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)

This report describes a clinical case of a large cell, immunoblastic plasmacytoid malignant B-cell lymphoma of the rectum in an AIDS patient coinfected with HTLV-I. The malignant cells showed clonal genetic rearrangement of the HC (JH) and LCK genes. Infection by EBV was demonstrated serologically and with slot blots using genomic DNA of the cancer cells. Southern blot analysis with DNA extracted from the lymphoma cells were negative for HTLV-I. The patient received seven cycles of VACO-B which induced complete but transient clinical remission of the tumor. The final outcome of the patient is unknown.
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PMID:Primary B cell lymphoma of the rectum in a patient coinfected with HIV-1 and HTLV-I. 128 27

Infection of human B cells by Epstein-Barr virus (EBV) causes transformation to immortalized lymphoblastoid cells capable of continuous proliferation. To identify biochemical changes induced by EBV infection of B cells, we have utilized isogenic EBV-positive and -negative B cell lymphoma lines as a model to determine whether EBV induces protein tyrosine phosphorylation. By utilizing two different methods, immunoblotting with phosphotyrosine antibodies and phosphoamino acid analysis, it was shown that the presence of EBV in these cells was reversibly associated with increased phosphorylation of a 50 kilodalton cytosolic protein on tyrosine residues. The characteristics of this protein were not consistent with any known EBV-encoded protein that is expressed in latency, and thus it likely represents a cellular protein that is phosphorylated by an endogenous tyrosine kinase. These results suggest that EBV induces protein tyrosine phosphorylation in human B cells, and this may represent an important event in the transformation of B lymphocytes by EBV.
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PMID:Conversion of a human B cell lymphoma line by Epstein-Barr virus is associated with increased tyrosine phosphorylation of a 50 kilodalton cytosolic protein. 165 26

Injection of a nonlymphomagenic ecotropic virus 24-666 isolated from a B cell lymphoma of AKR origin into young AKR mice (1-60 days old) inhibited spontaneous T cell lymphoma development. The reduction in T cell lymphoma incidence (16/106-15%) was accompanied with the appearance of B cell lymphomas (16/106-34%) in older mice (500 days mean latency). Infection of newborn to 60-day-old AKR mice with 24-666 prevented changes in thymus subpopulations and expression of MuLV-related cell surface antigens, normally observed in the thymus of 5- to 6-month-old AKR mice prior to lymphoma development. Thymuses of 24-666-infected 9- to 12-month-old mice lacked recombinant dual tropic virus (DTV) expression and retained the thymus pattern of 2-month-old AKR mice. At 12 months after 24-666 administration a striking decrease in Thy1.1 level and in the CD4+ CD8+ population and an increase in CD4- CD8- cells and in mu+ B cells, predominantly Ly1+, were observed. The presence of B cells in these thymuses was also reflected in the high response of thymocytes to LPS blastogenesis accompanied by a decreased response to PHA. Although T cell lymphoma development was markedly reduced by 24-666 administration, the establishment of potential lymphoma cells (PLC) was not affected. Transfer of lymphoid cells from 12-month-old grossly normal 24-666-infected mice to the appropriate recipients resulted in a high incidence (64-80%) of B cell lymphoma development. Thus, 24-666 seems to act through interference with the establishment of DTV in the thymus, thereby preventing PLC promotion to overt T cell lymphomas. Lack of the favorable microenvironment for PLC development in the T cell pathway enables PLC development in the B cell pathway in older mice.
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PMID:Prevention of spontaneous AKR T cell lymphomagenesis by 24-666, a virus isolated from an AKR B cell lymphoma. 167 38

Infection of young chickens with RAV-1, a subgroup A isolate of avian leukosis virus, results in the development of lymphoid leukosis, a B-cell lymphoma characterized by provirus insertion into the c-myc locus. We report here that when 12- to 13-day-old embryos rather than 1-day-old chickens were infected with RAV-1, a novel B-cell lymphoma developed in which proviral insertions had activated expression of the c-myb gene. These tumors expressed elevated levels of a 4.5-kilobase myb-containing mRNA transcript that contained c-myb sequences not found in v-myb. The c-myc locus in these tumors appeared normal. The biological properties of the activated myb lymphoma were distinct from those of lymphoid leukosis. Metastatic disease developed within 7 weeks of infection. Distinct intermediate pathogenic stages with preneoplastic and primary neoplastic lesions were not detected. Although bursal tissues appeared to be nonmalignant on gross examination, Southern analyses of bursal DNA revealed the presence of tumor with the same clonal origin as abdominal lymphoma masses. The dependence on embryonic infection for development of activated myb lymphoma suggests that the target cells in which c-myb is activated are found only in embryos and are distinct from those cells that give rise to lymphoid leukosis.
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PMID:RAV-1 insertional mutagenesis: disruption of the c-myb locus and development of avian B-cell lymphomas. 253 46

Since 1985 organ donors are routinely tested for the presence of HIV-antibodies, but prior to that time several patients acquired HIV-infection from grafts. In May 1984 a 65-year-old woman on hemodialysis received a cadaver kidney graft from a young iv drug addict. The transplant functioned perfectly with cyclosporin A immunosuppression. Retrospectively, 22 days after surgery HIV antigen was detected. At this time only a faint band of anti-p24 antibodies was found in the Western blot. Two years after surgery splenomegaly was found in the apparently healthy patient. During the third year thrombocytes fell and she developed lymphadenopathy and constitutional symptoms. Up to this time the immunological parameters were in the range of 10 healthy renal transplant patients with cyclosporin A treatment. In the 4th year T-lymphocytes dropped to values below 200 and the patient developed Pneumocystis carinii pneumonia. A few months later a pulmonary node, which later proved to be a B-cell lymphoma, appeared. Slightly less than 5 years after transplantation the patient died from clinically diagnosed pulmonary embolism. The progression of the HIV-Infection in this patient and in one of 18 patients in published reports show that the incubation period is several years shorter in renal transplant patients than in those who acquire HIV from blood products.
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PMID:[HIV infection caused by kidney transplant: case report and review of 18 published cases]. 267 39

Infection with the human immunodeficiency virus-type 1 (HIV-1) may produce a variety of central nervous system (CNS) symptoms and signs. CNS involvement in patients with the acquired immunodeficiency syndrome (AIDS) includes AIDS dementia complex or HIV-1 associated cognitive/motor complex (widely known as HIV encephalopathy), progressive multifocal leucoencephalopathy (PML), opportunistic infections such as Toxoplasma gondii, TB, Cryptococcus and infiltration by non-Hodgkin's B cell lymphoma. High resolution structural imaging investigations, either X-ray Computed Tomography (CT scan) or Magnetic Resonance Imaging (MRI) have contributed to the understanding and definition of cerebral damage caused by HIV encephalopathy. Atrophy and mainly high signal scattered white matter abnormalities are commonly seen with MRI. PML produces focal white matter high signal abnormalities due to multiple foci of demyelination. However, using structural imaging techniques there are no reliable parameters to distinguish focal lesions due to opportunistic infection (Toxoplasma gondii abscess) from neoplasm (lymphoma infiltration). In this manuscript we review the use of radionuclide brain imaging techniques in the investigation of HIV infected patients. Brain perfusion single photon emission tomography (SPET), neuroreceptor and positron emission tomography (PET) studies are reviewed. Greater emphasis is put on the potential of some radiopharmaceuticals, considered to be brain tumor markers, to distinguish intracerebral lymphoma infiltration from Toxoplasma infection. SPET with 201Tl using quantification (tumour to nontumour radioactivity ratios) appears a very promising technique to identify intracerebral lymphoma.
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PMID:Radionuclide brain imaging in acquired immunodeficiency syndrome (AIDS). 755 47

A 61-year-old pig farmer was found to be suffering from meningitis caused by Streptococcus suis type II. He was successfully treated with intravenous penicillin G but was left with permanent deafness. B-cell lymphoma was also diagnosed one year later. S. suis is a zoonotic pathogen which causes meningitis, septicemia and endocarditis in pigs. Human infection is rare and often presents as meningitis with the sequela of permanent deafness. It has previously been reported in pig rearing countries such as Holland or Hong Kong. This is the second documented case of human meningitis caused by S. suis in Taiwan, which is also a major pig rearing country in Asia. Infections caused by viridans streptococci or other beta-hemolytic streptococci in Taiwan may therefore actually be due to S. suis. Further investigation of the possibility of the underlying deficiency of humoral immunity is warranted.
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PMID:Streptococcus suis meningitis complicated with permanent perceptive deafness: report of a case. 791 82

Single or multiple lung nodules or masses were noted at chest radiography in 25 (9.7%) of 257 patients after cardiac transplantation. Two episodes occurred in each of three patients, for a total of 28 (10.9%) episodes in the 257 patients within the first 18 months after transplantation (transplantation performed between July 1987 and December 1990). Bronchoscopy, percutaneous needle biopsy, and open lung biopsy were performed as clinically warranted to establish a diagnosis. Infection was found in 21 instances (8.2%) in 18 patients. The most frequent pathogens were Aspergillus (n = 9 [3.5%]) and Nocardia (n = 7 [2.7%]). Aspergillus was hospital acquired in eight (89%) of nine patients and had a right-sided predominance (20 [74%] of 27 lesions). The nodules or masses appeared a median of 2 months after transplantation for Aspergillus (range, 0.5-12 months) and 5 months for Nocardia (range, 1-10 months). B cell lymphoma manifested as numerous nodules in two patients (0.8%). Although a variety of causes were found for post-cardiac transplantation nodules or masses, the majority (75%) were infectious.
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PMID:Lung nodules and masses after cardiac transplantation. 832 3

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

Infection with hepatitis C virus (HCV) may affect not only the liver but also various nonhepatic tissues and organs and may combine with many etiologically unrelated diseases and morbid conditions. Numerous nonhepatic manifestations in HCV infection have been previously reported. For some (eg, cryoglobulinemia), the association is well established. For others, such as sialadenitis and lichen planus, the association is probable (but not completely documented) and, for the remainder, the associations are weak. Extrahepatic manifestations may result from immunological mechanisms as well as virus invasion and replication in the affected extrahepatic tissues and organs. Thyroid abnormalities, primarily Hashimoto's disease, and isolated increases of anti-thyroid antibodies (ATPO) appear to be more frequent in chronic hepatitis C than B or D, with high ATPO titers clustering mainly among females. Interferon-alpha (IFN-alpha) therapy is associated with development of thyroid dysfunction in 5.5-12.9% of patients, usually exposing preexisting subclinical thyroid abnormalities. Mixed cryoglobulinemia (MC) is commonly found (36-45%) in patients with chronic HCV infection; however, only in a minority of cases does it become clinically manifested as systemic vasculitis with purpura, neuropathy, or Raynaud's phenomenon. In a number of patients, MC may terminate in non-Hodgkin's B-cell lymphoma. Treatment of these lymphoproliferative disorders with IFN-alpha is advocated. Idiopathic thrombocytopenia is now recognized more frequently in association with chronic HCV infection and is usually aggravated by IFN-alpha therapy. Patients with porphyria cutanea tarda (PCT) have demonstrated serological markers of HCV infection in 62-82% of cases. The usefulness of IFN-alpha in PCT remains to be demonstrated. Lichen planus has also been found in association with chronic HCV infection, particularly when severe or affecting the oral cavity. Other nonhepatic manifestations have also been reported in HCV infection such as diabetes, corneal ulceration, uveitis, and sialadenitis. These manifestations deserve further study and documentation. Finally, markers of autoimmunity occur with high frequency in chronic HCV infection; however, combination with the classical syndrome of autoimmune hepatitis is rare. In the presence of various autoantibodies, the clinical features of chronic hepatitis C do not appear to be modified and, contrary to general perception, IFN-alpha therapy within randomized controlled trials should not be withheld since the response rate to IFN-alpha does not appear to differ in the presence or absence of low titers of these markers.
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PMID:Nonhepatic manifestations and combined diseases in HCV infection. 901 79


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