV negative patients in Queen Mary Hospital, Hong Kong. One case of post-transplantation lymphoproliferative disease (PTLD) was positive for Epstein Barr virus (EBV) encoded RNA (EBER) by in situ hybridization. All the remaining 17 immunocompetent cases were classified as diffuse large B-cell lymphoma, except for one case of Burkitt's lymphoma. EBER expression was negative in all 13 cases tested. Immunostaining for bcl-2 and bcl-6 was positive in 8/11 and 6/11 cases tested, with heterogeneous combination of expression and intensity. The incidence rate of PBL in immunocompetent patients was stable at 1.03 per million per year. The incidence of PBL in post transplantation (0.16%) and HIV related setting (0.29%) is also low in Chinese. PBL in Chinese patients is almost uniformly represented by EBV negative, diffuse large B-cell lymphoma, confined to the brain. However, the molecular pathogenesis may be heterogeneous.
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PMID:Incidence and pathology of primary brain lymphoma in Hong Kong Chinese patients. 1072 83

It has been known for 30 years that Epstein-Barr virus (EBV), a ubiquitous human herpesvirus, is the etiologic agent of acute infectious mononucleosis and is closely associated with the genesis of Burkitt's lymphoma and undifferentiated nasopharyngeal carcinoma. Recent studies have demonstrated that EBV is also implicated in a variety of other diseases, such as EBV-associated hemophagocytic syndrome, chronic active EBV infection, T-cell lymphoma, natural killer cell leukemia/lymphoma, lymphoproliferative diseases in immunocompromised hosts, Hodgkin's disease, pyothorax-associated B-cell lymphoma, smooth-muscle tumors, and gastric carcinoma. Thus, the virus continues to attract worldwide attention, and it is now appropriate for a reappraisal of the relation between EBV and human diseases. This review summarizes the recent progress in research on EBV and the clinical findings of EBV-associated diseases and provides a basis for the development of new therapeutic strategies.
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PMID:Epstein-Barr virus--associated diseases in humans. 1074 21

Cancer susceptibility genes have been classified into two groups: gatekeepers and caretakers. Gatekeepers are genes that control cell proliferation and death, whereas caretakers are DNA repair genes whose inactivation leads to genetic instability. Abrogation of both caretaker and gatekeeper function markedly increases cancer susceptibility. Although the importance of Ku80 in DNA double-strand break repair is well established, neither Ku80 nor other components of the non-homologous end-joining pathway are known to have a caretaker role in maintaining genomic stability. Here we show that mouse cells deficient for Ku80 display a marked increase in chromosomal aberrations, including breakage, translocations and aneuploidy. Despite the observed chromosome instabilities, Ku80-/- mice have only a slightly earlier onset of cancer. Loss of p53 synergizes with Ku80 to promote tumorigenesis such that all Ku80-/- p53-/- mice succumb to disseminated pro-B-cell lymphoma before three months of age. Tumours result from a specific set of chromosomal translocations and gene amplifications involving IgH and c-Myc, reminiscent of Burkitt's lymphoma. We conclude that Ku80 is a caretaker gene that maintains the integrity of the genome by a mechanism involving the suppression of chromosomal rearrangements.
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PMID:DNA repair protein Ku80 suppresses chromosomal aberrations and malignant transformation. 1078 75

Chromosomal rearrangements observed in T-cell prolymphocytic leukemia involve the translocation of one T-cell receptor gene to either chromosome 14q32 or Xq28, deregulating the expression of cellular protooncogenes of unknown function, such as TCL1 or its homologue, MTCP1. In the human hematopoietic system, TCL1 expression is predominantly observed in developing B lymphocytes, whereas its overexpression in T cells causes mature T-cell proliferation in transgenic mice. In this study, using a newly generated monoclonal antibody against recombinant TCL1 protein, we extended our analysis mainly by immunohistochemistry and also by fluorescence-activated cell sorting and Western blot to a large tumor lymphoma data bank including 194 cases of lymphoproliferative disorders of B- and T-cell origin as well as reactive lymphoid tissues. The results obtained show that in reactive lymphoid tissues, TCL1 is strongly expressed by a subset of mantle zone B lymphocytes and is expressed to a lesser extent by follicle center cells and by scattered interfollicular small lymphocytes. In B-cell neoplasia, TCL1 was expressed in the majority of the cases, including lymphoblastic lymphoma, chronic lymphocytic leukemia, mantle cell lymphoma, follicular lymphoma, Burkitt lymphoma, diffuse large B-cell lymphoma (60%), and primary cutaneous B cell lymphoma (55%). TCL1 expression was observed in both the cytoplasmic and nuclear compartments, as confirmed by Western blot analysis. Conversely, TCL1 was not expressed in Hodgkin/Reed-Sternberg cells, multiple myelomas, marginal zone B-cell lymphomas, CD30+ anaplastic large cell lymphoma, lymphoblastic T-cell lymphoma, peripheral T-cell lymphoma, and mycosis fungoides. These data indicate that TCL1 is expressed in more differentiated B cells, under both reactive and neoplastic conditions, from antigen committed B cells and in germinal center B cells and is down-regulated in the latest stage of B-cell differentiation.
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PMID:Regulation of TCL1 expression in B- and T-cell lymphomas and reactive lymphoid tissues. 1078 66

In this study the authors explored the value of immunostaining for follicular center B-cell markers, BCL-6 and CD10, in paraffin sections as a tool for the differential diagnosis of B-cell lymphomas. The cases studied comprised reactive lymphoid hyperplasia (RLH; n = 19), follicular lymphoma (FL; n = 50), low-grade mucosa-associated lymphoid tissue (MALT) lymphoma (n = 24), mantle cell lymphoma (n = 19), splenic marginal zone lymphoma (n = 13), diffuse large B-cell lymphoma (DLBCL; n = 54), Burkitt's lymphoma (BL; n = 20), nodular lymphocyte predominance Hodgkin's disease (NLPHD; n = 16), and classic Hodgkin's disease (CHD; n = 13). In RLH, CD10 and BCL-6 were expressed almost exclusively by the follicular center cells. In contrast in FL, the expression of CD10 (39/50) and BCL-6 (34/36) was seen in both follicular and interfollicular neoplastic B cells. Marginal zone/MALT lymphomas and mantle cell lymphoma were always negative. In DLBCL the expression was variable for both CD10 (21/54) and BCL-6 (39/47), with some tumors, including cases of transformed follicular lymphoma (9/10), coexpressing CD10 and BCL-6, and others expressing only BCL-6, and a small group expressing neither marker, possibly reflecting the underlying primary pathogenetic events such as the rearrangement of BCL-2 or BCL-6 genes. BL was always both CD10 and BCL-6 positive. In NLPHD the L&H cells expressed BCL-6 (11/13) but not CD10, whereas in CHD BCL-6 expression was seen in half of the cases. This study demonstrates that both CD10 and BCL-6 are reliable markers of follicular center B-cell differentiation. CD10 and BCL-6 immunostaining have an important role in differential diagnosis of FL from RLH and other low-grade B-cell lymphomas. The results also suggest that a CD10/BCL-6 expression pattern may be helpful in identifying main subsets of DLBCL. However, additional studies comparing genotype with immunophenotype are required.
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PMID:CD10 and BCL-6 expression in paraffin sections of normal lymphoid tissue and B-cell lymphomas. 1084 87


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