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)

We have developed and tested a rapid and sensitive method of detecting expansion of T-cell clones using the polymerase chain reaction (PCR) and a single set of consensus primers for the V and J regions to amplify rearranged T-cell receptor-gamma (TCR-gamma) genes. Monoclonality was continued in all of the 18 cases of T-cell neoplasms tested, but not in reactive lymphadenopathy, non-Hodgkin's B lymphomas, and Hodgkin's disease. PCR analysis, using the primer sequence outlined in this study, had an overall specificity of 100% when compared with Southern blot analysis. No false-negative results were observed, certainly owing to the choice of consensus primers and to the control of PCR reactions on agarose gels before testing for clonality by separation of PCR products on polyacrylamide gels. This method for the detection of T-cell monoclonality can be especially useful in cases that are diagnostically problematic with standard histological and immunological analysis and in cases where the material available is limited.
Diagn Mol Pathol 1995 Jun
PMID:Improved polymerase chain reaction detection of clonal T-cell lymphoid neoplasms. 755 Dec 90

The utility of polymerase-mediated assays in the detection of the t(11;14) involving the bcl-1 major translocation cluster (bcl-1 MTC) was evaluated by analyzing DNA from 33 patients with mantle cell lymphoma, 14 patients with other non-Hodgkin's lymphomas, and five patients with reactive lymphoid hyperplasia. The polymerase chain reaction (PCR) assay was performed using a consensus immunoglobin heavy-chain joining region primer in conjunction with a chromosome 11 specific oligonucleotide primer flanking the translocation site. The sensitivity and specificity of the assay were confirmed by correlation of the (PCR) assay data with restriction analysis. Rearrangements at the bcl-1 MTC were detected in 13 (39%) of 33 cases of mantle cell lymphoma by PCR and in 13 (48%) of 27 cases by restriction analysis. Amplicons were detectable by PCR in 85% (11 of 13) of the cases shown to be bcl-1 rearranged by restriction analysis. Failure to detect amplification products in DNA samples from non-mantle cell lymphomas and reactive follicular hyperplasia further confirmed the specificity of the assay. Sequential hybridization of the PCR products with oligonucleotide probes 3' to the bcl-1 MTC primer revealed that the breakpoints in the bcl-1 MTC were clustered around an Sst I restriction site over a range of 170 base pairs. The study demonstrates that PCR-mediated assay for the detection of the t(11;14) at the bcl-1 MTC is specific and sensitive and can be used as an adjunct to restriction analysis in routine diagnostics.
Diagn Mol Pathol 1995 Mar
PMID:Polymerase chain reaction detection of the t(11;14) translocation involving the bcl-1 major translocation cluster in mantle cell lymphoma. 773 55

Two groups of children with acute lymphoblastic leukemia or non-Hodgkin lymphoma, treated with anthracyclines (ANT), were studied: group I, consisting of 10 patients, with coenzyme Q10 (CoQ) therapy; group II, consisting of 10 patients without CoQ therapy. The ANT cumulative dose was 240 +/- 20.0 mg/m2 in group I and 252.0 +/- 20.1 mg/m2 in group II. Echocardiographic study was performed at the beginning, at the cumulative dose of 180 mg/m2 and at the end of therapy with ANT. Percentage left ventricular fractional shortening (%LVFS) decreased from baseline (40.36 +/- 4.6) to end value (35.82 +/- 5.02) (P < 0.05) in group I; %LVFS decreased from baseline (39.89 +/- 4.37) to end value (33.43 +/- 3.46) (P < 0.002) in group II. Interventricular septum wall thickening decreased only in group II from baseline (46.10 +/- 10.1) to end therapy (27.00 +/- 18.54) (P < 0.01). Septum wall motion abnormalities were detected only in 2 patients of group II. These data demonstrate a protective effect of CoQ on cardiac function during therapy with ANT.
Mol Aspects Med 1994
PMID:Protective effect of coenzyme Q10 on anthracyclines cardiotoxicity: control study in children with acute lymphoblastic leukemia and non-Hodgkin lymphoma. 775 32

Clonal rearrangements of the bcl-1 and bcl-2 protooncogenes are found in many B-lineage non-Hodgkin's lymphomas (NHL) and may play a role in their pathogenesis. We investigated rearrangements of the bcl-1 and bcl-2 protooncogenes in 13 cases of B lineage diffuse small cleaved-cell lymphoma (DSCL), and correlated the results with clinical history, immunophenotype, and outcome. Six cases showed bcl-2 rearrangements, including four patients with an antecedent follicular small cleaved-cell lymphoma (FSCL). Two patients had a bcl-1 rearrangement, including one with a previous FSCL. Of the five patients who lacked detectable bcl-1 or bcl-2 rearrangements, one had an FSCL history. Similar to the lack of correlation between clinical history and genotype, there was no correlation between genotype and immunophenotype. Our results indicate that although DSCL is a morphologically uniform disease, different molecular genetic pathways are involved in its genesis. Follow-up showed four of the six DSCL patients with bcl-2 rearrangements were alive with a median survival of 56 months, whereas the median survival of the seven patients lacking a bcl-2 rearrangement was 17 months and included only one survivor. Thus bcl-2 rearrangements in DSCL may define a patient subset with a more indolent genetic abnormality and prolonged survival.
Diagn Mol Pathol 1994 Sep
PMID:The presence of bcl-1 and bcl-2 gene rearrangements in diffuse small cleaved-cell lymphoma. A disease with diverse molecular and immunophenotypic findings. 798 93

Epstein-Barr virus (EBV) has been detected in African Burkitt's lymphoma, posttransplant lymphoproliferative disease, and a variable fraction of Hodgkin's lymphomas. To assess if EBV is associated with other lymphoid proliferations, we evaluated a wide variety of benign and malignant lymphoid lesions, using polymerase chain reaction and a sensitive in situ hybridization method. Abundant EBV+ cells were seen in posttransplant lymphomas, some B cell immunoblastic lymphomas, and in tonsils from patients with infectious mononucleosis. Intermediate numbers of EBV+ cells were seen in a mixed B cell lymphoma, peripheral T cell lymphomas, and in syncytial variants of Hodgkin's disease as well as a lymph node from a patient with infectious mononucleosis. Low numbers of EBV+ cells were detected in normal and reactive lymph nodes, B and T cell lymphomas, and Hodgkin's lymphomas. The variable extent of EBV infection in lymphoid lesions suggests that EBV may play a variety of roles in the development of malignant and nonmalignant lymphoid lesions.
Diagn Mol Pathol 1994 Mar
PMID:Presence of Epstein-Barr virus in many types of benign and malignant lymphoid lesions. Detection by polymerase chain reaction and in situ hybridization. 816 52

Several recent studies reported the detection of partially deleted HTLV-I provirus in biopsies of lesions from patients with mycosis fungoides (MF) and T-cell anaplastic large-cell lymphoma. We studied lesions from 59 patients (21 B-cell lymphomas: 16 diffuse and five follicular; 11 cutaneous T-cell lymphomas, including seven MF; one T-immunoblastic lymphoma; 10 diffuse anaplastic large-cell lymphomas: two B, four T, and four of indeterminate phenotype; three Hodgkin's lymphomas; eight atypical lymphoid proliferations; four other lymphoid lesions, and one squamous-cell carcinoma) using primers to the gag, pol and pX regions of HTLV-I in the polymerase chain reaction (PCR) to detect relevant sequences. A total of 10 patients showed one or more PCR-amplifiable products, including five of 11 patients with cutaneous T-cell lymphomas (45%) as compared with one of 21 patients with B-cell lymphomas (4.3%). We did not find a high incidence of positivity in anaplastic large-cell lymphomas, as reported previously. Detectable HTLV-I sequences were not limited to any subtype of lymphoma, and a pX sequence was detected in a squamous-cell carcinoma. Sequence analysis of one amplified product from each of the three regions studied showed a 94.2, 100, and 98.9% homology to the corresponding prototypical gag, pol, and pX HTLV-I sequences, respectively, indicating that the amplified sequences were derived from HTLV-I or a very closely related virus. HTLV-I sequences were detected in a significant proportion of patients with cutaneous T-cell lymphoma, but their role in the pathogenesis of the neoplasm is still unclear.
Diagn Mol Pathol 1993 Sep
PMID:HTLV-I sequence in lymphoproliferative disorders. 828 32

Latent Epstein-Barr virus (EBV) infection is associated with a variety of malignancies. Rapid in situ hybridization techniques have been described for various lytic viral infections because of limited gene expression. However, EBERS (Epstein Barr early RNAs) are expressed in abundance in tumour cells which are latently infected with EBV. We have targeted these transcripts in a rapid (3 h) in situ hybridization assay fo the detection of latent EBV in clinical specimens, including formalin-fixed paraffin-embedded material. EBER RNA was detected in control cell lines which have two copies of the EBV genome and in paraffin-embedded biopsy specimens from patients with nasopharyngeal carcinoma, EBV-associated Hodgkin's disease, Burkitt's lymphoma and post-transplant lymphoma. The technique did not detect EBER RNA in oral hairy leukoplakia, a pathologic process previously characterized as associated with lytic EBV infection. The sensitivity, specificity and rapidity of this technique make it ideal for the diagnostic detection of EBV in latently infected clinical specimens.
Mol Cell Probes 1993 Apr
PMID:Rapid in situ hybridization for the diagnosis of latent Epstein-Barr virus infection. 839 39

In Drosophila melanogaster, sex determination in somatic cells is controlled by a cascade of genes whose expression is regulated by alternative splicing [B. S. Baker, Nature (London) 340:521-524, 1989; J. Hodgkin, Cell 56:905-906, 1989]. The master switch gene in this hierarchy is Sex-lethal. Sex-lethal is turned on only in females, and an autoregulatory feedback loop which controls alternative splicing maintains this state (L. R. Bell, J. I. Horabin, P. Schedl, and T. W. Cline, Cell 65:229-239, 1991; L. N. Keyes, T. W. Cline, and P. Schedl, Cell 68:933-943, 1992). Sex-lethal also promotes female differentiation by controlling the splicing of RNA from the next gene in the hierarchy, transformer. Sosnowski et al. (B. A. Sosnowski, J. M. Belote, and M. McKeown, Cell 58:449-459, 1989) have shown that the mechanism for generating female transformer transcripts is not through the activation of the alternative splice site but by the blockage of the default splice site. We have tested whether an activation or a blockage mechanism is involved in Sex-lethal autoregulation. The male exon of Sex-lethal with flanking splice sites was placed into the introns of heterologous genes. Our results support the blockage mechanism. The poly(U) run at the male exon 3' splice site is required for sex-specific splicing. However, unlike transformer, default splicing to the male exon is sensitive to the sequence context within which the exon resides. This and the observation that the splice signals at the exon are suboptimal are discussed with regard to alternate splicing.
Mol Cell Biol 1993 Mar
PMID:Regulated splicing of the Drosophila sex-lethal male exon involves a blockage mechanism. 844 86

Myxococcus xanthus, a bacterium that forms fruiting bodies, moves by gliding motility utilizing dual motility systems that differ both genetically and morphologically [system A, having at least 21 genetic loci and moving mainly single cells, and system S, having at least 10 genetic loci and moving groups (rafts) of cells] [Hodgkin, J. & Kaiser, D. (1979) Mol. Gen. Genet. 172, 177-191]. In this study, we found that A- and S-gliding-motility systems have different selective advantages on surfaces containing different concentrations of agar. We observed that colonies of A+S- cells (A-motile cells) swarmed better than A-S+ cells (S-motile cells) on relatively firm and dry surfaces (e.g., 1.5% agar). In contrast, colonies of A-S+ cells swarmed much better than A+S- cells on soft and wet surfaces (e.g., 0.3% agar). Individual A-motile cells moved at a rate of 2-4 microns/min on 1.5% agar but they barely moved on 0.3% agar (< 0.5 microns/min); in contrast S-motile cells moved 3-5 times faster on 0.3% agar than on 1.5% agar. Wild-type cells with both A- and S-motility systems were able to move well over a wide range of surfaces. These results suggest that dual motility systems enable the myxobacteria to adapt to a variety of physiological and ecological environments and show similarities in function to the dual motility systems of flagellated bacteria such as Vibrio spp.
 ...
PMID:The two motility systems of Myxococcus xanthus show different selective advantages on various surfaces. 847 84

The murine monoclonal antibody, LL2, is a B-cell (CD22)-specific IgG2a which has been demonstrated to be clinically significant in the radioimmunodetection of non-Hodgkin's B-cell lymphoma. The antibody carries a variable region-appended glycosylation site in the light chain and is rapidly internalized upon binding to Raji target cells. Humanization of LL2 was carried out in order to develop LL2 as a diagnostic and immunotherapeutic suitable for repeated administration. Based on the extent of sequence homology, and with the aid of computer modeling, we selected the EU framework regions (FR) 1, 2 and 3, and the NEWM FR4 as the scaffold for grafting the heavy chain complementarity determining regions (CDRs), and REI FRs for that of light chains. The light chain glycosylation site, however, was not included. Construction of the CDR-grafted variable regions was accomplished by a rapid and simplified method that involved long DNA oligonucleotide synthesis and the polymerase chain reaction (PCR). The humanized LL2 (hLL2), lacking light chain variable region glycosylation, exhibited immunoreactivities that were comparable to that of chimeric LL2 (cLL2), which was shown previously to have antigen-binding properties similar to its murine counterpart, suggesting that the VK-appended oligosaccharides found in mLL2 are not necessary for antigen binding. Moreover, the hLL2 retained its ability to be internalized into Raji cells at a rate similar to its murine and chimeric counterparts.
Mol Immunol 1995 Dec
PMID:Construction and characterization of a humanized, internalizing, B-cell (CD22)-specific, leukemia/lymphoma antibody, LL2. 864 11


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