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)

Epstein-Barr virus (EBV) DNA is frequently identified in benign and malignant lymphoproliferative conditions. As shown by in situ hybridization studies viral DNA is localized within malignant cells as well as benign lymphocytes. Clonal and nonclonal EBV genomes are present in Hodgkin's disease (HD), lymphomas of the immunocompromised host and reactive lymph node hyperplasia. Lytic infection with formation of linear genomes is observed in the same conditions but appears to be infrequent in HD as shown by quantitation of mRNA coding for viral capsid antigen. Expression of the oncogene LMP (latent membrane protein) is seen in Sternberg-Reed (SR) cells and immunoblasts of AIDS-related lymphoma and infectious mononucleosis (IM). In HD, the region of the BNLF1 oncogene coding for the amino terminal and transmembrane domains (associated with oncogenic function) of LMP appears to be homogeneous whereas the region coding for the intracytoplasmic (carboxy terminal) domain of LMP is heterogeneous. Cytological similarities between SR cells and immunoblasts of IM and AIDS-related lymphomas are consistent with the hypothesis that the BNLF1 oncogene is one possible inducer of morphological features of SR cells. Whether chromosomal integration of EBV DNA is an important factor in activation of such a transforming activity remains to be elucidated. EBV DNA positive and negative HD cases with numerous SR cells lack significant mRNA expression of the two recombinase activating genes (RAG-1 and RAG-2). Therefore the SR cells appear to be derived from lymphocytes beyond the pre-B-cell or common thymocyte stage which may or may not subsequently become infected by EBV.
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PMID:Significance of the detection of Epstein-Barr virus DNA in lymph nodes in patients with Hodgkin's disease. 133 49

To investigate the range of pathology shown by acquired immune deficiency syndrome (AIDS)-related lymphomas arising in an epidemiologically well-defined group of patients, all cases of lymphoma recognized in Danish human immunodeficiency virus (HIV)-infected individuals up to the end of 1988 were studied. Twenty-seven cases (26 high-grade non-Hodgkin's lymphoma [NHL], 1 Hodgkin's disease) were found, to give a cumulative incidence rate of 8% among Danish AIDS patients. Morphologically most NHL patients were classified into two groups: 1) high-grade tumors with a predominant population of immunoblasts, either monomorphic or more often polymorphic with plasmacytic differentiation; 2) Burkitt-type. Of 26 NHLs, 22 had a B-cell paraffin-section immunophenotype and 4 were non-B, non-T. Epstein-Barr virus (EBV) DNA was demonstrated in tumor cells of 12 of 24 cases (50%) using in situ nucleic acid hybridization with a 35S-labeled probe in paraffin sections. Epstein-Barr virus DNA was found in 65% of group 1 and 20% of group 2 tumors. This study suggests the existence of two main groups of AIDS-related lymphoma with different pathogeneses. First there are immunoblast-rich lesions, which usually are associated with EBV and morphologically resemble lymphomas described in immunosuppressed organ-transplantation patients. Second there are Burkitt-type tumors in which EBV sequences are less common and that may be pathogenetically analogous to sporadic Burkitt's lymphoma.
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PMID:AIDS-related lymphoma. Histopathology, immunophenotype, and association with Epstein-Barr virus as demonstrated by in situ nucleic acid hybridization. 184 63

Non-Hodgkin's lymphomas with particular clinicopathologic features occur with a high incidence in homosexual men affected by AIDS. More frequently than in the general population, these lymphomas have an extranodal location including the gastrointestinal tract. We have recently observed four cases of AIDS-associated lymphomas whose primary location is in the lower rectum and anus. The patients were 27 to 44 years of age, had greatly depressed helper-suppressor T-cell ratios, and antibodies to human immunodeficiency virus (HIV). All four presented with anorectal symptoms and originally had surgery for anorectal fistulas or tumor masses. When staged, three patients had no other organ involvement, the fourth only had lymphoma in an axillary lymph node, and all four had large tumor masses confined within the rectum. In terms of histology, the lymphomas were of undifferentiated or of large cell type and of B-cell phenotype. Lymphomas with primary or major location in the rectum are a rare occurrence in the general population, and until recently, are rare even among the lymphomas associated with the immune deficiency syndrome. At the Lenox Hill Hospital in New York City, no rectal lymphoma among the 58 cases of AIDS-related lymphoma diagnosed during the past 4 years was recorded until 10 months ago. The recognition of the new feature in presentation, a neoplasm associated with AIDS, is obviously important for its early diagnosis and treatment. Its unusual occurrence at the suspected portal of entry of the HIV infection is of interest because it may provide new clues to the association between AIDS and neoplasia.
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PMID:Primary anorectal lymphoma. A new manifestation of the acquired immune deficiency syndrome (AIDS). 295 43

Acquired immunodeficiency syndrome (AIDS) is a lethal infectious disease that has reached epidemic proportions in urban centers of the United States. Intraabdominal opportunistic infections and malignancies are common features of this syndrome. A prodromal phase or possibly milder form of infection is known as the AIDS-related complex. Abdominal computed tomography (CT) in patients with AIDS-related complex often demonstrates a triad of mild retroperitoneal and mesenteric adenopathy, splenomegaly, and perirectal inflammation. Lymph node enlargement greater than 1.5 cm is unusual in the AIDS-related complex and should prompt CT-guided biopsy. Abdominal adenopathy (greater than 1.5 cm) in AIDS, in our experience, is most commonly related to non-Hodgkin lymphoma, Kaposi sarcoma, or infection with Mycobacterium avium-intracellulare. In most instances, CT-guided biopsy with appropriate staining technique can readily distinguish these entities. However, the subtyping of non-Hodgkin lymphoma by fine-needle aspiration biopsy alone remains controversial. Unusual features of abdominal malignancies are common in AIDS. These include a purely lymphadenopathic form of AIDS-related Kaposi sarcoma and a predilection for extranodal sites of lymphoma in AIDS. In general, patients with AIDS-related lymphoma present with advanced stages of disease with highly malignant histologic subtypes. Abdominal CT may be useful clinically for diagnosing intraabdominal complications of AIDS.
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PMID:Abdominal CT in acquired immunodeficiency syndrome. 351 46

The number of cases HIV-associated non-Hodgkin's lymphoma continues to increase as the AIDS epidemic grows. Approximately 3% of AIDS-defining illnesses are non-Hodgkin's lymphoma. The number of non-Hodgkin's lymphoma cases may actually be higher because many cases go unreported. There is also evidence that increasing numbers of patients who are surviving longer on antiretroviral therapy are developing non-Hodgkin's lymphoma. A majority of HIV-related lymphomas are large cell, either high-grade immunoblastic or aggressive intermediate grade, diffuse cleaved, or small noncleaved (Burkitt's-like). HIV-related non-Hodgkin's lymphomas behave aggressively. They are predominantly extranodal and often show unusual patterns of organ involvement. They are typically stage III or IV at the time of diagnosis. Current treatment strategies involve the use of combination chemotherapy regimens with or without antiretroviral therapy. Current studies are evaluating the efficacy of low-dose chemotherapy regimens versus standard-dose regimens with granulocyte-macrophage colony-stimulating factor support. New strategies for treating AIDS-associated non-Hodgkin's lymphoma will incorporate our current knowledge of AIDS-related lymphoma pathogenesis. Factors that reflect a patient's state of immunodeficiency seem to be the most important prognostic features determining clinical outcome after treatment. Patients with good prognostic features may benefit the most from aggressive treatment regimens. AIDS-related primary central nervous system lymphomas continue to comprise approximately 15% of AIDS-related non-Hodgkin's lymphoma cases. Treatment is limited. Although whole-brain radiation therapy can result in an improved neurologic status, the median survival remains 3 to 4 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical aspects of HIV-related lymphoma. 821 98

The sonographic studies of 72 patients with pathologically proven Hodgkin's or non-Hodgkin's hepatic lymphoma were retrospectively reviewed. Sixty-eight patients (94%) had secondary hepatic lymphoma (nine of them had AIDS-related lymphoma) and four patients (6%) had primary lymphoma of the liver. Forty-six of 72 patients (64%) had diffuse hepatic involvement, and 26 of 72 patients (36%) had focal liver lesions as demonstrated by sonography. Four patterns of disease were identified: (a) hepatomegaly was depicted by sonography in 26 of the 59 patients with secondary hepatic lymphoma not related to AIDS, in two of the nine patients with AIDS-related secondary hepatic lymphoma, and in one of the four patients with primary hepatic lymphoma; (b) multiple rounded well-delineated hypoechoic liver lesions were found in 22 of the 68 patients with secondary hepatic lymphoma; (c) a large heterogeneous echoic mass, which was an evocating clue to the diagnosis of primary lymphoma of the liver, was found in the four patients with primary lymphoma of the liver; and (d) an absence of sonographic abnormalities was found in 20 of the 59 patients with secondary lymphoma not related to AIDS. Liver involvement with lymphoma should be considered in any patient who develops multiple homogeneous hypoechoic liver masses, even in the absence of known underlying lymphomatous disease.
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PMID:Hodgkin's and non-Hodgkin's hepatic lymphoma: sonographic findings. 822 32

We used the polymerase chain reaction, in situ hybridization, and immunohistochemical stains against latent membrane protein, CD23, and Epstein-Barr viral nuclear antigens 1 and 2 to identify Epstein-Barr virus (EBV) in fixed and unfixed (cryopreserved) AIDS-related lymphoma (ARL) specimens. The study included 17 cases of large-cell (immunoblastic) lymphoma, 11 cases of small non-cleaved cell lymphoma, and two cases of Hodgkin's disease. The EBV DNA was more frequently detected by polymerase chain reaction in cryopreserved specimens (94%) than in fixed specimens (17%). Significantly, the immunohistochemical and in situ hybridization studies detected evidence of EBV in only a small (< 10%) subset of the cells in 27 of 30 ARL specimens. We conclude that tissue fixation reduced the ability to detect EBV in ARL by polymerase chain reaction and that EBV was detectable in only a minority of cells in most ARL tissues.
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PMID:Incidence of Epstein-Barr virus in AIDS-related lymphoma specimens. 839 Oct 77

Detection of novel DNA sequences in Kaposi's sarcoma (KS) and AIDS-related body cavity-based, non-Hodgkin's lymphomas suggests that these neoplasms are caused by a previously unidentified human herpesvirus. We have characterized this agent using a continuously infected B-lymphocyte cell line derived from an AIDS-related lymphoma and a genomic library made from a KS lesion. In this cell line, the agent has a large episomal genome with an electrophoretic mobility similar to that of 270-kb linear DNA markers during clamped homogeneous electric field gel electrophoresis. A 20.7-kb region of the genome has been completely sequenced, and within this region, 17 partial and complete open reading frames are present; all except one have sequence and positional homology to known gammaherpesvirus genes, including the major capsid protein and thymidine kinase genes. Phylogenetic analyses using both single genes and combined gene sets demonstrated that the agent is a gamma-2 herpesvirus (genus Rhadinovirus) and is the first member of this genus known to infect humans. Evidence for transient viral transmission from infected to uninfected cells is presented, but replication-competent virions have not been identified in infected cell lines. Sera from patients with KS have specific antibodies directed against antigens of infected cell lines, and these antibodies are generally absent in sera from patients with AIDS without KS. These studies define the agent as a new human herpesvirus provisionally assigned the descriptive name KS-associated herpesvirus; its formal designation is likely to be human herpesvirus 8.
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PMID:Primary characterization of a herpesvirus agent associated with Kaposi's sarcomae. 852 68

While there is a clear association between several types of immunodeficiency-related lymphomas and Epstein-Barr virus (EBV), the association of EBV infection in AIDS-related lymphoma in Brazil, where the incidence of AIDS is high, has remained unknown. The authors report their findings from an analysis of tissue samples from 24 cases of AIDS-related lymphoma in Brazil. The samples were analyzed for morphologic classification, immunophenotype, and EBV association. 20 cases were classified as non-Hodgkin's lymphoma, while 4 were Hodgkin's disease. 11 non-Hodgkin's lymphomas were classified as diffuse large cell type, 5 as small, non-cleaved cell, Burkitt-type, and 4 as large cell immunoblastic non-Hodgkin's lymphoma. 18 cases were of B-cell phenotype; one was a T-cell lymphoma and one was classified as null. EBV was demonstrated in the tumor cells of 11 of the 20 non-Hodgkin's lymphoma cases and in 3 of the 4 cases of non-Hodgkin's disease.
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PMID:AIDS-related lymphoma in Brazil. Histopathology, immunophenotype, and association with Epstein-Barr virus. 860 50

The incidence of non-Hodgkin's lymphoma is greatly increased in human immunodeficiency virus (HIV)-infected individuals. Most are clinically aggressive B-cell lymphomas exhibiting Burkitt-type, immunoblastic or large-cell morphology. Approximately 80% arise systemically (nodal or extranodal), and the remaining 20% arise in the central nervous system. A small proportion are body cavity-based (primary effusion) lymphomas associated with Kaposi's sarcoma-associated herpesvirus (KSHV) infection. Possible factors contributing to lymphoma development include HIV-induced immunosuppression, chronic antigenic stimulation, and cytokine overproduction. These phenomena are associated with the development of oligoclonal B-cell expansions. The appearance of malignant lymphoma is characterized by the presence of a monoclonal B-cell population displaying a variety of genetic lesions including Epstein-Barr virus (EBV) infections, c-myc gene rearrangement, bcl-6 gene rearrangement, ras gene mutations, and p53 gene mutations/deletions. The number and type of genetic lesions varies according to anatomic site of origin and histopathology. In the case of Burkitt-type lymphoma, virtually 100% exhibit c-myc gene rearrangement, two thirds display p53 gene mutations, one third contain EBV, and none exhibit bcl-6 gene rearrangements. In contrast, in the case of immunoblastic lymphoma, virtually 100% contain EBV, 25% display c-myc gene rearrangements, 20% display bcl-6 gene rearrangements, and few exhibit p53 gene mutations. These findings suggest that more than one pathogenetic mechanism is operational in the development and progression of acquired immunodeficiency syndrome (AIDS)-related lymphoma. Further work is necessary to develop a thorough understanding of the origin and pathogenesis of malignant lymphoma in the setting of HIV infection. AIDS-related lymphoma remains an important biologic model for investigating the development and progression of high-grade non-Hodgkin lymphomas as well as malignant lymphomas that develop in immune-deficient hosts.
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PMID:Molecular pathology of acquired immunodeficiency syndrome-related non-Hodgkin's lymphoma. 904 11


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