Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma cell neoplasia occurs much less frequently than high-grade B-cell non-Hodgkins lymphoma in HIV-infected patients, but is nevertheless an AIDS-associated malignancy. In this report, we describe the fine-needle aspiration (FNA) findings of a mass in the left parotid region with plasmablastic features that occurred in a 41-yr-old HIV-infected homosexual man whom we diagnosed as having anaplastic myeloma. The patient had normochromic, normocytic anemia with a hematocrit of 21%, a white blood count of 2.2 x 10(9)/l with 76% neutrophils, and a CD4 count of 31%. He also had elevated levels of calcium (13.2 mg/dl), alkaline phosphatase (25,400 IU/l), blood urea nitrogen (2,600 mg/dl), and creatinine (2.5 mg/dl). Serum protein electrophoresis showed polyclonal hypergammaglobulinemia without any monoclonal component. A bone survey revealed multiple punched-out lytic lesions. FNA smears showed large plasmacytoid cells with eccentrically placed nuclei, prominent nucleoli, and moderate amounts of basophilic cytoplasm. By immunocytochemical staining, tumor cells were negative for CD19, CD20, and leukocyte-common antigen (LCA), but strongly positive for CD38 and kappa light chain. Anaplastic myeloma and plasmablastic lymphoma were considered in the differential diagnosis. Although the cytomorphologic and immunophenotypic findings of our case overlapped with those of plasmablastic lymphoma, the pattern of bone involvement with punched-out lytic lesions and absence of localization of the tumor to the mucosa of the oral cavity led us to a diagnosis of anaplastic myeloma. The patient initially received antiretroviral therapy followed by thalidomide and pulse dexamethasome therapy, but his response was poor. His HIV load increased, and his malignancy rapidly progressed with the development of multiple vertebral lesions, extraosseous extension, and eventually cord compression. He died of the disease less than 2 mo after presentation.
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PMID:Fine-needle aspiration cytology of a case of HIV-associated anaplastic myeloma. 1235 99

Whereas L26 (anti-CD20) is well established as a B-cell marker of high specificity for use in paraffin-embedded tissues and JCB117 (anti-CD79a) is increasingly used, a comparable additional pan-B-cell antibody has hitherto not yet been identified. Here we have studied the use of a novel anti-pan-B-cell marker Pax-5 for use in diagnostic pathology. Pax-5 encodes for BSAP (Pax-5), a B-cell-specific transcription factor, the expression of which is detectable as early as the pro-B-cell stage and subsequently in all further stages of B-cell development until the plasma cell stage where it is downregulated. Pax-5 is essential for B-lineage commitment in the fetal liver, whereas in adult bone marrow this transcription factor is required for progression of B-cell development beyond the early pro-B (pre-BI) cell stage. Among the B-cell genes that are present in early B-cell development and are upregulated by Pax-5 are CD19 and Igalpha (CD79a). We have tested a commercially available anti-Pax-5 antibody (anti-BSAP, clone 24) in a series of 592 routinely fixed and paraffin wax-embedded biopsies, including lymph nodes, bone marrow, and various other organs containing lymphoid tissues. Pax-5 protein (BSAP) was detected in all cases of precursor and mature B-cell non-Hodgkin lymphomas/leukemias. In addition, in 97% of classic Hodgkin lymphomas, Reed-Sternberg cells expressed Pax-5. However, Pax-5 was not detected in any of the multiple myelomas, solitary plasmacytomas, and 4% of diffuse large B-cell lymphomas. Among those diffuse large B-cell lymphomas not expressing Pax-5 were only those with terminal B-cell differentiation. All T-cell non-Hodgkin lymphomas, including ALCL and lymphoblastic lymphomas and leukemias, were negative. There was a strong association between Pax-5 and CD20 expression. We conclude that anti-Pax-5 is an excellent pan-B and pan-pre-B-cell marker. We have found that anti-Pax-5 is superior to anti-CD20 in the diagnosis of pre-B acute lymphoblastic leukemia and classic Hodgkin lymphoma versus ALCL of T and "null" cell type. It was also useful in differential diagnosis between lymphoplasmacytic lymphoma and plasmacytoma. Even though there is an excellent correlation between CD20 and Pax-5 expression, anti-Pax-5 exceeds the specificity and sensitivity of L26 (anti-CD20) because of its earlier expression in B-cell differentiation and its ability to detect all committed B cells, including classic Hodgkin lymphoma.
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PMID:The value of anti-pax-5 immunostaining in routinely fixed and paraffin-embedded sections: a novel pan pre-B and B-cell marker. 1236 49

B lymphomagenesis is an uncontrolled expansion of immature precursors that fail to complete their differentiation program. This failure could be at least partly explained by inappropriate expression of several oncogenic transcription factors, such as Pax5 and Myc. Both Pax5 and c-Myc are implicated in the pathogenesis of non-Hodgkin lymphomas. To address their role in lymphomagenesis, we analyzed B-cell lymphomas derived from p53-null bone marrow progenitors infected in vivo by a Myc-encoding retrovirus. All Myc-induced lymphomas invariably maintained expression of Pax5, which is thought to be incompatible with terminal differentiation. However, upon culturing in vitro, several cell lines spontaneously down-regulated Pax5 and its target genes CD19, N-Myc, and MB1. Unexpectedly, other B-cell markers (eg, CD45R) were also down-regulated, and markers of myeloid lineage (CD11b and F4/80 antigen) were acquired instead. Moreover, cells assumed the morphology reminiscent of myeloid cells. A pool of F4/80-positive cells as well as several single-cell clones were obtained and reinjected into syngeneic mice. Remarkably, pooled cells rapidly re-expressed Pax5 and formed tumors of relatively mature lymphoid phenotype, with surface immunoglobulins being abundantly expressed. Approximately half of tumorigenic single-cell clones also abandoned myeloid differentiation and gave rise to B lymphomas. However, when secondary lymphoma cells were returned to in vitro conditions, they once again switched to myeloid differentiation. This process could be curbed via enforced expression of retrovirally encoded Pax5. Our data demonstrate that some Myc target cells are bipotent B-lymphoid/myeloid progenitors with the astonishing capacity to undergo successive rounds of lineage switching.
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PMID:Oscillation between B-lymphoid and myeloid lineages in Myc-induced hematopoietic tumors following spontaneous silencing/reactivation of the EBF/Pax5 pathway. 1240 13

Activation-induced cytidine deaminase (AID) induces somatic hypermutation (SHM), class switch recombination (CSR), and immunoglobulin gene conversion in B-lymphocytes. Here we report for the first time the expression of AID in healthy human B-lymphocytes and in B-cell non-Hodgkin lymphomas (B-NHL). AID mRNA expression in humans is restricted to the CD19(+)CD38(+)IgD(-) germinal center cells, namely the CD19(+)CD38(+)CD44(-) centroblasts. After in vitro stimulation of naive human B cells by CD40-L and IL-4, AID mRNA is strongly induced for only 48 hours. In a survey of human B-NHL AID was found to be constitutively expressed in follicular lymphoma and in diffuse large B-cell lymphoma but to be absent in B-precursor lymphoblastic leukemia, in mantle cell lymphoma, and in plasma cell myeloma. In B-cell chronic lymphatic leukemia, in immunocytoma, and in extranodal marginal zone B-cell lymphoma of MALT, AID mRNA was expressed only in some samples. In follicular lymphoma and diffuse large B-cell lymphoma, the expression of AID mRNA was coincident with the presence of SHM in the variable region exons of the immunoglobulin heavy-chain gene. In human B-NHL, the AID mRNA is spliced into 4 different variants but does not contain point mutations. Thus AID, which is highly regulated during healthy B-cell development, is constitutively expressed in human germinal center B-NHL and in subsets of nongerminal center B-NHL. This constitutive expression of AID may promote illegitimate DNA recombinations and somatic mutations in B-NHL.
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PMID:Expression of activation-induced cytidine deaminase in human B-cell non-Hodgkin lymphomas. 1251 17

Chronic hepatitis C virus (HCV) infection is frequently associated with type II mixed cryoglobulinaemia (MC), a benign lymphoproliferative disease (LPD). More recently, HCV has been implicated as a possible aetiologic factor of B-cell non-Hodgkin lymphoma (B-NHL). CD81, a B-cell surface receptor, has been proposed as a receptor for HCV binding and entry in circulating B cells. The stimulation of CD81 complex enables B cells to respond to lower concentrations of antigen and finally induces B-cell proliferation. We studied the phenotypic expression of CD81, CD19 and CD5 on circulating B cells in HCV patients LPD-positive or LPD-negative. Sixty-two patients were anti-HCV antibody positive. Among HCV positive patients, 44 were HCV RNA positive with an histologically proven chronic active hepatitis of whom 10 had a B-NHL, 14 an MC and 24 no extrahepatic manifestation. Eighteen patients were HCV RNA negative with evidence of resolved infection. A control group included 40 healthy subjects. Peripheral blood mononuclear cells (PBMC) were stained for surface expression of CD81, CD19 and CD5 using monoclonal antibodies, and were analyzed by flow cytometry. The percentage of PBMC expressing CD81, CD19 and CD5 receptors were compared between the groups by univariate analysis. Logistic regression model variables were then evaluated to correlate the presence of an LPD with HCV infection characteristics (i.e. age, gender, genotype, duration of infection, HCV RNA positivity, liver histological lesions), or phenotypic expression of CD81, CD19 and CD5 receptors on PBMC. HCV antibody-positive compared with HCV-negative subjects had a higher expression of CD19 receptor (23 +/- 13 vs 13 +/- 1%, P = 0.003). Among HCV RNA positive-patients, LPD+ compared with LPD- patients had a lower expression of CD81 (58 +/- 28 vs 82 +/- 18%, P = 0.001) and CD5 receptor (66 +/- 16 vs 74 +/- 13%, P = 0.04). In multivariate analysis, the expression of CD81 receptor was a negative (OR = 0.15, 95% CI = 0.04-0.64, P = 0.01) and CD19 receptor a positive (OR = 4.81, 95% CI =1.29-17.88, P = 0.02) predictive factor for an LPD. We found two negative predictive factors for HCV RNA positivity, i.e. age (OR = 0.23, 95% CI. = 0.08-0.62, P = 0.003) and the expression of CD81 receptor (OR = 0.34, 95% CI = 0.13-0.89, P = 0.02). In patients with a chronic active HCV infection, the presence of a lymphoproliferative disease, either MC or B-NHL, is associated with lower expression of CD81 and higher expression of CD19 receptor on peripheral B cells.
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PMID:Lower expression of CD81 B-cell receptor in lymphoproliferative diseases associated with hepatitis C virus infection. 1255 6

In this paper we present the results of the distribution of a cell surface protein with molecular weight 104-110 kDa (p104-110) detected by monoclonal antibody made in our laboratory. The protein is expressed by a number of cell lines belonging to B lymphoid cells, but not to the other blood cell lineages. In healthy donors the expression of p104-110 is restricted to a minor population of human peripheral blood mononuclear cells shared by both CD20(+) and CD20(-) subpopulation. No expression of p104-110 has been found on resting and activated T cells as well as on monocytes and polymorphonuclear cells. FACS analysis of mononuclear cells derived from normal human bone marrow has revealed the presence of p104-110 on committed CD34(-); CD38(+) mononuclear cell subset that composes only the minor part of mature CD20(+) B cells being mostly CD20 negative. Furthermore, CD19(+)CD5(+)CD20(-) malignant cells derived from the patients with chronic lymphoid leukemia express p104-110 at high level. Similarly, it has been shown that some patients with malignant non-Hodgkin's lymphomas can have the increased contents of CD20(+) cells bearing that surface antigen. Possible associations of p104-110 expression on human B lymphoid cells with their differentiation and activation are discussed.
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PMID:Expression of the Protein with Molecular Weight 104-110 kDa by Normal and Malignant Human B Lymphoid Cells. 1268 16

The role of flow cytometry (FC) in the diagnosis of lymphoid lesions by fine-needle aspiration (FNA) is well established. However, studies evaluating the usefulness of FC in serous cavity effusions (SCE) are few. We performed a retrospective review of 115 consecutive SCE with concurrent FC analysis, comparing the provisional cytopathologic diagnosis (PCD), i.e., before the FC results were added, with final diagnoses as modified by subsequent FC immunophenotyping. The predominant clinical indication for the FC analysis was the presence of a spontaneous SCE in a patient with a history of malignant lymphoma. Three- or four-color analysis was performed using antibodies against CD45, CD71, CD33, CD22, CD19, CD20, kappa, lambda, CD5, CD3, and CD56. The PCD was benign in 47%, atypical in 16%, and malignant in 37% of cases. The latter category consisted mostly of malignant lymphoma (n = 32), but also included acute lymphoblastic leukemia (1 case), T-cell lymphoma/leukemia (2 cases), acute myelogenous leukemia (1 case), multiple myeloma (1 case), Hodgkin's lymphoma (1 case), sarcoma (1 case), and adenocarcinoma (4 cases). In 18 cases (16%), the PCD was later modified by the FC results from atypical/suspicious to benign (8) and from benign or atypical/suspicious to malignant (10 cases). The latter group included acute natural killer (NK) cell leukemia (1 case), chronic lymphocytic leukemia (1 case), mantle cell lymphoma (2 cases), follicular lymphoma (3 cases), angioimmunoblastic lymphoma (1 case), large cell lymphoma (1 case), and multiple myeloma (1 case). As expected, FC was noncontributory in cases of Hodgkin's lymphoma and nonlymphoid malignancies. In summary, immunophenotyping by FC modified the PCD significantly in 16% of SCE, permitting appropriate cancer staging and management. The above data underscore the importance of FC as an adjunct to cytomorphology in SCE.
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PMID:Flow cytometry as an adjunct to cytomorphologic analysis of serous effusions. 1288 43

Mantle cell lymphoma is non-Hodgkin's B-cell lymphoma characterized by the t(11;14)(q13;q32) translocation. Peripheral blood involvement of mantle cell lymphoma is usually associated with a poor prognosis and therefore, its identification is clinically important. In this study, we performed cyclin D1/IgH-probe fusion fluorescence in situ hybridization analysis on 223 peripheral blood samples: 185 from 125 mantle cell lymphoma patients, and 38 normal controls. The cutoff values for the test were established using normal controls. Flow cytometry on peripheral blood and corresponding bone marrow samples was used to evaluate this test. In all, 26% of the 185 peripheral blood samples and 27% of the 161 corresponding bone marrow samples were flow cytometry positive for mantle cell lymphoma. The mean numbers of single and- double-fusion signals and the mean number of CD5/CD19-positive cells, absolute blood lymphocyte count, and white blood cell count were significantly higher in peripheral blood and corresponding bone marrow samples with mantle cell lymphoma-positive flow cytometry. Double-fusion signals were more specific than single-fusion ones. Fluorescence in situ hybridization was far more likely to be positive for mantle cell lymphoma when the peripheral blood and the corresponding bone marrow samples had positive flow cytometry results or morphology (P<0.01). Our study indicates that cyclin D1/IgH-fusion fluorescence in situ hybridization analysis could be used to determine the presence and character of circulating mantle cell lymphoma cells in peripheral blood, thus enhancing our ability to evaluate leukemic mantle cell lymphoma and minimum residual disease.
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PMID:Evaluation of peripheral blood involvement of mantle cell lymphoma by fluorescence in situ hybridization in comparison with immunophenotypic and morphologic findings. 1500 94

Human herpesvirus 8 (KSHV/HHV-8) is associated with all forms of Kaposi sarcoma (KS), with a rare high-grade B-cell non-Hodgkin lymphoma characterized by serous effusions in body cavities called primary effusion lymphoma (PEL) and with some forms of multicentric Castleman disease (MCD). Although mostly observed during AIDS, such disorders have also been described with a lower incidence in human immunodeficiency virus-negative patients. We describe here the features of two novel cases of AIDS-unrelated PEL. Two patients, a 78-year-old man (case 1) and a 86-year-old woman (case 2), both of French origin, presented exudative ascitic effusion containing numerous KSHV/HHV-8(+) EBV(-) large lymphomatous cells of B-cell clonal origin, characterized by a CD45(+) CD30(+) CD19(-) CD20(-) immunophenotype. The PEL tumor cells harbored a homogenous and isolated trisomy 12 in case 1 and an aberrant expression of the T-cell lineage antigen CD7 in case 2. Both patients were lymphopenic at the time of PEL diagnosis and rapidly died with progressive lymphoma. Moreover, patient 2 had a previous history of classic KS and MCD clinically improved after treatment with all-trans-retinoid acid and a concomitant metastatic breast adenocarcinoma. Compared to AIDS-related PEL, these two cases displayed distinct features in particular the advanced age of patients, as observed for Mediterranean KS, and the absence of EBV coinfection.
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PMID:Human herpesvirus 8 (HHV-8)-associated peritoneal primary effusion lymphoma (PEL) in two HIV-negative elderly patients. 1511 7

To evaluate the normalization of lymphocyte subsets several years after autologous peripheral blood stem cell transplantation (aPBSCT) and to detect any differences based on the underlying lymphoproliferative diseases, we analyzed the immunological recovery of 149 patients with Non Hodgkin's Lymphoma (NHL), Hodgkin's Disease (HD), Multiple Myeloma (MM). Lymphocyte recovery was assessed before the transplant, on days 15, 30, 60, 90, 120 and on years 1, 2, 4, 6. Analysis of a total of 709 lymphocytes, including total lymphocyte count, CD3 +, CD4 +, CD8 +, CD4 +/CD8 + ratio, CD19 +, CD3 + HLA-DR +, CD16 + 56 +, was performed. The normalization of total lymphocyte counts was achieved between days 14 to 22 following PBSCT. CD3 + cells count showed a normalization after 2 years in the HD and NHL groups and after 4 years in MM group. CD4 + subset achieved normalization during the sixth year in the 3 groups. The CD8 + and CD19 + lymphocytes subsets achieved normal values in the 3 groups at day 60 and at day 120 respectively. CD16 + 56 + and CD3 +/HLA-DR + lymphocytes showed median values above the normal range starting from day 30. Immunological recovery was similar in all 3 groups. Moreover, the recovery of all subsets evaluated was similarly demonstrated within 6 years after aPBSCT.
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PMID:Immune recovery of lymphocyte subsets 6 years after autologous peripheral blood stem cell transplantation (PBSCT) for lymphoproliferative diseases. A comparison between NHL, HD and MM in group of 149 patients. 1537 Feb 51


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