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)

The malignant cells in a patient with hairy cell leukemia responded most evidently to lipopolysaccharide (LPS) in in vitro culture for 3 1/2 days when the conventional tritiated thymidine uptake method was used. Since the malignant cells from patients with several other forms of leukemia and the peripheral blood mononuclear cells from healthy individuals did not show a comparable degree of responsiveness to LPS, we could exclude the possibility that this response was due to effects on contaminating normal mononuclear cells or to the nonspecific conditioning effect through LPS-affected contaminating normal monocytes. Morphological changes were observed with photo- and electronmicroscopy. It is likely that the hairy cells from the patient did respond to LPS, and whether or not this phenomenon may be confined to this type of lymphoid leukemia is not being investigated.
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PMID:Lipopolysaccharide responsiveness of malignant lymphoid cells in a patient with hairy cell leukemia. 45 53

Using a sister chromatid differentiation (SCD) technique, cell cycle analysis in lymphocytes from two patients with hairy cell leukemia (HCL) revealed it to be similar to cell cycle progression of normal lymphocytes stimulated with lipopolysaccharide W from Escherichia coli 0.55:B5 (LPS). It appears that LPS can readily stimulate the leukemic cells of HCL into mitosis. In the two cases of B cell HCL studied, one (case 1) was revealed to have an abnormal clone with a missing chromosome #22 that was related to the production of lambda-chains.
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PMID:Cytogenetic studies of stimulated lymphocytes in hairy cell leukemia. 298 37

Cytogenetic analyses were performed on cells from 17 patients with hairy cell leukemia stimulated with polyclonal B-cell activators (in 155 different cultures). No mitosis was obtained in samples from four cases (23.5%). Of 14 bone marrows, four (28.6%) showed mitoses, two with clonal abnormalities. All four samples from the spleen had mitoses with four clonal changes; eight of 13 (37.5%) blood samples had mitoses with three clonal changes. Of the polyclonal B-cell activators (PBA), lipopolysaccharide and protein A seemed to be effective for the detection of clonal abnormalities in hairy cell leukemia. Among the clonal aberrations, chromosomes #3, #10, and #17 were affected in two cases each; frequent numerical changes were monosomies of #10 and #17 and structural changes were deletions at band 3p21 (two cases), 6q-, and der(9)t(9;?)(p22;?). The chromosomal bands involved in structural changes were close to accepted constitutive fragile sites.
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PMID:Cytogenetic studies in hairy cell leukemia. 349 70

What appears to be the first hairy cell leukemia case with a 14q+ anomaly is described. In addition to the 14q+ anomaly, a 6q- and a ring chromosome were seen in a blood sample stimulated with lipopolysaccharide, a B-cell mitogen. The clinical course of the present case was short, stormy, and had a poor response to therapy. The correlation between the clinical course and the presence of a ring chromosome in myelo- and lymphoproliferative blood disorders is discussed in relation to the various blood disorders with this karyotype anomaly described in the literature.
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PMID:Chromosomes and causation of human cancer and leukemia. LI. A hairy cell leukemia case with 14q+ and ring chromosomes: significance of ring chromosomes in blood disorders. 688 1

1. Freeze-fracture electron microscopy and 31P-NMR spectroscopy on native and electrodialyzed lipopolysaccharide from Escherichia coli K12 cells, both above and below the phase transition temperature, are described. 2. Freeze-fracture electron microscopy of native lipopolysaccharide shows ribbon-like structures below (0 and 22 degrees C) and large vesicles above (37 degrees C) the phase transition temperature. Electrodialyzed lipopolysaccharide (sodium salt) occurs in ribbon-like structures at 0, 22 and 37 degrees C if sodium lipopolysaccharide is hydrated in water. If sodium lipopolysaccharide is hydrated in Tris-HCL/NaCl buffer these ribbon-like structures occur only below the phase transition temperature. Above the phase transition temperature stacked sheets are observed. Moreover, in the latter case, the fracture planes contain particles and pits. Upon etching, sodium lipopolysaccharide when hydrated in water appears to form rods and when hydrated in buffer appears to form mainly stacked lamellae both above (37 degrees C) and below (0 degrees C) the phase transition temperature. 3. High resolution 31P-NMR spectra show that the chemical shifts of the phosphorus atoms in native lipopolysaccharide differ from those in electrodialyzed lipopolysaccharide, probably due to conformational and compositional (the disappearance of ions and (poly)electrolytes) changes. The 31P-NMR spectra of native lipopolysaccharide dispersed in Tris-HCL/NaCl buffer are very broad at 20 and at 40 degrees C indicating little motion. At 22 degrees C electrodialyzed lipopolysaccharide also gives a broad spectrum; at 40 degrees C the spectrum is narrower, indicating more motion, and two peaks are visible. After dispersion in H2o and subsequent addition of buffer, the spectrum of electrodialyzed lipopolysaccharide is narrow both at 20 and 40 degrees C, which can be correlated with the rods observed in freeze etching. After treatment with Ca2+, electrodialyzed lipopolysaccharide shows a very broad spectrum at 40 degrees C probably due to immobilization of the lipopolysaccharide. 4. Freeze-fracture electron microscopy and 31P-NMR spectroscopy of liposomes consisting of native lipopolysaccharide and total phospholipids indicate that the phospholipids and the lipopolysaccharide are mainly organized in bilayers. Lipopolysaccharide in such liposomes undergoes more motion than in the absence of phospholipids. Ca2+ does not influence this behaviour.
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PMID:31P nuclear magnetic resonance and freeze-fracture electron microscopy studies on Escherichia coli. II. Lipopolysaccharide and lipopolysaccharide-phospholipid complexes. 699 Sep 86

The results of cytogenetic studies are reported in 76 patients with B-chronic lymphoproliferative disorders (B-CLPD): 60 patients with chronic lymphocytic leukemia (CLL), six with follicular lymphoma in leukemic phase (FLLP), five with splenic B-cell lymphoma with villous lymphocytes (SLVL), two with chronic prolymphocytic leukemia (CPL), two with hairy cell leukemia (HCL), and one with plasma cell leukemia (PCL). PHA (phytohemagglutinin), PWM (pokeweed mitogen), LPS (lipopolysaccharide from Escherichia Coli), TPA (phorbol 12-myristate acetate), IL6 (interleukin 6), and DxS (dextran sulfate) were used as mitogens. Mitoses were obtained in 75 cases. Clonal aberrations could be demonstrated in 34 cases (44%). In CLL, classical type, chromosomes 6, 11, and 13 were more frequently involved, whereas trisomy 12 was frequently found in CLL mixed-cell type, in FLLP, and CPL. In SLVL the deletion del(7)(q32) is noteworthy and miscellaneous chromosome abnormalities in the remaining patients were observed. Regarding the efficiency of mitogens, PHA turned to be the most effective in obtaining metaphases and in detecting clonal chromosomal aberrations.
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PMID:Cytogenetic studies in seventy-six cases of B-chronic lymphoproliferative disorders. 907 2

We report on a male Japanese patient with hairy cell leukemia (HCL). A cytogenetic study with lipopolysaccharide stimuli showed a novel translocation (11;20)(q13;q11) in 10% of the analyzed cells. Northern blot analysis and RT-PCR analysis for cyclin D1 revealed the overexpression of cyclin D1, although the southern blot analysis of PRAD1 gene showed no rearrangement. In this particular case, the t(11;20)(q13;q11) might play some role in the oncogenesis of HCL and the overexpression of cyclin D1.
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PMID:Hairy cell leukemia with translocation (11;20)(q13;q11) and overexpression of cyclin D1. 1045 74

We evaluated the effect of HCL-31D, a novel cAMP-specific phosphodiesterase inhibitor, on the induction of inducible nitric oxide synthase (iNOS) in lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma)-treated rat aortic smooth muscle cells (RASMC) and on survival in a murine model of severe endotoxaemia. Treatment of cultured RASMC with LPS and IFN-gamma resulted in an increase of nitrite, tumour necrosis factor (TNF-alpha) production and induction of iNOS mRNA. However, incubation with HCL-31D (1 approximately 50 microM) for 24 h caused significant attenuation of nitrite and TNF-alpha formation as well as iNOS mRNA induction in a dose-dependent manner but no effect on iNOS activity in RASMC. In addition, administration of HCL-31D (5 mg/kg, i.p.) resulted in that the increase of both plasma nitrate and TNF-alpha levels induced by LPS in vivo was significantly reduced in LPS-treated rats. Treatment of conscious mice with a high dose of LPS (60 mg/kg, i.p.) to ICR mice resulted in a 24-h survival rate of only 10%. However, administration of HCL-31D (5 mg/kg, i.p. at 0 h and 6 h after LPS) improved the 24-h survival to 50%, indicating that HCL-31D has a beneficial effect in murine model endotoxaemia. These effects may be mainly due to inhibition of TNF-alpha formation and of the induction of iNOS. We proposed that the elevation of cAMP levels by HCL-31D may be involved in the prevention of TNF-alpha formation and iNOS induction.
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PMID:Beneficial effect of HCL-31D in murine models of endotoxaemia. 1152 Nov 63