Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytogenetic analysis was performed on peripheral blood cells stimulated with interleukin 6 (IL-6), lipopolysaccharide from Escherichia coli (LPS), phytohemagglutinin (PHA), pokeweed mitogen (PWM) and tetradecanoyl-phorbol-acetate (TPA), in a patient with B-chronic lymphocytic leukemia, showing a t(1;19;?) translocation as the sole abnormality. To our knowledge, this translocation has not been described before in any human neoplasia. In this case, the poor response to therapy (survival time 4 months) suggested that t(1;19;?) could be related to an aggressive course of the disease.
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PMID:New chromosomal abnormality. t(1;19;?) in a case of B-chronic lymphocytic leukemia. 160 55

In B chronic lymphocytic leukemia (B-CLL) cells, lipopolysaccharide (LPS) and phorbol esters fail to activate the plasma membrane-associated Na+/H+ antiporter and, subsequently, to elicit a rise in cytosolic pH. Since these events are thought to be a prerequisite for LPS-induced proliferation of B normal lymphocytes, we analyzed the kinetic properties of Na+/H+ antiporter in B-CLL cells as compared to both CD5- and CD5+ normal B lymphocytes. In the present work we report that Na+/H+ exchange rate after acid loading is drastically decreased in B-CLL cells, as compared to normal CD5- B lymphocytes, although the antiporter affinity for external Na+ and internal H+ is not significantly different in both cell populations. Kinetic data account for a reduction in the number of operating antiport units in B-CLL. The Na+/H+ antiporter of CD5+ normal B lymphocytes exhibits both an exchange rate and an ion affinity significantly higher than that observed in both CD5+ B-CLL cells and CD5- B normal lymphocytes, thus suggesting a possible explanation for their activated phenotype.
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PMID:Na+/H+ antiporter has different properties in human B lymphocytes according to CD5 expression and malignant phenotype. 170 1

The production of tumor necrosis factor (TNF) by lipopolysaccharide (LPS)-triggered peripheral-blood mononuclear cells (PBM) was investigated in 23 patients with untreated B-cell chronic lymphocytic leukemia (B-CLL) and 14 control donors. Cells were stimulated at concentrations that reflect cell density in peripheral blood. Under these conditions, PBM from 11/23 of the CLL patients produced at least 10-fold less TNF as compared with controls. Monocyte numbers were decreased in percentage, while absolute numbers (normal range 233 +/- 120 X 10(3)/mm3) were decreased only in 2, normal in 17 and increased in 4 patients indicating that the deficiency is not a result of monocytopenia in most patients. Cell separation experiments indicate that after removal of leukemic B cells, percentages of monocytes return to control range and TNF production is improved (7/7). In mixing experiments, we found a suppression of TNF production in control mononuclear cells by CLL cell samples (75 X 10(6) cells/ml) in 5/19 cases, while control cells from thymus exhibited no or little suppression in these conditions. In 2-chamber experiments, leukemic samples suppress TNF production by normal monocytes across a 0.45 micron membrane indicating that a soluble factor is responsible for suppression. The factor exhibits higher stability in serum-free conditions and its molecular weight is below 20 kDa. Prostaglandins are not involved, since indomethacin did not abrogate suppression.
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PMID:Deficient production of tumor necrosis factor by peripheral-blood monocytes in chronic lymphocytic leukemia. 230 94

Blood lymphocytes from 50 patients with chronic B-lymphocytic leukaemia (B-CLL) were cultured in vitro with and without the polyclonal B-cell activators (PBA) dextran sulphate (DxS), lipopolysaccharide from E. coli (LPS), and Epstein Barr virus (EBV). Patients with blood lymphocytes that showed a high spontaneous or PBA-induced 3H-thymidine uptake in 4 d cultures had a significantly shorter therapy-free survival than patients whose lymphocytes showed a low thymidine uptake. The DxS-induced cellular thymidine uptake was the most powerful predictor of prognosis. Eighteen patients with leukaemic cells responding to DxS stimulation had a median therapy-free survival of 17 months and a probability of 5 year therapy-free survival of less than 0.1, whereas for 30 patients with DxS unresponsive cells the corresponding figures were greater than 120 months and greater than 0.7, respectively (log rank, P less than 0.0001). A multivariate Cox's regression analysis revealed that the DxS-induced leukaemic cell response was of greater prognostic importance than clinical features such as blood counts and staging according to Rai and Binet. Therefore PBA-induced leukaemic cell thymidine uptake seems valuable in the prediction of prognosis in B-CLL.
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PMID:Prognostic value of B-cell mitogen-induced and spontaneous thymidine uptake in vitro in chronic B-lymphocytic leukaemia cells. 241 8

CLL-cell proliferation in vitro, as indicated by tritium-labelled thymidine uptake, was studied in 4-day cultures with or without the B-cell mitogens lipopolysaccharide (LPS), dextran sulphate (DxS) and Epstein-Barr virus (EBV). Thymidine uptake was not associated with Rai or Binet stage, but following mitogenic stimulation it was significantly greater in CLL-cell clones with an extra chromosome 12 or multiple chromosomal aberrations as compared to cell clones with normal karyotypes. Unstimulated thymidine uptakes did not predict outcome, but high proliferative responses to LPS- or DxS-stimulation were significantly associated with poor survival.
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PMID:Clinical implications of CLL cell proliferation in vitro. 246 92

Chromosomal aberrations occur in both B-CLL and T-CLL. The polyclonal B-cell mitogens, in particular Epstein-Barr virus and lipopolysaccharide from E. coli, have been used successfully to reveal chromosomal abnormalities in 40-60% of patients with B-CLL, while T-cell mitogens have shown chromosomal aberrations in T-CLL. The most common clonal chromosomal aberration in B-CLL is an extra chromosome 12, alone or together with other abnormalities. Other common aberrations are 14q+, structural aberrations on 6, 11, 12 and 13. Proto-oncogenes are frequently located close to breakpoints. The proto-oncogene c-K-ras is located on chromosome 12 and an abnormal transcript has recently been implicated in a subset of B-CLL-patients. An extra chromosome 12 as well as multiple chromosomal abnormalities in B-CLL appear to predict a less favourable prognosis. T-CLL is in most patients characterized by an inv(14), an extra 8q and structural abnormalities in chromosome 7. The genes for the specific T-cell receptor as well as the immunoglobulin heavy chain are located on these chromosomes. Chromosomal aberrations appear to have pathogenetic importance in both B-CLL and T-CLL.
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PMID:Role of chromosomal abnormalities in chronic lymphocytic leukemia. 333 2

The mitogenic response patterns as well as surface membrane receptors of peripheral blood lymphocytes were investigated repeatedly during progression of the disease in 27 patients with chronic lymphocytic leukemia. Each patient was characterized by a reproducible mitogenic response pattern. Eleven patients, who required treatment within 0-24 months after diagnosis, had significantly higher cellular responses to dextran sulphate (DxS) and lipopolysaccharide (LPS) than 10 patients who have not required treatment within an observation time of 10-40 months from diagnosis. The high LPS and DxS responses, which may indicate leukemias composed of more immature cells, appear to predict a poor prognosis.
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PMID:Clinical significance of mitogen-induced responses in lymphocytes from patients with chronic lymphocytic leukemia. 615 7

In the present study the B-cell mitogens from Epstein-Barr virus (EBV) and lipopolysaccharide-B from E. coli (LPS) were used to stimulate the blood cells of 27 patients with chronic lymphocytic leukemia (CLL) to undergo mitosis. In 14 CLL cases EBV was used as the only mitotic stimulant and in 5 cases both EBV and LPS. In 8 cases neither EBV nor LPS caused mitotic cells to appear. In 9 cases the cells were characterized by abnormal clones, including 5 cases with +12 (including 1 case with a possible Philadelphia chromosome), 2 cases with 14q+ and 1 case with an i(17q). No correlation was found between the types of surface membrane immunoglobulins and the chromosome abnormalities in the leukemic lymphocytes. The effects of EBV on normal lymphocytes were also investigated and found to be nonspecific (e.g., tetraploidy), although in every case EBV caused a definite increase in the mitotic index. The results indicate that 1) EBV and LPS stimulate leukemic cells of CLL to undergo mitosis, 2) about 50% of the patients have clonal abnormalities in the leukemic cells, and 3) CLL is associated with karyotypic changes seen in lymphoma (14q+), although the most common anomaly in our material was a +12.
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PMID:Chromosomes and causation of human cancer and leukemia. XLV. Chromosome patterns in stimulated lymphocytes of chronic lymphocytic leukemia. 626 49

Lymphocytes from 33 out of 63 patients with B-cell chronic lymphocytic leukaemia (B-CLL) were successfully stimulated for cytogenetic analysis by means of two B-cell mitogens: pokeweed mitogen and lipopolysaccharide-B, used after pretreatment of the cells with neuraminidase and galactose oxidase. All patients had abnormal clones in 30-100% of the cells analysed. Chromosomes more frequently involved were Nos. 1, 3, 6, 11, 12, 13 and 14. The most common abnormality was a marker 14q+ (breakpoint 14q32) seen in 17 cases; trisomy 12 was observed in seven cases. A clinical scoring system was used to investigate the correlation of chromosome abnormalities with prognosis. The group with 14q+ was often associated with features of progressive disease, namely; prolymphocytoid or Richter transformation, refractoriness to therapy, high WBC and advanced staging. A significant difference in survival was observed between patients with 14q+ and the rest: median survival from diagnosis being 45 months and over 64 months, respectively (P less than 0.05); when survival was calculated from the time of chromosome analysis the values were 8 months and more than 41 months, respectively (P less than 0.01). It is suggested that 14q+ is acquired during the evolution of CLL and that this development may be a key event in the clinical progression of B-CLL. Other abnormalities, including trisomy 12, were not found to be associated with a worse prognosis.
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PMID:Prognostic significance of chromosome abnormalities in chronic lymphocytic leukaemia. 633 48

Four consistent markers, involving chromosomes 8, 11, 14, 18, 21 and 22, were found in the majority of metaphases obtained after stimulation of peripheral blood and bone marrow from a patient with a T-cell chronic lymphocytic leukemia (CLL) and a concomitant IgA/lambda myeloma with phytohemagglutinin (PHA), lipopolysaccharide of E. coli (LPS) and S. aureus strain Cowan I bacteria (Cowan). A second malignant clone with three additional markers was observed after stimulation with Concanavalin A (Con A). A chromosome 14 aberration, inv(14) (q11-q32), may be of significance in the T-cell malignancy and may suggest a common clonal origin of the two tumors.
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PMID:Chromosomal aberrations in a case of T-cell CLL with concomitant IgA myeloma. 641 31


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