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Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
 11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

T- and B-cell markers of lymphocytes in peripheral blood, involved node and spleen, PHA response of peripheral blood lymphocytes, serum immunoglobulin levels, and skin test reactivity to six common antigens were studied in 16 cases of untreated non-Hodgkin's lymphoma. Impaired response of peripheral lymphocytes to PHA was observed in 13 of 16 cases, regardless of the proportion of T lymphocytes. Of 12 cases in which skin tests were done, two were positive and had a normal PHA response, seven cases were positive in spite of low PHA response, and three were negative with low PHA response. In the lymph nodes from involved areas two cases showed monoclonal increase of B-cells, five showed "null" cell increase, and the remaining nine showed no increase or decrease of subpopulation of lymphocytes. No correlation with surface marker of lymphocytes to histologic classification was seen. From the above observations it was concluded: 1) a low PHA response in non-Hodgkin's lymphoma was not due to the decreased population of T-cells; 2) a low PHA response may not necessarily indicate impaired delayed hypersensitivity; and 3) non-Hodgkin's lymphoma can be classified in the following ways--B-cell proliferative type, "null" cell increase type, and normal T/B proportion type.
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PMID:T and B lymphocytes in non-Hodgkin's lymphoma: a comparison of tumor-derived cells and peripheral blood lymphocytes. 108 88

Maintenance of remission solely by repeated BCG vaccinations in seven patients with non-Hodgkin's lymphoma who had achieved a complete clinical remission with initial standard therapy has provided sufficient encouragement to begin a randomized clinical trial. In vitro lymphocyte responses to mitogens and PPD used as parameters of cell-mediated immunity have not proved to be of value in predicting early or late recurrence in six pre-trial and trial patients. Eight out of twenty-one patients with malignant melanoma have shown a satisfactory clinical response (10-34 months) to immunotherapy. Those who respond must show immunological reactivity to the stimulating agent, however the best clinical responses were not associated with the highest degrees of in vivo and in vitro sensitization. The skin reactivity and the in vitro lymphocyte response to PPD as well as a 2-3-fold increase in the appearance of colony-forming units in the peripheral blood following the intratumour injection of BCG or PPD are helpful in prognosis and management of these patients. All patients with malignant melanoma who presented with a PHA response less than 40% of normal made a poor response to immunotherapy. Autopsies performed on seven patients dying with extensive melanocarcinomatous disease failed to show any serious adverse toxic reactions or infections from oral and intratumour injections of BCG.
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PMID:Observations in immunotherapy of lymphoma and melanoma patients. 110 63

We have analyzed cultures of malignant lymphoma cells and cells from patients with acute lymphoid leukemia in methylcellulose for their ability to from colonies. Clonogenic growth was examined in the presence or absence of fetal calf serum (FCS), platelet-poor plasma (PPP), medium conditioned by phytohemagglutinin-stimulated leukocytes (PHA-LCM), or irradiated allogeneic bone marrow stroma cells. Cells from 25 lymphoma patients--17 with non-Hodgkin's lymphoma (NHL), eight with Hodgkin's disease (HD)--and from 19 patients with acute lymphocytic leukemia (ALL) were investigated. We show that colony growth can be obtained in a minority of cases (in 3 NHL, 5 HD, and 2 ALL) and that the use of FCS and allogeneic irradiated stroma cells may be required for optimal colony formation.
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PMID:Stimulation of growth of human malignant lymphoma and lymphoid leukemia cells in vitro. 155 97

A case of an intravenous drug user who, over the course of less than 18 months, was diagnosed as having multiple opportunistic infections, the acquired immunodeficiency syndrome (AIDS) and a non-Hodgkin's lymphoma is presented. Cytogenetic findings on both bone marrow and lymph nodes revealed a consistent translocation involving chromosome 10 and 14 with trisomy for chromosomes 7 and 12, i.e. 48,XX,+7,+12,t(10,14) (q24;q32) in lymph node and bone marrow cells. These are abnormalities which heretofore have not been reported. Peripheral blood lymphocytes after PHA stimulation revealed a normal 46,XX karyotype. The number of reports describing cytogenetic findings in AIDS patients are limited. However, as there are a number of recurring, consistent chromosomal abnormalities in neoplasia, patients with AIDS should also be evaluated for chromosomal aberrations, especially in light of the increased number of secondary malignancies being described in such patients. It would be of great clinical importance to report as many chromosomal abnormalities as are found in this cohort of patients whose clinical outlook is so apparently poor.
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PMID:Acquired immunodeficiency syndrome and concomitant non-Hodgkin's lymphoma in a patient with new chromosomal abnormality. 311 36

After culture with 20-30% autologous or allogeneic T cells and PHA, at least a proportion of the pathological cells from a variety of B-cell proliferations (common acute lymphoblastic leukaemia, prolymphocytic leukaemia, non-Hodgkin's lymphoma with blood involvement by mature lymphoid (cleaved and non-cleaved) cells) expressed true endogenous sheep erythrocyte (E) receptors. In contrast, plasma cells and a variety of myeloid cells failed to express E receptors after similar in vitro stimulation. These data, taken in conjunction with previous findings with B cells from normals and patients with hairy-cell and chronic lymphocytic leukaemia, suggest that B cells earlier than plasma cells can express E receptors after appropriate stimulation. The findings provide an in vitro counterpart of the leukaemic proliferations expressing both E receptor and surface immunoglobulin described from various laboratories, and further question the lineage specificity of the E receptor.
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PMID:Stimulated lymphoid cells of B lineage, but not plasma or myeloid cells, can express E receptor. 315 85

In the PHA-leukocyte feeder colony assay--a fluid assay on top of an agar underlayer--colonies might not be the product of clonogenic cells but rather from aggregates, as was already shown for hairy cell leukemia (Leukemia Res. 11, 911 (1987)). To study the role of aggregation in this colony assay in other B-cell malignancies, we irradiated cells from B-chronic lymphocytic leukemia, B-non-Hodgkin's lymphoma and multiple myeloma. In nearly all cases, viable "colonies" were seen after irradiation, albeit in lower numbers. These data indicate that in the PHA-leukocyte feeder colony assay, a considerable percentage of colonies from a large variety of B-cell malignancies originate from aggregating rather than from proliferating cells.
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PMID:Radioresistant pseudo-colony formation in the PHA-leukocyte feeder colony assay. 326 67

Suppressor cells can be identified in vitro either by specific antibodies or by functional test assays. On investigation of the latter, a close relationship was demonstrated between spontaneously active and in vitro induced (ConA) suppressor cells. The activity of these cells, however, showed a wide day to day variation. Hence, no clinically relevant conclusions could be drawn from a comparison of patients and controls. This was shown both for SLE and myeloma. However, in multiple myeloma indirect evidence of increased activity of short-lived suppressor cells emerged from a different methodological approach. Helper and suppressor cells were evaluated using monoclonal antibodies. Patients with Hodgkin's disease in long-term remission had decreased proportions of T-lymphocytes. Helper T-cells but not suppressor T-cells were strongly diminished. The helper-suppressor ratio was changed from 2.1 in controls to 1.2 in patients. The stimulation (PHA-stimulation) index of the patients was half of the control value. The interactions of suppressor and tumour cells were investigated in non-Hodgkin's lymphoma. In general, a marked reactive infiltration of neoplastic lymph nodes was found. The pattern of suppressor cell distribution argued in favour of a functional role of these cells in tumour growth.
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PMID:[Immunologic detection and in vitro activity of suppressor cells]. 622 47

Serum levels of immunosuppressive acidic protein (IAP) in 105 patients with hematopoietic malignancies, there were 12 cases of acute myeloblastic leukemia, 1 acute monocytic leukemia, 13 myelomonocytic leukemia, 4 acute promyelocytic leukemia, 26 chronic myelogenous leukemia, 22 non-Hodgkin's lymphoma, 5 Hodgkin's disease, 6 adult T-cell leukemia, 5 acute lymphoblastic leukemia, 3 chronic lymphocytic leukemia, and 8 multiple myeloma. High levels of serum IAP were detected in all of the patients except chronic phase of CML, malignant lymphoma in stage I and II, and multiple myeloma. In the cases of malignant lymphoma, serum IAP levels in stage III and IV were higher with statistical significance (p less than 0.01) than those in stage I and II. Serum IAP levels in the patients with CML in blastic crisis were higher than in the chronic phase, so serum IAP levels are useful as one diagnostic parameters in blastic crisis. However, in patients with ANLL in relapse, serum IAP levels showed normal values. Serum IAP levels paralleled those of acute phase reactants such as alpha 1-acid glycoprotein , C-reactive protein, alpha 2-globulin, and alpha 1-antitrypsin, and had inverse correlations with PPD and PHA skin test.
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PMID:[Quantitative measurement and clinical analysis of serum levels of immunosuppressive acidic protein (IAP) in hematopoietic malignancies]. 673 51

The splenic T and B cell distribution in 79 patients with untreated Hodgkin's disease was quite similar to that in 15 control patients with non-Hodgkin's lymphoma or carcinoma. The mean T lymphocyte percentage was slightly higher in involved spleens than in uninvolved spleens of patients with Hodgkin's disease. There was no significant difference in the T and B cell distribution between tumor area and tumor-free area of the same spleens of Hodgkin's disease patients. Splenic T and B cell distribution did not correlate well with the clinical features of Hodgkin's disease. The splenic T cell percentage was significantly lower than that of the peripheral blood T cell percentage (P less than 0.05), while the splenic B cell percentage was significantly higher than peripheral blood B cell percentage (P less than 0.01) in 13 patients with untreated Hodgkin's disease. The splenic T lymphocyte response to PHA was significantly higher than the peripheral blood T lymphocyte response (P less than 0.05), and the splenic B lymphocyte response to PHA, in the presence of irradiated autologous splenic T lymphocytes, was also significantly higher than the peripheral blood B lymphocyte response (P less than 0.05) in 8 and 6 patients with untreated Hodgkin's disease, respectively. Since the control splenic cells, utilized in this study were obtained not from patients with non-neoplastic disease, but from patients with neoplastic disease other than Hodgkin's disease, our data are not conclusive, but only suggestive of normal T and B cell distribution and function in uninvolved spleens of patients with untreated Hodgkin's disease.
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PMID:Splenic T and B lymphocytes and their mitogenic response in untreated Hodgkin's disease. 696 6

Pleural fluid from a patient with non-Hodgkin's lymphoma was examined for lymphocyte subpopulations and their proliferative response to PHA, Con A, and PWM. T lymphocytes were present in a high proportion; in contrast only few B lymphocytes were present when compared to peripheral blood T and B lymphocytes. Among T-cell subsets, Tmu cells were present in high numbers. By contrast Tgamma cells were lacking. Proliferative response to PHA and Con A were normal; however, PWM-induced proliferation was subnormal. This study demonstrates selective migration of a subset of T cells in pleural fluid.
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PMID:Selective migration of T-cell subset in pleural fluid from non-Hodgkin's lymphoma. 701 85


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