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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adhesion molecules CD58 and CD54 are involved in cell-cell interactions that are potentially important in the biology of acute leukemia (AL). Expression of these molecules was studied in 79 cases of adult AL including 50 cases of acute non-lymphoid leukemia (ANLL) and 29 cases of acute lymphoid leukemia (ALL) using an indirect immunofluorescence technique. CD58 was expressed in 45 +/- 26% of ANLL cells and 43 +/- 32% of ALL cells, and its expression did not correlate with any other marker. In ALL, the expression of CD58 was inversely correlated with the presence of a clinical tumoral syndrome (p = 0.0009), leucocytosis (p = 0.005), and the percent of peripheral blast cells (p = 0.001). The major finding in this study was the association between CD58 expression and prognosis. In ANLL, higher expression of CD58 was independently associated with higher CR rate (p = 0.04), longer overall survival (p = 0.02), and longer disease-free survival (p = 0.007). In ALL, higher expression of CD58 was associated with longer survival (p = 0.05). CD54 was expressed only on 17 +/- 16% of ANLL cells and 11 +/- 11% of ALL cells; its expression on ANLL was positively correlated with that of CD11 (p = 0.03), CD15 (p = 0.001) and CD34 (p = 0.01). CD54 expression did not correlate with clinical and hematologic characteristics. We conclude that the expression of adhesion molecule CD58, but not CD54, in AL is related to initial characteristics and evolution of the disease.
Leukemia 1992 Apr
PMID:Expression of surface adhesion molecules CD54 (ICAM-1) and CD58 (LFA-3) in adult acute leukemia: relationship with initial characteristics and prognosis. 137 2

We review the role of adhesion molecule expression on malignant lymphoid cells as delineated by experimental studies and clinical observation. Adhesion molecules of the Ig superfamily, integrins, selectins, and the lymphocyte homing receptor CD44 mediate cell-to-cell and cell-to-extracellular matrix interactions. These molecules have been investigated with the aim (i) of defining certain biological features of the malignant cells, (ii) of providing a rationale to understand tumor organization, metastasis and organ specificity, and (iii) of detecting disease subsets and prognostic groups.
Leukemia 1992 Nov
PMID:Expression of adhesion molecules in lymphoproliferative disorders. 143 29

Adhesion to cells and extracellular matrices is a fundamental feature of leukocyte physiology, a process crucial to the generation of immune and inflammatory responses. Adhesive interactions between lymphocytes, monocytes/macrophages, granulocytes and vascular endothelial cells are mediated by specific cell-adhesion molecules (CAMs). The Leu-CAMs (CD111/CD18) belong to a large family of cell-surface molecules known as intergrins, a family which also includes receptors for extracellular matrix components. In man, inherited deficiency of Leu-CAMs is characterised by recurrent, sometimes fatal, bacterial infections. In animals, on the other hand, Leu-CAM blocking by monoclonal antibodies has been found beneficial in inflammatory disorders. As some lymphoid malignancies are devoid of CAMs, it is possible that their absence may be a contributing factor in the development of leukaemia and lymphoma.
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PMID:[Leukocyte adhesion: a fundamental process in immunologic and inflammatory reactions]. 199 69

Adhesion to glass and silicone-coated surface of leukemia cells (L1210 and L5222) and their motion on an inclined plane have been investigated. The cells in quiescent fluid are subjected to the action of gravitational force; its component parallel to the surface ranges from 4.0 x 10(-14) N to 4.5 x 10(-13) N. The prolonged action of the gravitational force at 45 degrees (3.3 x 10(-13) N) causes the separation from the substratum of numerous cells which have adhered on a horizontal plane. When the cells passively move on the slope they are frequently arrested by adhesion which is partly short-lived. The analysis of the leukemia cell velocity reveals good agreement with the theory describing the motion of a sphere in quiescent fluid. The translation movement of nucleated cells on an inclined plane is not, however, accompanied by rotation. On the other hand, the cells flowing in mid-stream rotate with an angular velocity predicted by the theory.
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PMID:Surface interactions of leukemia and red cells passively moving in a quiescent fluid. 709 56

Adhesion receptors from the very late activation (VLA) (beta 1) integrin subfamily play a role in the cooperation of hematopoietic progenitors with bone marrow stroma, and the disregulated expression of these molecules, as evaluated by immunophenotyping, has been implicated in the acquisition of the malignant phenotype by hematopoietic cells. In the present study, Northern hybridization was used to determine the pattern of expression of transcripts for VLA subunits in: (i) leukemic blasts obtained from the peripheral blood of ten patients with acute myelogenous leukemia (AML) of different FAB subclasses; (ii) the human leukemic cell lines KG-1, HL-60, K-562, HEL and U-937; and (iii) normal hematopoietic cells. Most of the AML blasts and the cultured leukemic cells expressed mRNAs for the beta 1 and alpha 5 subunits (the only exception among the cell lines was KG-1 cells) and these transcripts were also found in normal bone marrow progenitors, peripheral blood mononuclear cells (PBMNC), and peripheral blood monocytes. While the alpha 4 transcript was detected in all cultured cells but K-562, and in normal circulating monocytes, it occurred in blasts from only two AML patients and was weakly expressed in mature PBMNC. No specific pattern of expression of beta 1, alpha 5, and alpha 4 transcripts could be related to cell differentiation or maturation in the AML blasts and leukemic cell lines tested. None of the primary AML blasts or cultured cells showed mRNA messages for alpha 2, alpha 3 or alpha 6 chains of the beta 1 integrins. The results suggest that, in some cases of AML, the malignant phenotype of leukemic blasts may be associated with down-regulated transcription of the alpha 4 integrin subunit.
Leukemia 1994 Sep
PMID:Expression of beta 1 integrin mRNAs in human leukemic blasts. 752 92

Adhesion of cancer cells to endothelium is thought to be a prerequisite to extravasation during the haematogenous phase of metastasis, and is enhanced after perturbation of the endothelium by interleukin-1 (IL-1). The inducible endothelial adhesion molecules, E-selectin, VCAM-1/alpha 4 beta 1 and vitronectin receptor have been reported to mediate attachment of cancer cells to IL-1-treated endothelial cells. We have examined the relative contribution of these molecules by quantifying the adhesion of a panel of 22 human, 125I-labelled cancer cells and the rat W256 tumour to untreated and IL-1-treated endothelial monolayers in the presence of relevant neutralising antibodies. Antibodies against E-selectin inhibited the adhesion of HL-60 leukaemia cells and two colon carcinomas. Anti-alpha 4 beta 1 antibodies blocked adhesion of four melanomas, five sarcomas and one lung carcinoma. Anti-vitronectin receptor antibodies inhibited adhesion of 14 of the 22 human cell lines to IL-1-treated endothelial cells. Adhesion of seven cell lines was inhibited by more than a single antibody. In contrast, adhesion of one of the cancer cell lines was unaffected by any of the antibodies, suggesting involvement of other IL-1-inducible endothelial adhesion molecules. Moreover, none of the antibodies altered the attachment of cancer cells to unstimulated endothelial monolayers. We conclude that the mechanisms of cancer cell adhesion to the endothelium are influenced by endothelial activation and by the adhesive repertoire of the cancer cell.
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PMID:The relative roles of vitronectin receptor, E-selectin and alpha 4 beta 1 in cancer cell adhesion to interleukin-1-treated endothelial cells. 753 92

Leukocyte adhesion to kidney cells is an early event in renal inflammation, such as glomerulonephritis. We developed an experimental model of monocyte adhesion to cultured human mesangial cells. U-937 myelomonocytic leukaemia cells, similar to peripheral blood human monocytes, irreversibly bound to mesangial cell monolayers upon 30-180 min coincubations (to a max. of 13,600 +/- 1100/cm2 monolayer), as assessed by cell counting, U-937 labelling with 3H-thymidine, and colorimetry of nuclear staining with crystal violet. Adhesion was enhanced in mesangial cells proliferating in response to 17% fetal bovine serum, indicating expression of a proinflammatory phenotype. E. coli lipopolysaccharide (LPS), tumour necrosis factor-alpha (TNF-alpha) and protein kinase C activation with phorbol myristate acetate (PMA) potentiated monocyte binding during either coincubation or 24-h pretreatment (0.1 microM PMA, +200 +/- 21%). Binding was also promoted by pretreatment with vasoconstrictors, such as the thromboxane A2 mimetic, U-46619 (10 nM-1 microM, max. +35 +/- 3%), or 1 microM angiotensin II (+64 +/- 4%). To elucidate the mechanisms of monocyte adhesion, we analysed the adhesion molecules expressed by human mesangial cells, employing reverse transcription/polymerase chain reaction to detect ICAM-1, VCAM-1 and E-selectin gene expression. Proliferating cells express VCAM-1 and ICAM-1, confirmed by immunocytochemical staining and 79 +/- 3% inhibition of stimulated adhesion by pretreatment of mesangial cells with an anti-ICAM-1 monoclonal Ab. E-selectin transcription was not detectable.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of U-937 monocyte adhesion to cultured human mesangial cells by cytokines and vasoactive agents. 754 54

Adhesion of hematopoietic progenitor cells to marrow-derived adherent cells has been noted for erythroid, myeloid, and lymphoid precursors. In this report, we have characterized very late antigen (VLA) integrin expression on normal CD34+ marrow progenitors, on leukemic cell lines, and on blasts from patients with acute myelogenous or monocytic leukemias. CD34+ progenitor cells expressed the integrin beta 1 chain (CD29), VLA-4 alpha (CD49d), and VLA-5 alpha (CD49e). The myeloid lines KG1 and KG1a also expressed CD49d and CD49e as did the Mo7e megakaryoblastic line. CD29, CD18, and CD11a were also present on each of these cell lines. Only the Mo7e line expressed the cytoadhesins GPIIbIIIa or GPIb. Binding of KG1a to marrow stroma was partially inhibited by antibodies to CD49d and its ligand, vascular cell adhesion molecule (VCAM-1). The majority of leukemic blasts studied expressed CD49d and CD49e as well. Blasts from patients with acute myelomonocytic leukemia consistently bound to stroma at levels greater than 20%, and adhesion to stroma could in some cases be partly inhibited by anti-CD49d. No role for glycosylphosphatidyl-inositol (GPI)-linked structures was demonstrated in these binding assays because the adhesion of leukemic blasts to stroma was not diminished after treatment with phosphatidylinositol-specific phospholipase C (PI-PLC). These studies indicate that CD34+ myeloid progenitors, myeloid leukemic cell lines, and leukemic blasts possess a similar array of VLA integrins. Their functional importance individually or in combination with other mediators of attachment in adhesion, transendothelial migration, and differentiation has yet to be fully elucidated.
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PMID:Expression of integrins and examination of their adhesive function in normal and leukemic hematopoietic cells. 767 62

Adhesion molecules of the integrin family are implicated not only in leukocyte migration but also in leukocyte activation. Here we characterize the expression and function of fibronectin receptor integrins on rat mast cells. A rat basophilic leukemia cell line (RBL-2H3) and phorbol ester-stimulated rat peritoneal mast cells adhered to fibronectin (FN), vitronectin and fibrinogen. These mast cells expressed fibronectin receptor integrins, including very late antigen (VLA)-4, VLA-5 and vitronectin receptor (VNR), as estimated by immunofluorescent staining and inhibition of FN adherence by newly established mAbs reactive with the rat alpha 4 (MR alpha 4-1), alpha 5 (HM alpha 5-1) or beta 3 (HM beta 3-1) chains of the integrin molecules. The beta-hexosaminidase release, a marker for mast cell degranulation, triggered by high affinity IgE receptor (Fc epsilon RI)-mediated stimulation, was enhanced by adhesion of RBL-2H3 cells to either immobilized FN, MR alpha 4-1, HM alpha 5-1 or HM beta 3-1. This FN enhancement of beta-hexosaminidase release was inhibited by soluble MR alpha 4-1, HM alpha 5-1 and HM beta 3-1 as well as by GRGDSP and DELPQLVTLPHPNHLGPEILDVPST peptides which abrogate VLA-5/VNR and VLA-4 binding to FN respectively. In vivo, passive cutaneous anaphylaxis induced by IgE anti-DNP and DNP-BSA was inhibited by concurrent s.c. injection of MR alpha 4-1, HM alpha 5-1 and HM beta 3-1. These results demonstrate that FN receptor integrins expressed on rat mast cells play an important role in regulating mast cell activation both in vitro and in vivo.
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PMID:Expression and function of fibronectin binding integrins on rat mast cells. 773 20

The physiological function of many cells is dependent on their ability to adhere via receptors to ligand-coated surfaces under fluid flow. We have developed a model experimental system to measure cell adhesion as a function of cell and surface chemistry and fluid flow. Using a parallel-plate flow chamber, we measured the binding of rat basophilic leukemia cells preincubated with anti-dinitrophenol IgE antibody to polyacrylamide gels covalently derivatized with 2,4-dinitrophenol. The rat basophilic leukemia cells' binding behavior is binary: cells are either adherent or continue to travel at their hydrodynamic velocity, and the transition between these two states is abrupt. The spatial location of adherent cells shows cells can adhere many cell diameters down the length of the gel, suggesting that adhesion is a probabilistic process. The majority of experiments were performed in the excess ligand limit in which adhesion depends strongly on the number of receptors but weakly on ligand density. Only 5-fold changes in IgE surface density or in shear rate were necessary to change adhesion from complete to indistinguishable from negative control. Adhesion showed a hyperbolic dependence on shear rate. By performing experiments with two IgE-antigen configurations in which the kinetic rates of receptor-ligand binding are different, we demonstrate that the forward rate of reaction of the receptor-ligand pair is more important than its thermodynamic affinity in the regulation of binding under hydrodynamic flow. In fact, adhesion increases with increasing receptor-ligand reaction rate or decreasing shear rate, and scales with a single dimensionless parameter which compares the relative rates of reaction to fluid shear.
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PMID:Receptor-mediated binding of IgE-sensitized rat basophilic leukemia cells to antigen-coated substrates under hydrodynamic flow. 803 94


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