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

To study adhesion, which is probably the initial step in malignant invasion, we associated tissue culture fragments with living substrates in vitro. Malignant HeLa, hepatoma, and PY cells, as well as nonmalignant BHK cells, were transplanted into cultured chick blastoderms and organ fragments from chick embryos. Adhesion was evaluated by time-lapse cinematography, by flushing with Tyrode's solution, and by histological examination after fixation. It was shown that the adhesion of these tissue culture fragments depends on the nature of the substrate. Substrates of connective tissue, mesenchyme, and the basal side of epithelia proved to be adhesive. In contrast, the apical side of intact epithelia was nonadhesive. Perforated epithelia allowed adhesion at the site of the perforation. In the presence of dilysine, HeLa cells adhere to the apical side of epithelia and to the dorsal side of the upper layer of the blastoderm. We concluded that the apical side of intact epithelia constitutes an inappropriate substrate for adhesion of a large variety of cells, in vitro as well as in vivo. Alteration of this characteristic in the presence of dilysine indicates that long-range electrostatic repulsion might be responsible for the nonadhesive character of the epithelia.
Cancer Res 1975 Nov
PMID:Adhesion of malignant and nonmalignant cells to cultured embryonic substrates. 17 Oct 65

A surface-adherent cell population developed spontaneously from Friend erythroleukemia cells (FLC745) which previously had grown continuously in suspension cultures. The adherent cells have been transferred through more than 60 passages and apparently represent a stable variant, herein designated FLC745-Ad. The cell size, chromosome complement, and tumorigenicity in DBA/2 mice were similar to the parental FLC745 line, although the FLC745-Ad cultures grew at a slightly slower rate and synthesized less hemoglobin in response to dimethyl sulfoxide. Production of C-type particles was abundant in both suspension and adherent cells, but the latter appeared to contain more intracisternal A-type particles. Scanning electron microscopy disclosed that most adherent cells were globoid and nonspreading. They attached to the substrate by a circumferential lamellar skirt of unusual breadth. Adhesion of the FLC745-Ad cells was not influenced by serum concentration, trypsinization, 5-bromodeoxyuridine, or N6, O2'-dibutyryl adenosine 3':5'-monophosphate. Treatment with cytochalasin B increased the cell size and the area of cell attachment.
Cancer Res 1976 Feb
PMID:Characteristics of a surface-adherent subline derived from Friend erythroleukemia cells in continuous suspension culture. 17 97

Cell Adhesion Factor, complexed to insoluble collagen-coated tissue culture dishes, is required for the attachment of fibroblasts to this substrate. In solution, the factor has no demonstrable affinity for cells in suspension following trypsin-EDTA removal of cells from monolayer. Cell surface receptors for the factor are present during the assay period since cells allowed to recover for 1 h at 37 degrees C, 4 degrees C or in the presence of 10(-6) M cycloheximide show exactly the same kinetics of adhesion as control cells. It is demonstrated that Cell Adhesion Factor acquires affinity for the cell surface only following its binding to collagen.
Int J Cancer 1978 Jul 15
PMID:Substrate activation of cell adhesion factor as a prerequisite for cell attachment. 68 Oct 24

The expression of the VLA-integrins alpha 2, alpha 3, alpha 5 and alpha 6 was studied immunohistochemically in tissue samples from ductal pancreatic cancer, chronic pancreatitis, normal pancreas and in 8 cell lines of ductal human pancreatic cancer. Furthermore, adhesion assays on purified extracellular matrix (ECM)-compounds were used to define the function of alpha 2, alpha 3, alpha 5 and alpha 6 in pancreatic cancer cells. Immunohistochemically, VLA alpha 2 and VLA alpha 6 were moderately to strongly expressed on the basal surface of ductal and acinar cells in normal pancreatic tissue, while centro-acinar cells predominantly expressed VLA alpha 3 and VLA alpha 5. Pancreatic carcinoma showed intense staining for VLA alpha 2 and VLA alpha 6 with a diffuse distribution on the cell surface. The redistribution of VLA alpha 2 and VLA alpha 6 may reflect a loss of spatial arrangement of tumor cells and their ability to interact randomly with extracellular matrix structures during invasion and metastasis. Expression of VLA alpha 3 and VLA alpha 5 in pancreatic carcinoma was heterogeneous, ranging from moderate to weak, and was lost in about 50% of the cells. Two pancreatic carcinoma cell lines (PC 3, PC 44) were further investigated in adhesion assays. Monoclonal antibodies (MAbs) against alpha 2 (GI 9, 10-G-11) were able to inhibit tumor-cell adhesion to collagen IV (59%-72%) in both cell lines. A MAb against alpha 6 (GoH3) inhibited tumor-cell adhesion to laminin (52%-86%) in both cell lines. These results suggest that alpha 2 is a collagen-binding site and alpha 6 a laminin-binding site in pancreatic cancer cells. The anti-alpha 5-MAb SAM I inhibited adhesion of PC3 to fibronectin (76%), being without effect in PC44. Adhesion of both cell lines to fibronectin was almost completely inhibited by RGDS (85%-88%). Thus, alpha 5 is a functionally important fibronectin binding site in some pancreatic carcinoma cells, suggesting further RGD-dependent fibronectin binding sites in other pancreatic carcinoma cells.
Int J Cancer 1992 Nov 11
PMID:Expression and function of VLA-alpha 2, -alpha 3, -alpha 5 and -alpha 6-integrin receptors in pancreatic carcinoma. 133 Sep 37

CD54/Intercellular Adhesion Molecule-1 (ICAM-1) is a cell adhesion molecule largely distributed among normal and neoplastic tissues. Through the binding to its ligand(s) CD54 plays a key role in cell to cell interactions leading to the immune response. Recently, CD54 expression has been investigated on hematopoietic cells: the antigen is predominantly expressed in the early stages of normal hematopoiesis and during the activation of blood cells. As regards to hematological malignancies, CD54 is strongly expressed on neoplastic cells from "stem cell derived" neoplasms. In AML, CD54 expression is related with other differentiation-linked molecules such as CD34 and HLA-DR and is significantly correlated with FAB morphological classification. In lymphoproliferative disorders, a high CD54 expression is associated with germinal centre lymphomas. This review summarizes our current understanding of CD54 with emphasis on recent advances and reference to unresolved issues such as its prognostic role in the clinical outcome of oncohematological diseases.
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PMID:Expression and functional role of CD54/Intercellular Adhesion Molecule-1 (ICAM-1) on human blood cells. 136 19

Adhesion molecules play an important role in the functioning of the immune system, particularly with regard to cell-cell interactions and antigen presentation. Several adhesion molecules are expressed on Hodgkin's disease-derived cell lines and these are important in their molecular interactions as antigen presenting cells (APC). There are no data regarding the expression of many of these adhesion molecules on Reed-Sternberg cells and its mononuclear variant (Hodgkin's cells (HC)) present in pathological material. To obtain this information we undertook an immunohistological study on material from 18 cases of Hodgkin's disease using a panel of MoAbs to examine the expression of adhesion molecules on HC. The HC were shown to express the integrin beta 1 subfamily molecules, LFA-1 (CD11a) and p150,95 (CD11c) in high density but lacked CR3 (CD11b). All of the immunoglobulin gene superfamily adhesion molecules studied were present to some degree on HC, with ICAM-2, in particular, showing moderate to strong expression in most cases. The Hermes antigen CD44 was present in high density but leukosialin (CD43), another molecule present on diverse leucocyte types, was, in general, not detected on HC. These new data showing that ICAM-1, ICAM-2 and LFA-3 are, like LFA-1, expressed on HC emphasize the ability of HC to act as APC. The known adhesion molecule phenotype of the recently defined haematopoietic lineage of human dendritic cells (DC) is broadly similar to that of HC, perhaps supporting the hypothesis that some HC represent a malignancy of an APC (DC) lineage.
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PMID:Hodgkin's cells express a novel pattern of adhesion molecules. 139 91

Adhesion molecules involved in leukocyte recruitment and lymphocyte recirculation impact on several aspects of tumor biology--the primary host response, the delivery of effective adoptive immunotherapy and the hematogenous spread of malignant cells. Common to all three processes are receptor-mediated adhesive interactions between circulating cells and the vessel wall. Recruitment of circulating lymphocytes, monocytes and natural killer cells is essential for an effective host response or successful adoptive immunotherapy. Thus poor induction or blockade of leukocyte binding sites on the microvasculature of tumor implants may help malignancies evade natural defenses. In addition, perturbation of adhesion receptor function during ex vivo expansion may alter the behavior of infused cells in adoptive immunotherapy protocols. Finally, circulating malignant cells may utilize receptors normally involved in recruitment and recirculation. This paper reviews the function and regulation of adhesion molecules involved in normal leukocyte trafficking. The evidence implicating specific adhesion receptors in the spread of lymphoid malignancies through the bloodstream is then discussed.
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PMID:Adhesion molecules involved in the trafficking of normal and malignant leukocytes. 139 99

Cancer metastasis poses the greatest challenge to the eradication of malignancy. The majority of clinical and experimental evidence indicates that metastasis is a non-random, organ-specific process. Tumor cell interaction with endothelium and subendothelial matrix constitutes the most crucial factor in determining the organ preference of metastasis. A plethora of cell surface adhesion molecules, which encompass four major families (i.e., integrins, cadherins, immunoglobulins and selectins) and many other unclassified molecules, mediate tumor-host interactions. Adhesion molecules and adhesion processes are involved in most, if not all, of the intermediate steps of the metastatic cascade. Decreased E-cadherin expression and increased CD44 expression are clearly correlated with the acquisition of the invasive capacity of primary tumor cells. Similarly, altered expression pattern of many other adhesion molecules such as upregulated expression of the laminin receptors and depressed expression of fibronectin receptors (alpha 5 beta 1) appears to be involved in tumor cell invasion into the subendothelial matrix. Tumor cell-endothelium interactions involve several well-defined sequential steps that can be analyzed by the 'Docking and Locking' hypothesis at the molecular level. Tumor cell-matrix interactions are determined by the repertoire of adhesion receptors of tumor cells and the unique composition of organ-specific matrices. Our experimental data, together with others', suggest that the integrin alpha IIb beta 3 is one of the major players in these tumor-host interactions. Tumor-host interaction is a dynamic process which is constantly modulated by a host of factors including various cytokines, growth factors and arachidonate metabolites such as 12(S)-HETE. Delineation of the molecular mechanisms of tumor-host interactions may provide additional means to intervene in the metastatic process.
Cancer Metastasis Rev 1992 Nov
PMID:Adhesion molecules and tumor cell interaction with endothelium and subendothelial matrix. 142 22

Appropriately activated mononuclear phagocytes mediate contact-dependent tumoricidal activity. Adhesion structures involved in contact-dependent tumor cytotoxicity have not been defined. The present study was aimed at identifying the adhesion structures involved in the tumoricidal activity of activated (IFN-gamma + LPS) human monocytes. Tumor cells of different histological origin were used as targets in a 48-hr cytolysis assay. Anti-CD18 (integrin beta 2 chain) monoclonal antibodies (MAbs) substantially (50-80%) inhibited human monocyte cytotoxicity. When the role of different a-chains was studied, anti-alpha L (CD11a, LFA1), anti-alpha M (CD11b, Mac-1) and anti-alpha X (CD11c, p150,95) caused marginal inhibition, but the effect of the 3 combined was comparable to that of anti-CD18. Anti-CD18 MAb did not affect the release of various cytotoxic molecules (e.g. TNF) by activated human monocytes. Activated monocytes showed augmented binding to target cells and anti-CD18 MAb inhibited the binding of resting and activated monocytes to tumor target cells. While IFN-gamma alone augmented expression of leukocyte integrins and LPS had no effect, the 2 activation signals, combined for optimal stimulation of tumoricidal activity, resulted in no appreciable increase in these leukocyte adhesion molecules, as assessed by flow cytometry. Our results suggest that the augmented CD18-dependent binding of activated monocytes on tumor cells depends mainly upon changes in the adhesive properties of these molecules rather than upon increased numbers on the cell surface. Anti-ICAM-1 MAb significantly reduced monocyte cytotoxicity on tumor cells, which is consistent with a role of the CD11/CD18 adhesion pathway. These results implicate "activated" leukocyte (beta 2) integrins (CD11/CD18) as important adhesion molecules in the contact-dependent tumoricidal activity of human monocytes.
Int J Cancer 1991 Sep 09
PMID:Involvement of leukocyte (beta 2) integrins (CD18/CD11) in human monocyte tumoricidal activity. 167 46

Intraperitoneal (I.P.) administration of chemotherapeutic agents, in particular, cisplatin and bleomycin is successfully used in the treatment of ovarian and gastrointestinal malignancies. Their use however, is limited by the rapid development of adhesions. The vinca alkaloid group of chemotherapeutic agents has been shown to impair the acute inflammatory reaction, which plays an important role in adhesion formation, thereby providing the rationale for addition of vindesine to an I.P. regimen containing cisplatin and bleomycin. A rat model was used to study the effects of various I.P. chemotherapeutic regimens on adhesion formation. Four groups were studied (30 rats/Group). Regimens used included Group A (Saline), Group B (Vindesine 0.1 mg/kg), Group C (Cisplatin 5 mg/kg and Bleomycin 0.2 mg/kg), and Group D (Cisplatin 5 mg/kg, Bleomycin 0.2 mg/kg and Vindesine 0.1 mg/kg). In order to grade adhesion formation, animals were sacrificed on days 2, 14 and 28, with the severity of adhesions graded on a scale of I-IV in order of increasing severity. Adhesion formation in Group A (Saline) and Group B (Vindesine) was similar. The addition of Vindesine to Group C (Cisplatin and Bleomycin) resulted in a significant reduction in adhesion formation (p less than 0.01). The results of this experimental study suggest that the local toxicity of I.P. chemotherapy may be reduced by the inclusion of a vinca alkaloid.
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PMID:Reduction of the local toxicity of intraperitoneal chemotherapy; an experimental model. 169 8


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