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)

A case is described of an HIV+ man who was successfully treated for Hodgkin's lymphoma, but who later developed non-Hodgkin's lymphoma 3 years later when his immune system became suppressed. The patient was 22 years old when he presented with fever, asthenia, weight loss, and cervical lymphadenopathy. With Hodgkin's lymphoma he also had positive serology for HIV and hepatitis B. He was treated with alternate courses of MOPP and ABVD chemotherapy. In 1990 he again appeared with high fever, progressive cervical, axillary and inguinal lymphadenopathy, with hilar and mediastinal lymph node enlargement on x-ray. CD4 lymphocytes were 577/cubic mm, and the CD4/CD8 ratio was 0.57 (normal 1.8). His cervical lymph node biopsy was classified as non-B non-T large-cell anaplastic lymphoma which was EBV-positive. A Western Blot was positive for small amounts of p24 and p18 antigens. The man was treated with MACOP-B chemotherapy, with some results, but died of sepsis 6 weeks later. The relationships between Hodgkins and non-Hodgkin's lymphoma, the timing of the neoplasm in the course of HIV infection, and the possible re-activation of hepatitis virus were discussed.
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PMID:Non-Hodgkin's lymphoma after prolonged remission of Hodgkin's disease in an HIV-infected patient. 166 42

Four Epstein-Barr virus-positive lymphoblastoid cell lines (LCL) were successfully infected in vitro with immunodeficiency virus type 1 (HIV-1) as demonstrated by reverse transcriptase activity and p24 HIV antigen in culture supernatants, positive cell staining for gag-encoded HIV proteins, presence of viral HIV genome by Southern blot analysis and ulstrastructural observations. In addition, both HIV-1-infected B cells and their supernatants efficiently transactivated the chloramphenicol acetyl transferase reporter gene which is under the control of the HIV-1 long terminal repeat. The LCL cells displayed long-term HIV-1 infection and production, but no cytopathic effects were observed. Cytofluorimetric analysis did not detect membrane CD4 presence in the LCL cells before and after HIV-1 infection; moreover, a minute amount of CD4 mRNA was observed only in one of the LCL. A monoclonal antibody specific for the viral binding site of the CD4 molecule delayed, but did not block, HIV-1 infection of the LCL cells. Following HIV-1 infection, changes in LCL phenotype were observed, consisting of a decrease in CD23- and CD39-positive cells, and a concomitant increase of cells with surface CD10 and Bac-1. Furthermore, HIV-1-infected LCL cells did not grow in tight clumps, as usually observed in uninfected LCL, but as disperse suspensions, and formed more agar colonies than control LCL. However, despite this apparent acquisition of a malignant-like phenotype, c-myc proto-oncogene rearrangement was not detected. The appearance of cells with new characteristics did not seem due to clone selection by HIV-1 infection, since all the LCL conserved their clonotypic pattern of IgH chain rearrangement. The acquisition of malignant-like features by HIV-infected B cells might be clinically significant in terms of the pathogenesis of non-Hodgkin's B cell lymphomas, which occur frequently in AIDS patients.
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PMID:Infection of Epstein-Barr virus-transformed lymphoblastoid B cells by the human immunodeficiency virus: evidence for a persistent and productive infection leading to B cell phenotypic changes. 217 Jan 47

Because of the T-cell abnormalities observed in Hodgkin's disease and the growing number of Hodgkin's disease cases observed in association with the acquired immunodeficiency syndrome (AIDS), concern has been expressed that a retrovirus may be the primary cause of Hodgkin's disease. We examined plasma specimens from 17 patients with Hodgkin's disease that were drawn in 1979. Because serum containing antibodies to either human T-lymphotropic virus type I (HTLV-I) or HTLV-II precipitate the major core protein, p24, of HTLV-I, lack of reactivity to HTLV-I p24 in all the specimens demonstrated absence of antibodies to HTLV-I or -II. None of the specimens was reactive to human immunodeficiency virus type 1 (HIV-1) by ELISA. None of the specimens were reactive on Western blot assays for HTLV-I or -II or HIV-1. Lack of evidence of cross-reacting antibodies to prototype strains of those retroviruses in specimens drawn before the AIDS epidemic suggests that classic Hodgkin's disease is not the result of infection with one of the known human lymphocytotropic retroviruses or a closely related agent.
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PMID:Lack of evidence of circulating retroviral antibodies in patients with classic Hodgkin's disease. 289 80

This report describes the experience of the Southeastern Cancer Study Group (SECSG) with the frozen-section immunoperoxidase phenotyping of 162 cases of B-lineage non-Hodgkin's lymphomas. The authors used a panel of 13 different markers with varying degrees of specificity for B lymphocytes and B-cell neoplasms. All lymphomas were classified according to the International Working Formulation. Several antibodies, including anti-immunoglobulin, B1, Leu 12, and Leu 14 were B-cell-specific markers that were generally pan-reactive. Several other monoclonal antibodies, however, were selectively reactive with subpopulations of B-cell lymphomas. Three "selective-B" antigens (BA1, p24, CALLA) were found on about half of the B-cell lymphomas tested, while another three (HB31, transferrin receptor, C3d receptor) were found on about two-thirds of the lymphomas tested. Leu 1 reacted with 18% of the B-cell lymphomas, particularly the small lymphocytic lymphomas. When the reactivity of the monoclonal antibodies was compared with the histologic classification, two important points became apparent. First, with the large panel of antibodies, there was tremendous phenotypic diversity even among histologically similar tumors. Second, however, not all possible combinations of antibody phenotypes were encountered. That is, clusters of antigenic phenotypes were seen, and these phenotypes correlated to some degree with the histologic diagnosis of the tumor. Small lymphocytic and follicular lymphomas tended to be phenotypically distinct, although there was some overlap. Intermediate- and high-grade lymphomas were phenotypically more diverse. The more common phenotypes of lymphomas encountered could not be reconciled with any simple linear scheme of neoplastic B-cell differentiation.
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PMID:Monoclonal antibody phenotyping of B-cell non-Hodgkin's lymphomas. The Southeastern Cancer Study Group experience. 293 60

With a seroprevalence rate (SPR) of 6%-10% among healthy adult blood donors (ABD), Nigeria and other African locales represent an endemic zone for HTLV-I. We studied SPR in patients with leukaemia, lymphomas, solid tumours, and chronic disorders, as well as in groups of men and women with varying sexual lifestyles. Serum specimens were screened with ELISA and then confirmed with Western blot (WB). Sexual practices were investigated among volunteers of different sexual backgrounds by means of a questionnaire. Female prostitutes (FP) (13.0%) and patients with sexually transmitted diseases (STDP) (16.7%) had the highest SPR while a low rate occurred in religious celibate males (RCM) but not in religious celibate females (RCF) (11.8%). Heterosexual activity as well as geographical location of the place of birth constituted the most important risk factors for HTLV-I. HIV antibodies were demonstrable in none of the study subjects. ATL was associated with 100% SPR (4/4) while SPR in other clinical states were not different from normal. Western blot profile was rarely of strong poly band but more frequently of weak oligo band pattern with absent or weak p19 compared to p24. Only 18% of non Hodgkin's lymphoma in Ibadan, Nigeria was seropositive compared to 50% and > 60% in Japanese and Caribbean endemic zones respectively. The high SPR and aberrant WB profiles indicate reactivity to HTLV-I and to an HTLV-II-like activity, probably a new virus in the region. Excluding the aberrant WB profile, SPR based on HTLV-I-related profile was 3.8%-4.8% in ABD, 13% in FP, 10% in STDP, 1.9% in RCM, 0% in RCF, and 25% in ATL patients. The HTLV-II-related profile showed no such heterosexual association, but occurred in 75% of ATL patients. HTLV-I and probably and an HTLV-II-like virus appear to play a role in STD and lymphoma epidemiology in Nigeria.
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PMID:Some epidemiological features of the human T-cell lymphotropic virus type I (HTLV-I) and ATL in Nigerians. 815 10

Sera from a small sample of adult blood donors, healthy school children and patients with lymphoma, leukaemia, non-haematologic cancer, congenital and inflammatory disorders from Ibadan, Nigeria were screened for HTLV-I antibody by an enzyme-linked immunoabsorbent assay and confirmed by investigational Western blot. Seventy-nine of 236 positively screened samples could not be tested for confirmation. Seropositive reactivity was observed in nine of 123 blood donors, and 3 of 46 healthy school children but banding patterns on Western blot were often sparse. Among non-Burkitt's non Hodgkin's lymphoma patients six of 30 were HTLV-I positive including four of four with clinical features of adult T-cell leukaemia (ATL). Other clinical conditions had a frequency of positivity indistinguishable from healthy donors. Western blot patterns ranged from strong with multiple bands, which were uncommon, to those with only p24 and p21 envelope positive which were frequent. Given the relative paucity of clinical ATL and the unusual Western blot patterns the true rate of HTLV-I infection may be lower than estimated. It is possible that a cross-reactive HTLV-I-like virus accounts for this pattern.
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PMID:Frequency of adult T-cell leukaemia/lymphoma and HTLV-I in Ibadan, Nigeria. 847 36

Comparative genomic hybridization was applied for a comprehensive screening of frequently occurring net gains and losses of chromosomal subregions in small populations of CD30+ Hodgkin cells and their morphological variants. In 12 Hodgkin's lymphomas, recurrent gains were detected on chromosomal arms 2p, 9p, and 12q (in six, four, and five tumors, respectively) and distinct high-level amplifications were identified on chromosomal bands 4p16, 4q23-q24, and 9p23-p24. In Hodgkin cells with 9p23-p24 amplification, fluorescence in situ hybridization revealed an increased copy number of chromosomal sequences spanning the tyrosine kinase gene JAK2. Several of the imbalances described, in particular a gain in chromosomal arm 9p that includes JAK2 amplification, are similar to the genomic changes detected in primary mediastinal B-cell lymphoma.
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PMID:Genomic imbalances including amplification of the tyrosine kinase gene JAK2 in CD30+ Hodgkin cells. 1067 35

Although HIV-positive patients are at higher risk for developing a variety of infection-related cancers, the prevalence of infections with the seven known cancer-associated viruses has not been studied. Luciferase immunoprecipitation systems were used to evaluate antiviral antibodies in four 23-person groups: healthy blood donors and HIV-infected patients with oral hairy leukoplakia (OLP), Kaposi's sarcoma (KS), or non-Hodgkin lymphoma (NHL). Antibody profiling revealed that all HIV-positive individuals were strongly seropositive for anti-gp41 and antireverse transcriptase antibodies. However, anti-p24 HIV antibody levels were highly variable and some OLP and KS patients demonstrated weak or negative responses. Profiling two EBV antigens revealed no statistical difference in antibody levels among the three HIV-infected groups. A high frequency of KSHV infection was detected in HIV patients including 100% of KS, 78% of OLP, and 57% of NHL patients. Most HIV-infected subjects (84%) showed anti-HBV core antibodies, but only a few showed antibodies against HCV. MCV seropositivity was also common (94%) in the HIV-infected individuals and KS patients showed statistically higher antibody levels compared to the OLP and NHL patients. Overall, 68% of the HIV-infected patients showed seropositivity with at least four cancer-associated viruses. Antibody profiles against these and other infectious agents could be useful for enhancing the clinical management of HIV patients.
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PMID:The Cancer-Associated Virus Landscape in HIV Patients with Oral Hairy Leukoplakia, Kaposi's Sarcoma, and Non-Hodgkin Lymphoma. 2292 24

Genome instability is a hallmark of cancer. Diffuse large B-cell lymphoma (DLBCL) is the most common form of non-Hodgkin lymphoma with high levels of chromosomal aberrations. The purpose of this study was to characterize chromosomal aberrations in Chinese DLBCL patients and to compare chromosomal abnormalities between germinal centre B-cell-like (GCB) and non-GCB subgroups. Fluorescence in situ hybridization, G-band cytogenetics and immunohistochemistry were performed in 231 cases of de novo DLBCL. We demonstrated that the rate of abnormal and complex karyotypes was 89.1% (139/156) and 92.8% (129/139), respectively. We found a total of 490 structural chromosomal aberrations, including 96 frequent and recurring structural alterations. Most importantly, we identified several rare or novel chromosomal alterations: eight gains (5, 13, 14q, 17, 19p, 20, 21p, Y), one loss (21) and three recurrent translocations [t(7;15)(q22;q22), t(3;20)(p24;q13.1), t(2;3)(q21;q25)]. Moreover, the frequent recurrent genomic imbalance between GCB and non-GCB subgroups was different. Finally, we discovered two cases of concurrent IGH-BCL6 and MYC rearrangements. The rate of abnormal karyotypes in DLBCL patients of Chinese descent was similar to that of Western countries, but some common karyotypes were different, as were the abnormal karyotypes of GCB and non-GCB subgroups. Our discovery of rare and novel abnormal karyotypes may represent unique chromosomal alterations in Chinese DLBCL patients.
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PMID:Chromosome abnormalities in diffuse large B-cell lymphomas: analysis of 231 Chinese patients. 2313 54

HIV-associated primary CNS lymphomas are well-recognized, almost exclusively EBV-driven neoplasms with poor clinical prognosis. We report a challenging, atypical case of an HIV-associated lymphoproliferative disorder with unusual morphologic features reminiscent of Hodgkin Lymphoma, accompanied by HIV encephalitis. A 52-year-old male presented with acute seizures after seven months of progressive neurocognitive decline that was clinically diagnosed as progressive supranuclear palsy. Clinical work-up revealed HIV infection along with two ring-enhancing lesions in the brain on MRI, and negative CSF EBV testing. Subsequent biopsy showed well-demarcated hypercellular regions in the brain comprised of scattered Reed-Sternberg-like cells in a background of small to medium-sized lymphocytes exhibiting focal angiocentricity and geographic necrosis. The atypical cells were positive for CD20, EBV, and CD79a, and negative for CD45, GFAP, CD15, CD30, and p24. These cells were admixed with numerous CD68-positive cells. The adjacent brain showed classic features of HIV encephalitis with perivascular, CD68 and p24-positive multinucleated giant cells. This case illustrates several diagnostic pitfalls in the work-up of HIV-associated brain lesions, as well as reporting a unique histomorphology for an HIV-related primary CNS lymphoproliferative disorder.
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PMID:An unusual and challenging case of HIV-associated primary CNS Lymphoma with Hodgkin-like morphology and HIV encephalitis. 2632 86


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