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

Only 2.0-6.8% of extranodal malignant lymphomas are found in the nasal region and paranasal sinuses. Primary malignant lymphoma of the paranasal sinuses usually occurs in the maxillary or ethmoid sinuses, and is very rare in the sphenoid sinus. Here we report a rare case of primary malignant lymphoma of the sphenoid sinus that was found accompanying orbital apex syndrome. The patient's progressively deteriorating neurological condition was improved after surgery via the transsphenoidal approach. A 52-year-old man was admitted with reduced left visual acuity, diplopia, and retroorbital pain. CT showed an isodense mass in the sphenoid sinus with slight enhancement, and MRI showed that the lesion was slightly hypointense on T1-weighted images, hypointense on T2-weighted images, and slightly enhanced by Gd-DTPA. On January 19, 1989, the patient suddenly became blind. An operation via the transsphenoidal approach was done as an emergency procedure to decompress the sphenoid sinus and the left optic canal. The histological diagnosis was non-Hodgkin's lymphoma of the diffuse large cell type (B cell lymphoma). Malignant lymphoma in the paranasal sinuses is usually biopsied and treated by chemotherapy and/or radiotherapy without surgical resection. In this rare case, an operation via the transsphenoidal approach was effective in improving the patient's visual acuity.
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PMID:[Primary malignant lymphoma in the sphenoid sinus with orbital apex syndrome; a case report]. 155 80

The lesion detection capability of a new technetium-99m labelled B-cell lymphoma monoclonal antibody (MoAb) imaging agent, LL2, was evaluated in 8 patients with non-Hodgkin's lymphoma and 1 patient with chronic lymphocytic leukaemia. The MoAb kit consists of a 1-vial, 1-mg Fab' form of LL2 ready for instant labelling with technetium. The patients were injected with approximately 925 MBq (25 mCi) of 99mTc-LL2 Fab' (1 mg), and planar and single photon emission tomography (SPET) studies were performed at 3-4 h post injection and at 24 h. There was no evidence of thyroid or stomach activity up to 24 h. Uniform splenic uptake was seen in all patients. Two non-lymphoma patients were also administered with the same agent and demonstrated a similar splenic distribution; therefore, splenic targeting was not scored as tumour-specific. A total of 29 from 48 tumour sites were detected by scintigraphy, including tumours of various grades and histological types. Excluding 1 patient who had a large tumour burden of over 500 g, 29 of 33 lesions were detected. One patient was free of disease at the time of the study and had a negative scan. Another patient showed excellent targeting of gallium-negative sites in the liver and bone. The bone involvement was not known prior to the antibody study and was subsequently confirmed by a bone scan. Additional sites of MoAb localization could not be followed in this group, since most patients went on to radioimmunotherapy immediately following the 99mTc-LL2 study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lymphoma imaging with a new technetium-99m labelled antibody, LL2. 161 28

A 38-year-old man with diffuse endobronchial infiltration with non-Hodgkin's lymphoma (NHL) is reported. He was admitted to our hospital on November 1990 because of lymph node swelling. Physical examination on admission revealed left axillary, bilateral cervical and inguinal lymph node swelling. Chest and abdominal CT scan showed para-aorta lymph node swelling, mild splenomegaly and heterogeneous density of the liver, although hilar and mediastinal lymphadenopathy were not found. Microscopic examination of the biopsy specimen obtained from the right inguinal lymph node and liver revealed NHL (B cell lymphoma, diffuse, mixed type). After two courses of chemotherapy, a chest roentgenogram showed bilateral hilar lymphadenopathy and reticular shadows. CT scan demonstrated a thickening of the left main bronchus. Bronchoscopic examination revealed a small submucosal nodule in the left main bronchus on February 1991, from which the biopsy specimen revealed NHL infiltration similar to that of the lymph node. At follow-up bronchoscopic examination, in spite of chemotherapy, scattered NHL infiltration was found in the submucosal space of the left vocal cord, carina and the bifurcation between left upper and lower bronchi. In patients with NHL, endobronchial involvement is rare. In this case, diffuse endobronchial infiltration was not thought to be direct invasion from the lymph node but hematogenous or lymphatic spread to the bronchi.
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PMID:[A case of diffuse endobronchial infiltration in a patient with non-Hodgkin's lymphoma]. 162 90

A 70-year-old man was admitted to our hospital on March 9, 1989 because of fever, superficial generalized lymphadenopathy, upper abdominal mass and right pleural effusion. The diagnosis of non-Hodgkin's lymphoma (follicular medium sized cell type, B cell) was made by a biopsy of the neck lymph node. Peripheral blood mononuclear cells were obtained from the patient by cytopheresis. The cells were cultured for 8 days with interleukin-2 (IL-2) to generate Lymphokine-activated killer (LAK) cells. The patient received a total of 7.7 x 10(9) LAK cells intravenously over a period of 3 weeks. He also received continuous intravenous infusion of IL-2 for 17 days, starting 2 days before the first infusion of LAK cells. After this therapy, although his superficial generalized lymphadenopathy disappeared or decreased in size, the size of the upper abdominal mass did not decrease. Therefore, it is suggested that adoptive immunotherapy is a beneficial treatments for B cell lymphoma. However, LAK cells should be generated in much larger quantities for a more successful therapeutic result.
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PMID:[Lymphokine-activated killer (LAK) cells and interleukin-2 (IL-2) therapy that improved lymphadenopathy in a patient with B cell non-Hodgkin's lymphoma]. 163 70

The application of hyperthermia to the treatment of neoplastic disease has focused on solid tumors. Since the hyperthermic sensitivity of human B-cell lymphoma cells is not known, we have examined the effect of hyperthermia on the growth of B-cell lymphoma cell lines (Raji and Daudi) in vitro to evaluate the ability to purge tumor cells from normal bone marrow by heat, utilizing a limiting-dilution assay to measure log depletion of tumor cells in a 20-fold excess of normal bone marrow. When exposed at 42 degrees C and 43 degrees C for 120 min, both clonogenic Raji and Daudi cells were dramatically decreased (a 4- to 6-log reduction) with exposure time, while leaving over half of the normal granulocyte-macrophage progenitor cells surviving at 42 degrees C and 10% at 43 degrees C. This high level of lymphoma-cell depletion by heat correlated with that obtained in immunologic and pharmacologic studies. These results suggest that in vitro hyperthermia might be applied effectively for the elimination of residual lymphoma cells in autologous marrow grafts before autologous bone marrow transplantation in B-cell non-Hodgkin's lymphoma.
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PMID:A simple elimination of clonogenic tumor cells from human bone marrow in vitro by heat: its application to autologous bone marrow transplantation for B-cell lymphoma. 163 79

The clinical features, morphology and immunophenotype of 20 cases of B non Hodgkin's lymphoma (B-NHL) with chromosome abnormalities involving 11q13-14 were studied, to determine if this abnormality was closely associated with a specific sub-type of B-NHL. A t(11;14)(q13;q32) was found in 11 cases of intermediately differentiated lymphocytic lymphoma (IDLL). A breakpoint in the major translocation cluster of the BCL-1 locus was found in six of these cases. These patients were male with lymphomatous involvement of the bone marrow, marked splenomegaly and frequently had mucosa associated lymphoid tissue involvement. One patient with IDLL had a t(8;11)(p21;q13) and a rearranged BCL-1 locus, suggesting that this may be a variant of t(11;14)(q13;q32). Diagnoses of IDLL, chronic lymphocytic leukaemia, lymphoplasmacytic lymphoma and monocytoid B cell lymphoma were made in all but one of the remaining cases. These cases had either a translocation involving 11q13-14 and various partner chromosomes or an 11q13 deletion. This study demonstrates that 11q abnormalities occur mainly in a group of low-grade B-NHL of non follicle centre cell lineage.
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PMID:Chromosome 11q rearrangements in B non Hodgkin's lymphoma. 164 18

The beta 2-adrenergic transmembrane signal transduction was investigated in malignant B-cells from 15 patients with low grade non-Hodgkin's lymphoma as compared with normal lymphocytes of seven healthy adults. The number of beta 2-adrenoceptors and the response of adenylate cyclase (AC) to isoproterenol were slightly decreased in lymphoma cells. The responsiveness of AC to forskolin was 8-fold lower in lymphoma cells, whereas the response to cholera toxin showed no difference. These findings demonstrate an impairment of the beta 2-adrenergic signal transduction in low grade lymphoma cells that particularly affects the function of AC. The comparison with forskolin resistant mutants of an adrenocortical tumor cell line, Y1 (Schimmer et al., J Biol Chem 262: 15521-15526, 1987), suggests that the availability of functional active alpha subunits of stimulatory G proteins (Gs) might be reduced in human B-cell lymphoma, although other mechanisms known to inhibit the AC activity might be involved.
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PMID:Reduced responsiveness of adenylate cyclase to forskolin in human lymphoma cells. 165 84

A pathogenetic relationship is postulated for the development of membranoproliferative glomerulonephritis type I in non-Hodgkin's lymphoma (B-cell lymphoma of low-grade malignancy) and myeloproliferative syndrome, which we have observed in eight patients. This hypothesis is supported by the fact that chronic lymphatic leukaemia and immunocytoma are often associated with immunodysregulative phenomena, and by the immunohistological and ultrastructural findings in the kidney, especially the frequent electron-microscopic finding of cryoglobulins, which results in the membranoproliferative type of immune-complex glomerulonephritis, an expression of a disturbance in immune balance. The pathogenetic mechanism may involve cryoglobulins themselves as immune complexes; it is also possible that monoclonal cryoglobulins combine with an antigen to form immune complexes or lead to in situ formation of immune complexes. In addition, other immune complexes, for example with endogenous tumour-associated antigens and exogenous antigens (e.g. hepatitis antigens), may be involved in the pathogenesis.
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PMID:[Membranoproliferative glomerulonephritis in non-Hodgkin's lymphoma nad myeloproliferative syndrome--a causal relationship?]. 172 39

This study reports six non-Hodgkin's lymphoma cases that we called histiocyte-rich B-cell lymphoma (BCL) because of the prominent reactive histiocytic infiltrate obscuring the malignant B-cell population. The involved lymph nodes are characterized by a mixed nodular and diffuse infiltrate and occasionally feature prominent sinuses. The infiltrate is composed of reactive lymphocytes and numerous histiocytes obscuring a tumor population composed of variably sized scattered cells with irregular or multilobar vesicular nuclei. Immunostaining of paraffin sections for the B-cell marker recognized by L26 helps in the identification of these neoplastic cells. The clonal nature and further evidence of the B-cell lineage of this condition is shown by immunoglobulin gene rearrangements detected in three cases. The six cases of histiocyte-rich BCL are remarkably similar clinically: all presented with stage IVB disease with splenomegaly and follow an aggressive clinical course. Except for these features, our series show striking similarities to paragranuloma lymphocyte-predominant Hodgkin's disease, including male preponderance (all patients are male), age distribution (mean age, 41 years), propensity to progress to a diffuse, large B-cell lymphoma (two cases), as well as morphology of the neoplastic B-cell population and expression of Hodgkin's cell markers (Leu-M1 positivity after neuraminidase digestion in three cases, Leu-M1 positivity without neuraminidase digestion in one case, and additional epithelial membrane antigen [EMA] positivity in two cases). Both morphologically and clinically, the present series can be differentiated from other types of infiltrate-rich BCL, such as T-cell-rich BCL. Although additional cases will have to be recognized, histiocyte-rich B-cell lymphoma most likely represents a distinct clinicopathological entity. We speculate that it develops from a subset of B cells that also gives rise to the lymphocytic-histiocytic (L/H) cell, the Hodgkin's cell variant of lymphocyte-predominant Hodgkin's disease, paragranuloma subtype.
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PMID:Histiocyte-rich B-cell lymphoma. A distinct clinicopathologic entity possibly related to lymphocyte predominant Hodgkin's disease, paragranuloma subtype. 172 95

The excess of NHL associated with HIV infection is well established. Clinically, HIV associated NHL is characterized by histological evidence of a high grade of malignancy, B cell origin, extensive extranodal involvement (most notably of the CNS) and poor prognosis. High grade B cell lymphoma or primary brain lymphoma in HIV infected individuals is considered diagnostic of AIDS by the Centers for Disease Control. The incidence of NHL among individuals with AIDS varies by subtype of lymphoma, age, sex, race and risk group. Younger individuals, males, whites and haemophiliacs are at higher risk than other groups. The incidence of HIV associated NHL is increasing. Because of the paucity of data on risk factors for this malignancy, the current possibilities for risk modification are limited to the prevention of HIV infection.
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PMID:Epidemiology of HIV associated non-Hodgkin lymphoma. 182 26


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