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

A Japanese patient with adult T-cell leukemia-lymphoma (ATL) showed a disease progression from the smoldering type to the chronic type and finally to the acute type. The patient was variously treated, including 2'-deoxycoformycin, with some beneficial effects. During the chronic type he developed a composite lymphoma consisting of T-cell lymphoma (ATL) of medium-sized cells and B-cell lymphoma of diffuse large cell type. At that time, he also suffered from miliary tuberculosis and adenovirus type 11-induced hemorrhagic cystitis, indicating that he was in a marked immunodeficient state. Southern-blot analysis revealed that the two malignancies have distinct clonal origin on the basis of the following results: (1) clonally rearranged T-cell receptor beta-chain gene (TcR-beta gene) and germline configuration of immunoglobulin heavy chain gene (IgH gene) in ATL leukemic cells, (2) clonal rearrangement of IgH gene in lymphoma cells, indicating a monoclonal B-cell lymphoma, (3) monoclonal integration of HTLV-I provirus in ATL leukemic cells, (4) definite presence and monoclonal origin of EBV genome in lymphoma cells. This is the first report of secondary EBV genome carrying monoclonal B-cell lymphoma in an ATL patient. It is suggested that the immunodeficient state in the patient with ATL allows the emergence of EBV-related B-cell lymphoma.
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PMID:Epstein-Barr virus (EBV) genome carrying monoclonal B-cell lymphoma in a patient with adult T-cell leukemia-lymphoma. 165 51

Various samples from lymphoproliferative diseases in the skin were analyzed by Southern blotting technique with probes from the T cell receptor gene, immunoglobulin genes, and human T cell leukemia virus-I genome. Samples were taken from 10 mycosis fungoides (MF) patients, 1 parapsoriasis en plaque patient, 10 Adult T cell leukemia/lymphoma (ATL) patients, 1 cutaneous T cell lymphoma (CTCL) patient, 4 lymphomatoid papulosis (LP) patients, 4 B cell lymphoma patients, and 2 actinic reticuloid (AR) patients. In MF, the monoclonality of the T cells became detectable first in the skin when plaques develop to tumors then in lymph nodes, and finally in the blood lymphocytes, indicating this disease develops from local (skin) malignancy to systemic malignancy. In parapsoriasis en plaque, no monoclonality was detected in any sample. We could distinguish cutaneous ATL from the carrier state by detecting the T cell monoclonality and HTLV-I integration with these probes. One patient with CTCL showed detectable T cell monoclonality; 1 out of 4 patients with LP did the same. Four samples from patients with B cell lymphoma revealed detectable monoclonal rearrangement of immunoglobulin heavy and light chain genes. In AR, no monoclonality was detected in any sample. From these data, we conclude that DNA analysis is useful in determining the monoclonality, cell origin, and distribution of monoclonal cells from skin samples.
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PMID:Characterization of the lymphoproliferative diseases in the skin by DNA analysis. 180 May 28

While B-cell lymphomas are frequently found in AIDS patients, reports on oral manifestations are rare. Among a group of 465 HIV-infected patients 5 presented with primary oral manifestations of a malignant B-cell lymphoma. The primary site of manifestation was the maxilla in 3 cases and the mandible in 2 cases. Based on the histological and immunohistochemical examination the tumors were differentiated as Burkitt's lymphoma (n = 1), as anaplastic large cell (ALC) lymphoma of the B-cell type (n = 1), as high-grade non-Hodgkin's lymphoma not classifiable according to the Kiel classification (n = 1), as immunoblastic-plasmoblastic lymphoma (n = 1), and as centroblastic lymphoma (n = 1). Serum samples were negative for HTLV-I antibodies in 5/5 cases.
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PMID:Oral manifestations of AIDS-associated non-Hodgkin's lymphomas. 189 Mar 20

There are rapidly increasing opportunities for dermatologists to see patients suffering from retrovirus infections. The HTLV-I was the first class of human oncogenic retrovirus that was found in cultured cells of a patient with skin manifestations similar or identical to those of CTCL (MF). It was soon recognized as the agent causing ATLL. The skin manifestations, histopathology, and immunophenotypes of ATLL share many similarities with MF and SS. Both HTLV-I and HIV-I (HTLV-III) cause immunodeficiency with an increased susceptibility to opportunistic infections. Persistent generalized lymphadenopathies are the initial manifestations of most of the HIV infections. The incidence of lymphoid malignancies is expected to become much higher as the life span of AIDS patients is prolonged. They can have both B-cell and T-cell non-Hodgkin lymphomas, although the incidence of the latter (B-cell lymphoma) is still much higher than that of the former. All human retroviruses are transmitted in similar ways.
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PMID:Lymphoid proliferation and lymphoma associated with human retroviruses (HTLV and HIV). 193 70

Type-C virus-like particles (VLPs) were found in an Epstein-Barr (EB) virus-infected human B-cell lymphoma cell line, SP-50B, that was established from a patient with non-Hodgkin lymphoma. The cell line continuously produces a small number of type-C VLPs, 150-200 nm in diameter, over 1 year. SP-50B cells were negative for HTLV-I and HTLV-II antigens and did not contain the HTLV-I genome. In addition, two EB virus nuclear antigen (EBNA)-positive B-cell lines, SP-54-Cord and SP-57-CLL, were established from human cord blood and chronic lymphocytic leukemia (CLL), respectively, by coculture with lethally irradiated SP-50B cells. Type-C VLPs with the same morphology were also found in both cell lines.
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PMID:Type-C virus-like particles in a human B-cell lymphoma cell line. 216 9

In a married couple, a T-cell and a B-cell lymphoma occurred at the same time in the husband (FR) and wife (FE), respectively. Serum antibodies of patient FE with less advanced tumor progression specifically recognized HTLV-I-related envelope precursor molecules of 66-68 kDa molecular mass on HTLV-I-infected T- and B-cell lines, but not on HTLV-II or HIV-infected cells. In addition, in vivo-activated CD8+ T-cell lines (TCL) from this patient specifically lysed autologous B-lymphoma cells, T-lymphoma cells from the husband (FR), as well as the HTLV-I-transformed MT2 T-cell line. All positive target cells shared an HLA-class-I cross-reactive determinant identified by the alloantiserum WER127. On a clonal level, the specificity of the cytotoxic T-cell response was unequivocally distinguishable from classical natural-killer-like cytotoxicity. Results imply the involvement of a common inductive agent in the manifestation of malignant lymphoma in both patients (FR and FE). Since antibodies from cases with classical HTLV-I-induced adult T-cell leukemias (ATLL) did not bind antigens on cells of either lymphoma (FR or FE) and active virus production was not demonstrable under various different conditions, these results argue against HTLV-1 itself being the transforming agent. However, humoral and cellular immune responses of one patient (FE), in addition to de novo HLA-class-1 antigen expression of both patients, are nonetheless consistent with the involvement of viral infections(s). These were responsble for the expression of HTLV-1-characteristic envelope determinants of the malignant progeny of respective T- and B-cell origin.
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PMID:Lymphoma-specific T- and B-cell responses suggest the involvement of HTLV-I in virus-non-productive lymphomas of a married couple. 289 49

This study examines the identification of unusual cell populations highly associated with lymphoma cells (UCP-L) in diagnostic biopsy specimens using three-color flow cytometry (3-FCM). Patterns of surface antigen expression were used to compare the morphology of distinct lymphoid cell populations present in biopsy specimens and determine the presence or absence of UCP-L. UCP-L were identified by their larger size as compared to admixed reactive lymphocytes, and the method is based on the concept that neoplastic lymphoma cells are larger than reactive lymphocytes. The comparison of relative cell sizes was determined by overlaying forward scatter histograms by multicolor gating using PAINT-A-GATE software. In order for separate gates to be set on UCP-L and reactive cell populations, UCP-L had to fulfill one or more immunophenotypic criteria. These included: (1) belonging to a subset of B cell antigen-positive cells showing restricted expression of kappa or lambda light chains; (2) belonging to a subset of CD4-positive cells having dim or absent expression of CD45RA; (3) showing alterations in antigen expression (loss, dimmer or brighter); or (4) expressing an immunophenotype that is present on only rare cell populations or is absent from reactive lymph nodes. The immunophenotypic profiles of the respective cell populations were demonstrated by cubic representations to assess more easily the co-expression of three antigens. The common morphology of UCP-L as defined by forward and side scatter grams was consistent with a 'lymphoid appearance' except in several cases of HTLV-I-positive T cell lymphoma and gammadelta T cell lymphoma. The immunophenotypic profiles of UCP-L were confirmed to correspond to the presumptive lymphoma cell population by use of a live gating procedure on the large cells, which eliminated interference by reactive cells or necrotic tissue fragments. Using this method, we identified UCP-L in 208 of 293 (71%) consecutive cases of non-Hodgkin's lymphomas, while no UCP-L were seen in 72 cases of non-specific hyperplasia of lymph nodes. Twenty-seven cases could not properly be examined about the existence of UCP-L because of massive necrosis, extensive fibrosis or strong non-specific staining reactions of unknown cause. When those cases were eliminated from the analysis, 80% of non-Hodgkin's lymphoma were found to contain UCP-L. In B cell lymphoma, the incidence of UCP-L in nodal lymphomas (80%) was much higher than in extranodal lymphomas (47%). Only one of 21 cases of Hodgkin's lymphoma was found to have UCP-L. The 3-FCM procedure was validated by the combined use of immunohistochemistry, morphologic examination, cytogenetic and antigen receptor gene rearrangement analysis by Southern blot hybridization. Our findings indicate that detection of UCP-L by 3-FCM is a reliable method to distinguish non-Hodgkin lymphomas from reactive hyperplasias in the majority of cases, even when the reactive cell population predominates over the malignant cell population.
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PMID:Three-color flow cytometry in the diagnosis of malignant lymphoma based on the comparative cell morphology of lymphoma cells and reactive lymphocytes. 936 23

The recently identified decoy receptor 3 (DcR3) binds to FasL and inhibits FasL-induced apoptosis, and is considered to play a role in the immune escape system of neoplastic cells. To examine the involvement of DcR3 in the immune evasions of virus-associated lymphoma, we analyzed the amplification and expression of DcR3, using dot blot and in situ hybridization (ISH), in 45 cases, which included 17 cases with Epstein-Barr virus (EBV)-associated lymphoma (seven pyothorax-associated B-cell lymphomas (PAL); ten natural killer lymphoma (NKL)), seven cases with adult T-cell leukemia lymphoma (ATLL), 13 Hodgkin's disease (eight EBV-associated cases; five non-EBV-associated cases), and eight control cases (three reactive lymphadenopathy; five non-EBV-associated-B-cell lymphoma). EBV-associated PAL and NKL exhibited DcR3 amplification and expression in lymphoma cells. ATLL also showed DcR3 expression and amplification. The cases with DcR3 amplification showed DcR3 expression; however, the expression was confined in the neoplastic cells, but not in the reactive cells. In Hodgkin's disease (HD), DcR3 was expressed only in Hodgkin and Reed-Sternberg giant (H-RS) cells. However, DcR3 was not expressed or amplified in reactive lymphadenopathy. Non-EBV-associated B-cell lymphoma also rarely expressed DcR3, and showed no amplification except in two cases, in which rare expression was present. Our results suggest that EBV and HTLV-I probably use DcR3 to escape from the immune system during lymphomagenesis, or virus-infected lymphoma cells with DcR3 expression might be selected in the multistep tumorigenesis.
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PMID:Amplification and expression of a decoy receptor for fas ligand (DcR3) in virus (EBV or HTLV-I) associated lymphomas. 1109 89

We report a 47-year-old woman with progressive multifocal leukoencephalopathy (PML). She was a carrier of HTLV-I virus, and developed subacute right hemiparesis and marked motor aphasia. She had a malignant lymphoma in the left neck and basal cell carcinoma in the right inguinal region. Three months after the onset, she became unable to walk because of the right leg weakness or to speak because of motor aphasia. Magnetic resonance imaging (MRI) revealed multifocal T2-high lesions in the white matter of the left frontal lobe, and a brain biopsy revealed demyelinating pathology. A biopsy of the left parotid gland revealed a diffuse pleomorphic type large B cell lymphoma. Although anti-HTLV-I antibody was positive in the serum and cerebrospinal fluid (CSF), no adult T-cell leukemia (ATL) cells were found in the blood or CSF. The patient was then admitted to our hospital. Neurological examinations revealed severe motor aphasia, mild sensory aphasia/cognitive impairment, right hemiplegia, mild right hemihypesthesia, limb-kinetic apraxia in the left hand, idiomotor apraxia, agraphia, perseveration, marked spasticity and brisk tendon reflex in four extremities, and positive bilateral pathological reflexes. MRI showed multifocal T2-high lesions mainly in the cerebral white matter, predominantly in the left hemisphere, and partly in the cerebral cortex. No gadolinium enhancement was found. In addition, 99mTcECD-SPECT showed a broad decrease in cerebral blood flow (CBF) in the cortex. Anti-HTLV-I antibody was positive but anti-HIV antibody was negative in serum. ATL cells were found in 1-3% of the peripheral white blood cells after admission. CSF examination revealed that the cell count (1/microl), protein level (24 mg/dl), and IgG index (0.4) were all normal. However, the myelin basic protein level (321 pg/ml; normal < 102) was increased, JC virus DNA was detected by PCR, and anti-HTLV-I antibody (x 8) was detected in CSF. The regulatory region of the JC virus DNA in the CSF was partly deleted; immunostaining with anti-JC virus protein antibodies revealed the existence of JC virus in biopsied brain specimens, and these findings were consistent with PML. Her symptoms such as motor aphasia, cognitive dysfunction and left hemiparesis were subacutely progressive, and she developed akinetic mutism two weeks after admission. Since the efficacy of cytosine arabinoside for PML has been reported, she was administered 80 mg/day of the drug for five days. After treatment, her communication function was mildly improved but the efficacy was transient. Since it has been reported that HTLV-I, as well as HIV, activates the JC virus promoter and its proliferation, the latent infection of HTLV-I in the central nervous system (CNS) in this case might have stimulated the JC virus proliferation, promoting lesion extension over the cerebral cortex. There have been only a few reports of broad decreases in CBF by SPECT in PML patients. Further MRI and SPECT studies on PML patients are therefore necessary to evaluate the significance of HTLV-I in promoting the JC virus infiltration into the CNS.
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PMID:[A case of progressive multifocal leukoencephalopathy presenting white matter MRI lesions extending over the cerebral cortex and a marked decrease in cerebral blood flow on SPECT, and associated with HTLV-I infection]. 1602 67


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