Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Viruses implicated in the development of human cancers include hepatitis B (and C) viruses in hepatocellular carcinoma; human papillomaviruses in anogenital cancers; Epstein-Barr virus in nasopharyngeal carcinoma and Burkitt's lymphoma; human T-cell leukaemia/lymphoma viruses in adult T-cell leukaemia/lymphoma; and indirectly, human immunodeficiency viruses in Kaposi's sarcoma and B-cell lymphoma. Together, they contribute significantly to the cancer statistics in the Southeast Asian region. Neoplastic proliferation may be instigated by the presence and expression of viral oncogenes which may be integrated into the host genome and/or exist in episomal molecules. Critical viral genes may also interfere with host genes, resulting in the activation of cellular proto-oncogenes and/or the inactivation of anti-oncogenes and their products. The molecular pathogenesis of virally-induced cancers has led to major breakthroughs in the understanding of carcinogenesis at a molecular level. The occurrence of some of these viruses in a significant proportion of normal individuals suggests long latency periods necessitating multi-step co-operating events arising from multi-factorial agents such as host genetic susceptibility, immunological and hormonal status, as well as chemical and physical cocarcinogens in the environment. Successful intervention achieved with effective vaccines such as the hepatitis B vaccine and measures to severe the chain of viral transmission culminating in reduced incidence of the corresponding cancer will provide conclusive evidence for the virus-cancer relationship.
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PMID:Cancer and viruses. 810 16

The recently developed strategy for the detection of monoclonal B-cell populations, based on the selective amplification of predominant immunoglobulin heavy chain gene (IgH) rearrangement, is seen to be a suitable alternative to Southern blot analysis. The new technique uses a pair of consensus primers for variable (VH) and joining (JH) regions. We first tested the accuracy of this new approach on a broad series of 67 samples that had been well characterized by both Southern blot and immunohistochemical techniques before being subjected to blind testing. Our results show that this technique gave 100% specificity (absence of false-positive results) and approximately 70% sensitivity (30% false-negative results). The only exception was the presence of an IgH polymerase chain reaction ambiguous result in a case of Sezary's syndrome. The polymerase chain reaction technique was then applied to a panel of 27 frozen gastric endoscopy biopsy specimens following previous clinical suspicion of lymphoma. Monoclonality was detected in nine of 13 samples previously diagnosed as lymphomas and in one of two carcinomas. Further examination of the gastrectomy specimen in the latter case disclosed a B-cell lymphoma associated with the carcinoma. In spite of its limited sensitivity, the high specificity attained by this technique in the detection of monoclonality makes it a useful adjunct to routine morphologic criteria, as it is sometimes capable of detecting true positive cases that conventional morphology studies show to be negative.
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PMID:The detection of B-cell monoclonal populations by polymerase chain reaction: accuracy of approach and application in gastric endoscopic biopsy specimens. 824 19

A 34-year-old woman was hospitalized for the investigation of a one-month history of intestinal disorders, gastric heaviness and transitory icteric episodes. Extensive clinical investigations suggested the diagnosis of gall bladder carcinoma or sclerosing cholangitis. At laparotomy, the proximal part of common bile duct was markedly thickened by a white, firm, fish-flesh like tumour extending in to the cystic duct, gall bladder wall and to the liver. Histological study showed a diffuse lymphoid proliferation of the common bile duct mainly composed of small cells mixed with scattered large atypical cells. Immunohistochemistry revealed that most of the small cells expressed T-cell markers with predominant CD 4 and alpha-beta T-cell receptors and without phenotypic gap, whereas large atypical cells showed monotypic B phenotype with co-expression of mu and delta heavy chains and light lambda chain restriction. No evidence of primary nodal lymphoma was found during extensive clinical, radiological, sonographic or scanographic examinations. Sequential chemotherapy (MACOP-B) was instituted and the patient was still alive 4 years after diagnosis. Morphological and immunohistochemistry findings fulfilled criteria for a primary high grade B-cell lymphoma (centroblastic type, Kiel classification) from common bile duct concealed by numerous small reactive T-cells, so called T-cell rich B-cell lymphoma, not previously described in this location.
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PMID:Primary T-cell rich B-cell lymphoma of the common bile duct. 829 Dec 24

In order to elucidate the factors influencing the takes of human tumor xenografts in nude mice, we compared the transplantability of human tumors in nude mice with additional genetic defects in the immune system. The nude mice strains tested were classified as follows by expression of the beige gene and the x-linked immunodeficiency (xid) gene: 1) high NK nude (C57BL/6N, nu/nu), 2) low NK nude (C57BL/6 bg/bg nu/nu), 3) high NK nude with B-cell defect (CBA/N nu/nu), and 4) low NK nude with B-cell defect (NIH(S)III). Takes of human tumor xenografts including gastric carcinoma, T-cell lymphoma and B-cell lymphoma were better in nude mice with xid (CBA/N and NIH(S) III nude mice) than in nude mice without xid (B6 and beige nude mice). In addition, among the nude mice with xid expression, the takes were slightly better in nude mice with a CBA/N background than in those with a NIH(S) background. Moreover, the xenotransplantation rate in (CBA/N x C57BL/6N)F1 male nude mice with xid expression was higher than in (C57BL/6N x CBA/N)F1 males without xid expression, but did not react the same level as that in CBA/N nude. On the other hand, introduction of the beige gene into nude mice minimally improved the takes of human tumor xenografts under limited experimental conditions (inoculation of 100 x 10(5) T-cell lymphoma and 1 x 10(5) gastric carcinoma cells) despite the reduction of NK activity. In xenotransplantation of human tumors directly from patients, the take rates of the tumors were also better in CBA/N nude mice than in BALB/cA nude mice. The results in the present report confirmed the effect of xid and CBA/N genetic background on human tumor xenografts in nude mice, suggesting the existence of serum factors, possibly present in serum IgM, mediating rejection of the xenografts.
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PMID:Role of x-linked immunodeficiency (xid) and NK activity in rejection of human tumor xenotransplants in nude mice. 832 95

The incidence of three malignancies has increased in conjunction with the epidemic of human immunodeficiency virus (HIV) disease, and they are currently considered acquired immunodeficiency syndrome (AIDS)-defining conditions. These are Kaposi's sarcoma, associated with AIDS since the onset of the epidemic in 1981; intermediate or high-grade B-cell lymphoma, which became AIDS-defining in 1985; and cervical carcinoma in HIV-infected women, formally recognized as an AIDS-defining diagnosis on January 1, 1993. Approximately 40% of all patients with AIDS have developed cancer during the course of HIV infection. Further, as survival has improved in HIV disease, the incidence of these malignancies has increased. It is thus expected that greater numbers of patients with AIDS-related lymphoma and cervical cancer will be diagnosed in the years ahead. The epidemiologic factors associated with neoplastic disease differ among patients with the three AIDS-related malignancies. The pathogenesis of neoplastic disease also differs. The specific etiologic steps in the development of AIDS-related Kaposi's sarcoma and lymphoma are currently unknown. However, a great deal of information has already been acquired, which may have bearing on the pathogenesis of malignant disease in general, as well as the elucidation of future therapeutic modalities. The specific epidemiologic, etiologic, and clinical characteristics of the AIDS-related malignancies will be described herein. It is hoped that this review will serve to outline our current understanding of this area, to introduce the questions and controversies which are apparent in the field, and to mention those areas in which future research might be focused.
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PMID:AIDS-related malignancies: the emerging epidemic. 835 Mar 62

The bcl-2 proto-oncogene product inhibits apoptosis. Increased levels of bcl-2 protein are associated with prolonged B-cell survival and have been demonstrated in a high proportion of follicular B-cell lymphoma. Recent studies have shown that bcl-2 protein expression in B cells immortalized by Epstein-Barr virus (EBV) in vitro is up-regulated by the EBV-latency-associated antigen, latent membrane protein (LMP) 1. The epithelial malignancy, undifferentiated nasopharyngeal carcinoma (UNPC), has a well-established association with EBV and the tumour cells characteristically display a restricted latent viral phenotype including LMP 1. This study has investigated the relationship between the presence of EBV DNA, EBV phenotypic profiles and bcl-2 protein expression in conventionally processed and cryopreserved samples of NPC using in situ hybridization, immunocytochemical and immunoblotting techniques. bcl-2 was detected in most (80%) samples of UNPC as well as in 1/3 samples of keratinizing NPC and 2/2 samples of nasopharyngeal adenocarcinoma. However, no close correlation was found between the presence of EBV DNA, and profiles for LMP 1 and bcl-2 protein expression in 45 UNPC. In addition, bcl-2 protein was shown to be selectively expressed in the basal compartment of normal nasopharyngeal epithelia. bcl-2 protein expression has not been reported previously in malignant tumours of epithelial origin. The findings in this study implicate a role for bcl-2 both in normal keratinocyte differentiation and in the pathogenesis of epithelial malignancy.
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PMID:Bcl-2 proto-oncogene expression in Epstein-Barr-virus-associated nasopharyngeal carcinoma. 838 56

Epstein-Barr virus (EBV) as a member of the herpesvirus family persists lifelong in the human body and causes diseases associated with virus replication (infectious mononucleosis, oral hairy leukoplakia) as well as neoplastic conditions such as nasopharyngeal carcinoma, B-cell lymphoma, Hodgkin's disease associated with viral latency. This complex biology relates to a highly regulated control of the persisting virus. Still, EBV is lytically produced in certain compartments of the human body. Epithelial cells were found to be of key importance for this. Various routes (cell fusion, IgA receptor-mediated uptake) were described for EBV to enter epithelial cells in the absence of CR2 receptor. Viral entry into cells, however, via CR2 receptor fusion or IgA mediated was not found to be sufficient for viral production. The molecular mechanisms for the lack of viral production in most target cells are primarily the presence of silencer activities and the early elimination of cells entering the lytic cycle. Only terminally differentiated epithelial cells are capable of supporting an efficient lytic cycle of EBV replication. EBV-mediated suppression of apoptosis as well as down-regulation of cellular and viral gene products, such as HLA molecules, which mediate recognition by the immune system, are important contributing factors to the development of these neoplasias where viral genes, possibly via interaction with anti-oncogenes, such as p53, in context with genetic and environmental factors play a key role. Novel diagnostic tools and a vaccine have been developed which could help to control EBV-related diseases.
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PMID:Epstein-Barr virus and its interaction with the host. 840 48

Introduction and expression of the proto-oncogene bcl-2 (B-cell lymphoma/leukemia 2) has been shown to extend the survival of certain hematopoietic cell lines after growth factor deprivation, by blocking apoptosis or programmed cell death. We investigated the effect of bcl-2 expression on cellular sensitivity to lysis by tumor necrosis factor (TNF), a cytokine capable of inducing apoptosis in several tumor cell lines. Introduction of the human bcl-2 gene in the highly TNF-sensitive L929 mouse fibrosarcoma cell line did not result in altered TNF sensitivity. Likewise, NIH3T3 and REF cells, which are resistant to TNF cytotoxicity but become TNF sensitive upon cotreatment with actinomycin D or upon expression of the adenovirus E1A gene, did not show altered TNF sensitivity upon bcl-2 transfection. Despite constitutive expression of the endogenous bcl-2 gene, human MCF7 breast carcinoma cells, as well as HL60 promyelocytic leukemia and U937 histiocytic lymphoma cell lines were found to be TNF sensitive. bcl-2-overexpressing derivatives of these cell lines did not acquire reduced TNF sensitivity and still exhibited the characteristic pattern of internucleosomal DNA fragmentation of TNF-induced apoptosis. Moreover, bcl-2 expression in the interleukin 3 (IL-3)-dependent myeloid cell line 32D protected these cells from apoptosis resulting from growth factor deprivation, but not from apoptosis induced by TNF. These data clearly establish the absence of a correlation between bcl-2 gene expression and cellular sensitivity to TNF-induced cell lysis. These findings are discussed in the context of the hypothesis of different pathways for induction of apoptosis, only some of which are affected by bcl-2 expression.
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PMID:Effect of bcl-2 proto-oncogene expression on cellular sensitivity to tumor necrosis factor-mediated cytotoxicity. 845 35

A 79-year-old women with upper abdominal pain, vomiting and weight loss was found at endoscopy to have a large tumour mass in the gastric body. Histology of forceps biopsies revealed an adenocarcinoma of intestinal type. Gastrectomy was performed, but extensive lymph node metastasis precluded a curative surgical approach. Histopathological study of the specimen, however, revealed two distict malignancies, which arose in the setting of Helicobacter pylori-associated chronic gastritis with partial mucosal atrophy. One tumour was a gastric carcinoma, while the other was a primary B-cell lymphoma of the stomach (CD20-positive). The lymphoma comprised both a low-grade component (mucosa-associated lymphoid tissue- or MALT-type lymphoma), and a high-grade component (large cell lymphoma with CD30-positive giant cells). Infection with H. pylori was confirmed by the serological presence of IgG antibodies to H. pylori-antigens, including antibodies against the 128 kDa protein of the cytotoxin-associated gene (cagA gene) of H. pylori.
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PMID:Simultaneous gastric adenocarcinoma and MALT-type lymphoma in Helicobacter pylori infection. 854 31

The authors describe a patient with gastric lymphoepithelioma-like carcinoma (LELC) and jejunal low grade B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) with histologic transformation to large cell lymphoma. In situ hybridization studies for Epstein-Barr virus (EBV) demonstrated abundant EBV RNA (EBER) within the neoplastic cells of the gastric LELC and the jejunal large cell lymphoma. The low grade MALT lymphoma was EBER negative. Polymerase chain reaction (PCR) studies confirmed the in situ hybridization results, and demonstrated a 30 base pair deletion in the 3' end of the latent membrane protein gene in both the gastric LELC and the jejunal large cell lymphoma. These results suggest that the same viral strain infected both the stomach and jejunal tumors. In addition, the finding of EBV in the large cell lymphoma, but not the low grade component suggests that EBV may have played a role in large cell transformation.
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PMID:Gastric lymphoepithelioma-like carcinoma and jejunal B-cell MALT lymphoma with large cell transformation. Demonstration of EBV with identical LMP gene deletions in the carcinoma and large cell lymphoma. 862 63


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