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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of B cell lymphoma with clinical and histological features of malignant histiocytosis was described. A 57-year-old male was admitted to Shinshu University Hospital because of transverse myelopathy. Five months before admission, he noticed urinary disturbance, which progressed to urinary obstruction. The following month, bilateral muscular weakness appeared in his legs. A few days later he could not stand up, and was admitted to a local hospital. Neurological examination revealed sensory disturbances below the level of Th12 in all modalities, and marked weakness and hyperreflexia in the lower limbs. A spinal tumor was suspected. However, myelography showed no abnormality. The patient's condition worsened and he became bed-ridden in February 1990. He was transferred to Shinshu University Hospital for further evaluation. On admission he was poorly nourished with fever, anemia, hepatomegaly, and bilateral pretibial pitting edema. No lymphadenopathy was observed. Neurological examination showed total sensory loss below the level of Th12, spastic paraplegia, hyperreflexia in the legs, and urinary obstruction. Laboratory findings revealed an elevated erythrocyte sedimentation rate, increased CRP, pancytopenia, and hypoalbuminemia. Serum level of IgG, IgA, IgM, LDH, ALP, GPT and total bilirubin were increased. CSF and MRI imaging of the spinal cord were normal. Proliferation of atypical histiocytes with marked erythrophagocytosis, which is a characteristic pathological feature of malignant histiocytosis, was observed in peripheral blood and aspirated bone marrow. Immunoenzyme staining of bone marrow using monoclonal antibody L-26, which is a B-cell marker, revealed B-cell lymphoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of B-cell lymphoma with clinical and histological features of malignant histiocytosis]. 130 24

Lymphokine requirements for the in vitro proliferation of the spleen-dependent B cell lymphoma BCL1 have been analysed. Cells were found to respond by proliferation to added recombinant (r) interleukin-4 (IL-4), r-IL-5 and recombinant granulocyte-macrophage colony-stimulating factor (r-GM-CSF). Inhibition by antibodies specific for each of these lymphokines has confirmed growth factor-dependent growth. Anti-GM-CSF has, however, been found to inhibit the proliferation of BCL1 cells induced by r-IL-4 and r-IL-5, as well as r-GM-CSF, suggesting that BCL1 cells may express receptors for GM-CSF and that GM-CSF may be able to act synergistically with IL-4 and IL-5 in promoting cell proliferation. Anti-IL-6 antibody was also found to be a very effective inhibitor of BCL1 proliferation induced by either IL-4 or IL-5 but not by GM-CSF. Added IL-6 did not stimulate BCL1 proliferation, suggesting that endogenous IL-6 may regulate the autocrine growth of BCL1 cells. BCL1 cell proliferation in vitro appears to be regulated by interactions between multiple growth factors.
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PMID:Proliferation of the BCL1 B cell lymphoma induced by IL-4 and IL-5 is dependent on IL-6 and GM-CSF. 147 97

The t(14;18) of human follicular B cell lymphoma translocates the Bcl-2 gene into the Ig H chain locus and markedly deregulates Bcl-2 expression. We sought to determine if Bcl-2 could be directly implicated in a growth-factor pathway. Consequently, we introduced a retrovirus containing the murine Bcl-2 gene (N2-M-Bcl-2) or the parental retrovirus (N2) into a series of factor-dependent hemopoietic cell lines. Overexpressed Bcl-2 resulted in no long term IL-2, IL-3, or IL-6 independent clones, indicating that Bcl-2 could not spare the need for a specific ligand-receptor interaction. However, Bcl-2 did extend the short term survival of IL-3-dependent cell lines after factor deprivation. Although viable, IL-3-deprived pro B lymphocytes (FL5.12) bearing N2-M-Bcl-2 were in Go, and deregulated Bcl-2 did not obviously influence cell-cycle progression. Bcl-2 predominant effects were to delay the onset of cell death and to modestly augment viable cell growth in the first 48 h after IL-3 deprivation. This death sparing was associated with increased levels of Bcl-2 RNA and protein in factor-deprived cells possessing N2-M-Bcl-2. This result was not restricted to prolymphocytes because an IL-3-dependent mast cell line (32D) as well as a promyeloid line (FDC-P1) demonstrated the same response to Bcl-2. Moreover, the effect was not limited to the IL-3/IL-3R signal transduction pathway in that promyeloid cells maintained in granulocyte-macrophage-CSF or IL-4 displayed a similar response. Yet, Bcl-2-enhanced cell survival was not universal as an IL-2-dependent T cell line, and an IL-6-dependent myeloma line demonstrated no consistent effect upon IL withdrawal. Thus, Bcl-2 appears to interfere with cell death but in a cell type and/or factor-restricted fashion.
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PMID:Deregulated Bcl-2 gene expression selectively prolongs survival of growth factor-deprived hemopoietic cell lines. 218 93

We found a unique thymocyte growth-promoting activity in supernatants (SN) from subclones of the B cell lymphoma CH12.LX. We have tentatively named this activity B-TCGF (for B cell-derived T cell growth factor) and characterized the activity produced by the CH12.LX.4866 subclone. This SN did not induce thymocyte proliferation alone, however, it enhanced both adult and fetal (Day 15 of gestation) murine thymocyte proliferation in the presence of IL-2, IL-4, or IL-7. Other known cytokines were screened for a B-TCGF-like activity using both adult and fetal thymocytes. IL-6 was found to be active only on adult thymocytes, while TNF alpha and GM-CSF were found to be active only on fetal thymocytes. However, neutralizing antibodies against these cytokines did not block the B-TCGF activity present in CH12.LX.4866 using either adult or fetal thymocytes. These observations suggest that the B-TCGF activity is mediated by a novel factor(s). The apparent molecular weight of this novel molecule(s) was 27-50 kDa determined by sizing HPLC.
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PMID:Identification of a novel thymocyte growth-promoting factor derived from B cell lymphomas. 219 78

Malignant lymphoma is classified roughly into Hodgkin's disease (HD) and non-Hodgkin's lymphoma (NHL) according to the biological characteristics. Malignant lymphoma in Japan has such characteristics as low incidence of HD, which is usually favorable in prognosis, and high incidence of NHLs, which have further distinctive features of less incidence of favorable follicular B cell lymphoma and of higher incidence of unfavorable diffuse T cell lymphoma including adult T cell leukemia/lymphoma (ATLL) in comparison with those in western countries. As a recent trend of progress in lymphoma study, the introduction of molecular diagnosis by means of gene rearrangement analysis of immunoglobulin and T cell antigen receptor has contributed diagnostically to a definitive determination of T and B cell lineage and cellular monoclonality in malignant lymphoma. On the other hand, remarkable progress has been made in the treatment of malignant lymphoma in recent years. After all, in HD even far advanced cases have been expected to be curable by the combination chemotherapy, for example, MOPP regimen in USA at the present time. Furthermore, in NHL even advanced cases with such aggressive lymphoma as diffuse large cell lymphoma of B cell type have also been able to survive for more than 10 years and may be curable with the frequency of more than 30% in several institutions. Nowadays, the treatment for malignant lymphoma has focussed on multidisciplinary cure-oriented therapy including chemotherapy and radiotherapy in a collaboration of surgical procedure and immunotherapeutic maneuvers. The recent chemotherapy regimen has been called "third generation" ones characterized by alternating non-cross resistant combination and frequent administration of intense drug dose. Furthermore, various biologics such as monoclonal antibodies, several BRMs including IFNs, IL-2 and TNF, and recombinant G-CSF and GM-CSF have been applied in lymphoma treatment to improve the efficacy of combination chemotherapy in new designs of clinical trials.
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PMID:[Malignant lymphoma]. 273 35

T cell-replacing factor (TRF)/IL-5 is a glycosylated polypeptide that acts as a key factor for B cell growth and differentiation. Since IL-5 action is probably mediated by specific cell surface receptor(s), we have characterized the binding of IL-5 to cells using biosynthetically [35S]methionine-labeled IL-5 and 125I-IL-5 that had been prepared using Bolton-Hunter reagent. The radiolabeled IL-5 binds specifically to BCL1-B20 (in vitro line) (a murine chronic B cell leukemic cell line previously shown to differentiate into IgM-secreting cells in response to IL-5) within 10 min at 37 degrees C. There are two classes of binding sites with high affinity (Kd = 66 pM) and low affinity (Kd = 12 nM) for IL-5 and an average number of binding sites for high affinity and for low affinity were 400 and 7,500 per cell, respectively. The specificity of binding of radiolabeled IL-5 has been confirmed by demonstrating that only unlabeled IL-5 and anti-IL-5 mAb but not by IL-1, IL-2, IL-3, IFN-gamma, and GM-CSF inhibit radiolabeled IL-5 binding to BCL1-B20 cells. Treatment of surface-bound radiolabeled IL-5 with bivalent crosslinkers identified a membrane polypeptide of Mr 46,500 to which IL-5 is crosslinked. A variety of cell types have been surveyed for the capacity to bind specifically radiolabeled IL-5 with high affinity. BCL1 cells MOPC104E (murine myeloma cell line) expressed IL-5-R, whereas BAL. 17 and L10 A (B cell lymphoma) did not. T cell line, mastocytoma cell line, or macrophage tumor cell line did not display detectable levels of IL-5-R. were hardly detectable on normal resting B cells but were expressed on LPS-activated B cells, fitting the function of IL-5 that acts on activated B cells for their differentiation into Ig-secreting cells. Intriguingly, early B cell lines (J-87 and T-88) that grow in the presence of IL-5 expressed significant but low numbers of high-affinity binding sites for IL-5. The biological effects of IL-5 were mediated by high-affinity binding sites. The identification and characterization of IL-5-R should provide new insight into the apparent diverse biological activities of IL-5.
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PMID:Receptors for T cell-replacing factor/interleukin 5. Specificity, quantitation, and its implication. 326 7

We describe the use of a panel of monoclonal antibodies, directed against leukocyte surface antigens to characterize CSF mononuclear cells with regard to malignancy when cytopathology was inconclusive. Cytocentrifuged preparations from three patients in which traditional modalities had not yielded a diagnosis were studied, utilizing a panel of antibodies for B and T cell antigens. All three patients were found to have B cell lymphoma of the CNS. Rapid institution of the appropriate therapy resulted in marked improvement of CNS symptoms in each case. Our results indicate that in patients with CNS disease and CSF pleocytosis of undefined nature, this technique may provide rapid and precise diagnostic information.
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PMID:Diagnosis of CNS lymphoma using immunofluorescent phenotyping of CSF mononuclear cells. 353 May 81

A case report of paraplegia secondary to a malignant B-cell lymphoma primary in the cauda equina is presented. Initial diagnosis was suggested on cytocentrifuge preparations of cerebrospinal fluid with subsequent tissue confirmation following bilateral laminectomy (T12-L3). Histologically, the tumor was a diffuse "histiocytic" lymphoma by Rappaport's or large noncleaved FCC lymphoma by Lukes and Collins classification. Immunologic studies typed the tumor as a B-cell neoplasm with lambda light chains. Following an extensive evaluation of the patient, the lymphoma was found to be limited to the lower spinal cord. Although radiotherapy was initiated there was no improvement of her neurological symptoms, and CSF cytology remains positive for rare malignant cells 2 months after diagnosis. A complete reevaluation at 3 months after laminectomy was negative for lymphoma involvement of other sites.
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PMID:Primary malignant lymphoma of the cauda equina. 634 66

The pathophysiology of cerebral tumor mass in cases of systemic non-Hodgkin's lymphoma is not well known. We experienced with two cases with this lesion. The purpose of this report is not only case presentation but also an analysis of cases from the literature from the clinical, radiological, histological, immunological and therapeutic aspects. Case 1 was a 82-year-old man who had weakness in the right arm and for the past month. For about two years he had been received anticancer chemotherapy because of a systemic malignant lymphoma at another hospital. Neurological examination revealed disorientation and right hemiparesis. Microscopic and immunological studies of the biopsy specimen of the enlarged supraclavicular node showed a non-Hodgkin's B-cell lymphoma of the diffuse large cell type according to the Lymphoma Study Group (LSG) classification. The clinical stage (CS) of the lymphoma was IV except for the CNS lesion by systemic examination including lymphography. CT scan on admission revealed remarkable enhancement of a nodular high density area near the lateral ventricle, accompanied by surrounding low density. Angiography failed to reveal a tumor stain. CSF cytology was positive although no pleocytosis was observed. Case 2 was a 70-year-old man who had weakness of the right foot for two weeks. About three years ago he underwent orchiectomy for a testicular tumor at another hospital. Neurological examination revealed disorientation, memory loss and right hemiparesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Localized cerebral tumor mass in systemic non-Hodgkin's lymphoma--report of two cases and review of the literature]. 646 9

A 73-year-old woman was diagnosed with seropositive destructive rheumatoid arthritis in 1981. She was treated with cortisone, chloroquine, and cyclophosphamide (Sendoxan) in 1982 and 1984 and contracted severe neutropenia. After that she only received cortisone. During 1991, again low neutrophilic counts were registered, especially granulocytopenia. At first, B-cell lymphoma was suspected, but later Felty's syndrome was established. The patient was treated with high-dose cortisone with some success and had a few minor septic episodes. In May 1992 she contracted a traumatic wound on the back of the lower leg. Conservative treatment resulted in a worsening of the condition and an increased wound area, most likely related to the neutropenic condition. In mid July the patient was hospitalized. Bacterial isolates yielded mixed gram-negative enteric bacteria from the wound. Parenteral antibiotic treatment was started, followed by oral drugs, rhG-CSF (filgrastim) was given subcutaneously once a day, starting 3 days after admission. This resulted in increased numbers of peripheral granulocytes. The ulcer started to heal and by mid August the patient received a transplant with autologous skin grafting. In mid September the wound was completely healed. It is concluded that the combination of antibiotics, skin transplantation, and G-CSF was necessary for the successful result. Actually, the bacterial growth did not call for antibiotics, but it was considered necessary to cover for staphylococci. No worsening of the underlying arthritis was observed.
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PMID:Successful treatment of chronic wound infection in neutropenia and rheumatoid arthritis with filgrastim (rhG-GSF) 752 58


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