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)

The third complementarity determining region (CDR3) of the hypervariable domain of immunoglobulin heavy chain (IgH) genes represents a highly variable and clone-specific IgH-CDR3 sequences in 10 non-Hodgkin's lymphomas (NHL), five chronic lymphocytic leukemias (CLL) and five acute lymphoblastic leukemias (ALL) of B cell lineage. The IgH-CDR3 sequences were amplified using DNA extracted from clinical specimens (bone marrow, peripheral blood and fresh-frozen or paraffin-embedded lymph nodes) by a semi-nested PCR with consensus primers directed to conserved regions within the variable (VH) and the joining (JH) gene segments. In 17/20 samples (85%), a distinct IgH-CDR3 PCR product was obtained. Individual PCR products were sequenced after cloning. The nucleotide sequences of 134 randomly chosen recombinant vectors were determined demonstrating in 17/20 cases (85%) monoclonal VH-N-DH-N-JH junctions. Analysis of PCR products by temperature-gradient gel electrophoresis (TGGE) confirmed the specificity of the IgH-CDR3 PCR/sequencing results. Moreover, the combination of PCR/TGGE technology allowed the rapid and specific characterization of clonal IgH-CDR3 junctions in B cell proliferations by direct sequencing even in the presence of admixed polyclonal B cells.
Leukemia 1995 May
PMID:Identification and structural analysis of rearranged immunoglobulin heavy chain genes in lymphomas and leukemias. 776 47

A t(8;21)(q22;q22) translocation without blood and bone marrow invasion by immature myeloid precursors was suspected in a conventional karyotype and confirmed by fluorescence in situ hybridization (FISH) with chromosome 8 and 21 painting in a patient previously treated for Hodgkin's lymphoma. Six weeks later, the diagnosis was confirmed by the onset of acute myeloid leukemia (AML) M2 with a t(8;21) in the bone marrow.
Leukemia 1995 Jan
PMID:FISH diagnosis of t(8;21) in a myelodysplasia secondary to Hodgkin lymphoma. 784 3

Tawam Hospital is the major paediatric oncology referral centre in the UAE. During the past 11 years, 352 patients (0-12 years of age) were diagnosed to have a childhood malignancy. Leukaemia and lymphoma accounted for 62.7% of all tumours. Stage distribution for Hodgkin's disease (HD) and non-Hodgkin's lymphoma (NHL) showed a relatively high proportion of advanced stage disease. Histological analysis demonstrated a preponderance of lymphocyte predominance and mixed cellularity cases in Hodgkin's disease, and 2/3 of the NHL patients had small, non-cleaved cell lymphoma. Children fell into three main ethnic groups based on the origin/nationality of their parents: Group 1: UAE nationals and Omanis; Group 2: other Arabs; Group 3: Indian/Pakistani (subcontinental) origin. When compared for the relative proportion of leukaemia/lymphoma/other tumours, children of subcontinental origin had significantly more acute lymphoblastic leukaemia (ALL) and less lymphoma than the other two ethnic groups. This is probably due to the higher level of education and smaller family size in group 3 and lends support to the proposed infectious aetiology in ALL.
Leukemia 1995 Jan
PMID:Ethnic differences in the lymphoid malignancies of children in the United Arab Emirates. A clue to aetiology? 784 16

The latent membrane protein 1 (LMP1) oncogene is one of the major proteins synthesized by the Epstein-Barr virus (EBV). It is expressed in Reed-Sternberg cells of Hodgkin's disease (HD), tumor cells of nasopharyngeal carcinoma (NPC), and immunoblasts of angioimmunoblastic lymphadenopathy (AILD). A particular LMP1 deletion mutant was recently identified in NPC and clinically and histologically aggressive HD. We studied two patients with AILD that subsequently progressed into immunoblastic lymphoma (IBL) in order to investigate whether the LMP1 deletion mutant was implicated in progression of AILD into IBL. Immunohistology and in situ hybridization were performed on diagnostic biopsies. DNA extracted from fresh frozen material was used for rearrangement studies and polymerase chain reaction (PCR) based amplification and sequencing of portions of the LMP1 gene. Immunohistochemistry revealed B cell origin of both cases of IBL. In the first patient clonal rearrangement of the immunoglobulin heavy-chain gene was present in IBL but not in AILD. In this patient, scattered immunoblasts of AILD and numerous tumor cells of B-IBL were shown to contain EBV transcripts (EBER1) and to express LMP1. Sequence analysis of the LMP1 gene from AILD and IBL in the first, and from IBL in the second patient, revealed identical deletions and point mutations. This LMP1 deletion mutant is identical to those which have been reported in HD and NPC. Its association with evolution of AILD into B-IBL, aggressive HD and NPC, suggests that this particular mutant is more widespread than originally thought and is clinically relevant.
Leukemia 1995 Mar
PMID:A deletion mutant of the LMP1 oncogene of Epstein-Barr virus is associated with evolution of angioimmunoblastic lymphadenopathy into B immunoblastic lymphoma. 788 44

In malignant non-Hodgkin lymphomas (NHL), cytogenetic analysis may provide prognostic information including prediction of histologic evolution and responsiveness to therapy. In this study, we correlate clinical data and chromosomal aberrations in 70 adult patients with newly diagnosed NHL followed for a median of 20 months. Clonal aberrations were detected in 68/70 patients (97%). Besides t(2;5)(p23;q35), observed exclusively in three patients with anaplastic large cell lymphoma, Ki-1 positive, none of the characteristic aberrations observed was specific for a given histological subtype. Aberrations of chromosome 7 (n = 21) occurred in all histological subtypes together with aberrations of chromosome 3 and of the short arm of chromosome 17. They were clinically associated with a high serum lactate dehydrogenase level (LDH) and a trend to short survival. Anomalies of the long arm of chromosome 13 (n = 10) were found in patients with high grade B-cell lymphomas and bulky disease. In t(14;18)(q32;q21) bearing lymphomas (n = 27), distinct patterns of additional aberrations were observed in low grade and high grade lymphomas: trisomy 3 and trisomy 18 occurred concomitantly in high grade lymphomas (n = 6, p < 0.001) as well as aberrations of 1q, 5q, 6q and +der (18)(q21). In conclusion, cytogenetic analysis provides information about the complexity of genetic changes in NHL. These changes act not only as indicators of disease activity, but influence clinical outcome as demonstrated by their stringent correlation to the International Index and might reveal more general rules of tumor growth and spreading.
Leukemia 1994 Nov
PMID:Karyotype and prognosis in non-Hodgkin lymphoma. 796 39

We have studied a diverse group of lymphoproliferative disorders (acute lymphoblastic leukaemia (ALL), chronic lymphocytic leukaemia (CLL), non-Hodgkin lymphoma (NHL) and myeloma) to determine if V kappa gene use is random or disease-specific and whether somatic mutations (a late event in B-cell differentiation) can provide additional information on the type of B cell involved in the neoplastic clone. In this group of disorders V kappa gene selection is not random and some members of each V kappa family are preferentially rearranged. V kappa genes from the distal portion of the locus are seldom used, possibly because rearrangement of the proximal locus by deletion is more efficient than rearrangement of the distal locus by inversion. Although pseudogenes account for 46% of the V genes in the kappa locus none were ever rearranged, even in non-functional rearrangements of lambda-producing leukemias, suggesting the existence of a mechanism which down-regulates the rearrangement of pseudogenes. N regions were noted at the VJ junction in 20% of alleles (in six CLL, three NHL, two ALL and one myeloma) possibly the result of kappa-chain recombination during the early period of B-cell maturation in which TdT is expressed. Nucleotide addition or imprecise joining at the VJ junction, resulting in a shift in the reading frame, were the commonest causes of non-functional rearrangement. The occurrence of somatic mutation broadly correlated with the stage of B-cell maturation from which the different disorders are thought to arise. However, there was no strict association and somatic mutations were demonstrated in 'typical CLL' while V kappa genes were germline in some follicular lymphomas; these findings suggest either heterogeneity in the stage of B-cell maturation at which these disorders arise or some variability in the process of somatic mutation.
Leukemia 1994 Jul
PMID:Variable kappa gene rearrangement in lymphoproliferative disorders: an analysis of V kappa gene usage, VJ joining and somatic mutation. 803 5

Ten months following the diagnosis of Hodgkin's disease (HD), a 46-year-old woman presented cutaneous and leukemic involvement by CD30+ anaplastic large cells, from which a continuously growing, exogenous growth factor-independent T cell line was established. The cultured cells are phenotypically and genotypically T cell in type, negative for EBV, HTLV-I and HTLV-II viral sequences, and release soluble CD30 into the supernatant. Karyotype analysis disclosed several chromosomal abnormalities, but none on chromosome 5q. The involvement of the short arm of chromosome 17 prompted us to investigate the TP53 gene by means of the polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) analysis, but no alterations were found in exons 5-8.
Leukemia 1994 Jul
PMID:A CD30-positive T cell line established from an aggressive anaplastic large cell lymphoma, originally diagnosed as Hodgkin's disease. 803 14

A polymerase chain reaction analysis of biopsy specimens from a total of 52 patients with Hodgkin's disease has revealed the presence of the t(14;18) chromosomal translocation in 14 cases (28%). Twelve involved the major breakpoint region and two included the minor cluster region of the bcl-2 gene. Direct sequencing of the amplified 14q+ junctions from the initial four positive cases (from 21 biopsies) has been previously published and demonstrated the similarity in nature of the break-points to those described in follicular lymphoma and lymphoid hyperplasia. The 52 biopsies have also been studied with a monoclonal antibody to immunolocalize the Bcl-2 protein. In all cases Bcl-2 positivity was observed in the majority of surrounding lymphocytes. However, in 11 cases, positive immunostaining in the Sternberg-Reed cells was also observed. Three of these cases contained the t(14;18) translocation, but 11 cases which were positive for the t(14;18) by PCR did not show Bcl-2 protein staining in the Sternberg-Reed cells. This data confirms the presence of t(14;18) in 28% of biopsies from Hodgkin's disease and demonstrates Bcl-2 protein staining in a variable proportion of Sternberg-Reed cells of some cases.
Leukemia 1994 Aug
PMID:The t(14;18) chromosomal translocation and Bcl-2 protein expression in Hodgkin's disease. 805 70

The Epstein-Barr virus (EBV) genome has recently been detected in various non-B cell neoplasms, including various T-cell leukemias and in Reed-Sternberg cells of Hodgkin's disease, but the contribution of EBV genes to the transformed phenotype remains unclear. We have investigated the possible effect which the EBV genes LMP1 and EBNA2, of which the expression has been reported in non-B cell neoplasms, may have on a variety of cell types. The LMP1 and EBNA2 genes were transiently expressed from heterologous promoters in two human T-cell lines (HPB-ALL and Jurkat), two human cell lines of the myeloid lineage (K562 and U937), one type I Burkitt's lymphoma cell line (Rael) and in human primary T cells and B-cell chronic lymphocytic leukemia cells. The cell surface expression of CD23, CD21, ICAM-1 and LFA-1 was monitored on transfected cells. In the cell lines, except U937, the surface antigens CD21 and ICAM-1 were upregulated in a dose-dependent and transient manner by the transient expression of LMP1, and EBNA2 slightly enhanced the effects of LMP1 on CD23 and CD21 upregulation. LMP1 also induced increased CD21, ICAM-1 and LFA-1 surface expression on transfected primary T-cells, and CD21 and ICAM-1 in four of five B-cell chronic lymphocytic leukemias tested. Finally, LMP1 transient expression caused increased cell size of the primary T cells and responding B-cell chronic lymphocytic leukemia cells. Our results strongly suggest that LMP1 can trigger specific responses in a variety of white cell types and thus is probably contributing to the phenotype of EBV-positive tumor cells not only in the B-cell lineage.
Leukemia 1993 Jan
PMID:Transient expression of the Epstein-Barr virus LMP1 gene in B-cell chronic lymphocytic leukemia cells, T cells, and hematopoietic cell lines: cell-type-independent-induction of CD23, CD21, and ICAM-1. 809 69

The intercellular adhesion molecule 1 (ICAM-1) is the ligand for the lymphocyte function-associated antigen 1 (LFA-1). The ICAM-1/LFA-1 complex mediates cell-cell and cell-matrix interactions and is believed to be crucial for several immunological functions, including non-MHC-restricted cytotoxicity. Recently, a circulating form of the surface ICAM-1 molecule, the 82 kDa cICAM, has been identified. Using enzyme-linked immunosorbent assay (ELISA) we have examined 82 kDa cICAM-1 levels in the sera of 45 age- and sex-matched healthy subjects and 130 consecutive patients with Hodgkin's disease (HD). The mean +/- SD concentration of the 82 kDa cICAM-1 was significantly higher (p < 0.001) in HD patients (725.6 +/- 141 ng/ml) than in healthy controls (403.5 +/- 54.5 ng/ml). Patients with B-symptoms (n = 66) had higher cICAM-1 levels than patients without systemic symptoms (n = 64) (825.1 +/- 202.9 ng/ml versus 671.7 +/- 164.9 ng/ml; p < 0.001). Serum levels of cICAM-1 were also significantly higher (p < 0.05) in patients with disseminated disease (stage III and IV) than in those with localized disease (stage I and II). The HD patients in stage III and IV with B-symptoms had significantly higher (p < 0.001 and p < 0.02, respectively) cICAM-1 levels then stage III/IV patients lacking B-symptoms. The increase of cICAM-1 concentrations was positively correlated to increases of soluble receptors for interleukin-2 (sIL-2R) (r = 0.69; p < 0.001). Since cICAM-1 is functionally able to bind to LFA-1, increased serum levels of this molecule could be a mechanism for promoting de-adhesion and inability of Hodgkin and Reed-Sternberg cells (H-RS) to be recognized by cytotoxic effector cells, and could thus represent a way for these cells to escape immunosurveillance and for progression and spreading of disease.
Leukemia 1993 Aug
PMID:Serum levels of circulating ICAM-1 are increased in Hodgkin's disease. 810 18


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