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

The topographic distribution of the dipeptidylaminopeptidase IV (DAP IV-CD 26) and II (DAP II) positive T-cell population in six reactive lymph nodes and seven follicular B-cell non-Hodgkin's lymphomas (NHL) was analysed with regard to the distribution of activated T-cells, as visualized by a panel of monoclonal antibodies including Tac-CD 25, HLA-DR, OKT 9-CD 71, ICAM-1-CD 54, LFA-1-CD 11a. For comparative studies serial frozen sections of the lymph nodes were tested by enzyme histochemistry and immunohistochemistry. In addition, cell suspensions obtained from 10 B-NHL and interleukin-2 (IL-2) activated T-cells were investigated by a combined cytochemical and immunological method for simultaneous visualization of DAP IV-CD 26 cytoplasmic activity and surface immunostaining for markers of lymphocyte activation. Both in reactive and lymphomatous lymph nodes the topographic distribution of DAP IV-CD 26+ and DAP II+ lymphocytes was rather similar to that of Tac-CD 25+ lymphocytes. On the contrary, the DAP IV-CD 26 and DAP II distribution pattern substantially differed from that of the other immunologic markers. In a cell suspension of IL-2 activated T-cells, more than 80% of the cells with a blastic morphology were DAP IV-CD 26+; DAP IV-CD 26+ cells coexpressing Tac-CD 25, OKT 9-CD 71, HLA-DR positivity, relative to the total number of DAP IV-CD 26 positive cells, were 90.5%, 70.5% and 87% respectively. Only small (not activated) lymphocytes expressed a focal cytoplasmic DAP II positivity. In cell suspensions from 10 cases of B-NHL the mean percentage of DAP IV-CD 26+ Tac-CD 25+ cells was 75.8. Only a small number of DAP IV-CD 26+ cells coexpressed HLA-DR, the mean percentage being 9.6. The results support the view that DAP IV-CD 26 may be considered as a marker of lymphocyte activation; this marker seems to be restricted to T lymphocytes that reside in the T dependent areas of reactive lymph nodes and to non malignant T-cells surrounding neoplastic follicles of follicular NHL.
 ...
PMID:Immunohistocytochemical correlation of DAP IV-CD 26 reactivity with immunologic markers of lymphocyte activation in human lymphoid tissues. 197 15

The total T cell population and T cell subsets in ten lymph nodes with reactive lymphoid hyperplasia (RLH) and 23 specimens (21 lymph nodes, one stomach, and one small bowel) involved by histologically and immunohistologically diagnosed B cell non-Hodgkin's lymphomas (NHLs) were determined by reactivity with monoclonal antibodies Leu 4-CD3, Leu 3-CD4, and Leu 2-CD8 in cytospin preparations from cell suspensions. T cell populations were also investigated for the coexpression of dipeptidylaminopeptidase IV (DAP IV) activity, which was visualized simultaneously with cell surface immunostaining by a combined cytochemical and immunocytochemical method. The mean absolute percentage of Leu 4-CD3+ (total T) and Leu 3-CD4+ cell populations was significantly lower in B cell NHL cases than in RLH cases (35% v 54%, P less than .001; 29.5% v 44.4%, P less than .01). No difference in the mean absolute percentage of the Leu 2-CD8+ T cell subset was found between the RLH cases and the B cell NHL cases classified as other than category A as described by the Working Formulation (WF) of NHLs. The relative percentage of Leu 4-CD3+ and Leu 2-CD8+ cells coexpressing DAP IV reactivity was lower in B cell NHL cases than in RLH cases (27.3% v 39.5%, P less than .05; 13.5% v 24.4%, P less than .10). There was no difference in the proportion of Leu 3-CD4+ cells expressing DAP IV reactivity between the NHL and RLH groups (34.5% v 36.1%). Since the mean relative percentage of Leu 2-CD8+ cells expressing DAP IV reactivity in the B cell NHL group in the other than category A according to the WF was lower than that of the RLH group (12.5% v 24.4%), and whereas the mean absolute percentage of total Leu 2-CD8+ cells was similar in the two groups (16.6% and 16.6%), a possible defective role of this Leu 2-CD8+ DAP IV+ subset, at least in B cell NHLs in the other than category A according to the WF, may be hypothesized.
 ...
PMID:Dipeptidylaminopeptidase IV activity in T lymphocyte subsets in B cell non-Hodgkin's lymphomas. 257 58

Death-associated protein kinase (DAP-Kinase) is a novel serine/threonine kinase whose expression is required for gamma interferon-induced apoptosis. A previous study suggested that DAP-Kinase expression may be lost epigenetically in cancer cell lines, because treatment of several nonexpressing cell lines with 5-aza-2'-deoxycytidine resulted in the expression of DAP-Kinase. Using methylation-specific polymerase chain reaction (MSP), we examined the DAP-Kinase CpG island for hypermethylation in cancer. Normal lymphocytes and lymphoblastoid cell lines are unmethylated in the 5' CpG island of DAP-Kinase. However, in primary tumor samples, all Burkitt's lymphomas and 84% of the B-cell non-Hodgkin's lymphomas were hypermethylated in the DAP-Kinase CpG island. In contrast, none of the T-cell non-Hodgkin's lymphoma samples and 15% or less of leukemia samples examined had hypermethylated DAP-Kinase alleles. U937, an unmethylated, DAP-Kinase-expressing leukemia cell line, was treated with gamma interferon and underwent apoptosis; however, Raji, a fully methylated, DAP-Kinase nonexpressing Burkitt's lymphoma cell line, only did so when treated with 5-aza-2'-deoxycytidine followed by gamma interferon. Our findings in cell lines and primary tumors suggest that hypermethylation of the DAP-Kinase gene and loss of gamma interferon-mediated apoptosis may be important in the development of B-cell malignancies and may provide a promising biomarker for B-cell-lineage lymphomas.
 ...
PMID:Hypermethylation of the DAP-kinase CpG island is a common alteration in B-cell malignancies. 1084 15

Aberrant promoter hypermethylation is a mechanism of tumour suppressor gene inactivation. We explored aberrant promoter hypermethylation of multiple genes in 88 human immunodeficiency virus (HIV)-non Hodgkin lymphomas (NHL), 25 post-transplant lymphoproliferative disorders (PTLD) and five common variable immunodeficiency (CVI)-related NHL. Twenty-six of 79 (32.9%) HIV-NHL, eight of 14 (57.1%) PTLD and two of five (40.0%) CVI-NHL showed aberrant hypermethylation of O6-methylguanine-DNA methyltransferase (MGMT). Aberrant hypermethylation of death-associated protein-kinase (DAP-K) occurred in 70 of 84 (83.3%) HIV-NHL, 19 of 25 (72.0%) PTLD and three of five (60.0%) CVI-NHL. These data implicate MGMT and DAP-K hypermethylation in lymphomagenesis of immunodeficient hosts. In particular, promoter hypermethylation of DAP-K represents the most frequent molecular alteration yet identified in immunodeficiency-related lymphomas.
 ...
PMID:Frequent aberrant promoter hypermethylation of O6-methylguanine-DNA methyltransferase and death-associated protein kinase genes in immunodeficiency-related lymphomas. 1461 9