Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Activation of endothelial cells by the two inflammatory mediators interleukin-1 (IL-1) and tumor necrosis factor strongly increases tumor cell adhesion. We describe antibody inhibition studies showing that the endothelial leukocyte adhesion molecule-1 (ELAM-1), a cell-surface glycoprotein selectively expressed by cytokine-activated endothelial cells and responsible for neutrophil adhesion, is the major, if not the only, mediator of colon carcinoma cell adhesion to activated endothelial cells. Among the different tumor cell lines tested, seven colon carcinoma cell lines were sensitive to ELAM-1 antibodies. Adhesion of melanoma, osteosarcoma, and lung, cervix, or kidney carcinoma cell lines to IL-1-treated endothelial cells was not affected by the ELAM-1 antibody. This result suggests that ELAM-1 is selectively recognized by colon carcinoma cells and that adhesion of tumor cells to activated endothelial cells could be mediated by different and specific mechanisms.
J Natl Cancer Inst 1991 Sep 18
PMID:Tumor cell adhesion to endothelial cells: endothelial leukocyte adhesion molecule-1 as an inducible adhesive receptor specific for colon carcinoma cells. 171 24

Phorbol esters which activate protein kinase C (PKC) have been shown to enhance experimental lung metastasis. Therefore, it was reasoned that inhibitors of PKC might also modulate metastasis. We have investigated this possibility using a PKC inhibitor, MDL 27,032 [4-propyl-5(4-pyridinyl)-2(3H)-oxazolone], as well as staurosporine and H-7. Treatment of B16F1 murine melanoma cells with MDL 27,032 for 24 h in culture and subsequent i.v. injection of the cells into mice resulted in greater than 90% inhibition of lung metastasis. Inhibition of metastasis was time dependent, with 90% of maximum inhibition occurring by 8 h of incubation. The 50% inhibitory concentration (IC50) for inhibition of metastasis with MDL 27,032 was 7 microM, a value similar to that for the inhibition of B16F1 membrane-associated PKC (IC50 = 13 microM) but not cytosolic PKC (IC50 = 54 microM). B16F1 cells treated with MDL 27,032 for 24 h were less adherent than untreated cells to extracellular matrix/basement membrane proteins. Adhesion to fibrinogen and collagen IV was inhibited (IC50 = 6 microM and 48 microM, respectively) by MDL 27,032, whereas adherence to laminin and fibronectin was not affected, indicating that the drug affects specific adhesion molecules. MDL 27,032-treated cells were also found to be less adherent than untreated cells to human umbilical vein endothelial cells. The phosphorylation of an 80-kDa B16F1 cell plasma membrane protein was stimulated under conditions known to stimulate PKC activity, and MDL 27,032 inhibited this phosphorylation in a dose-dependent manner. MDL 27,032 was more potent than H-7 for the inhibition of metastasis but was significantly less potent than staurosporine. These results support the hypothesis that there is a critical role for PKC-mediated phosphorylation of cell surface adhesion receptors in metastasis.
Cancer Res 1992 Mar 01
PMID:Inhibition of experimental metastasis and cell adhesion of B16F1 melanoma cells by inhibitors of protein kinase C. 173 79

Adhesion molecules are expressed on the surface of various cells and establish cell-cell interaction, playing important roles in development, inflammatory reaction, immune response, and tissue regeneration. Neural adhesion molecules, found on neurons or glial surfaces, are involved in the migration of neurons, neurite formation, myelination, and denervation--reinnervation. The roles of cell adhesion molecules in malignancies, normal and abnormal development and as receptors in viral infections, constitute major fields of research and may have important diagnostic and therapeutic implications.
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PMID:Neural cell adhesion molecules. 179 2

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 has been evaluated for tumor cell populations derived from Kirsten murine sarcoma virus (KiMSV)-transformed BALB/c 3T3 cells responding to substrata coated with intact plasma fibronectin (pFN), a family of related proteolytic fragments from pFN or cellular fibronectins (FNs), and the heparan sulfate-binding platelet factor-4 (PF4). Both early-passage KiMSV cells, harboring the viral Kirsten ras oncogene (v-Ki-ras+), and late-passage KiMSV cells, in which most cells have lost the oncogene (v-Ki-ras-), are compared with primary tumor and lung metastatic tumor cells after three routes of injection into nude mice; nontumorigenic v-Ki-ras- revertant cells have been cloned from the late-passage KiMSV population. Attachment of early-passage KiMSV, primary tumor, and lung metastatic tumor cells was optimal and resistant to soluble RGDS peptide in the medium on intact pFN, on fragment F-155 from pFN containing the RGDS cell-binding domain and the heparinII domain, and on PF4 but decreased for metastatic cells on F110 containing only the RGDS domain (and sensitive to RGDS peptide). Cytoplasmic spreading of early-passage KiMSV and all tumor cells was good to excellent in polygonal patterns on pFN and on F155, while most cells remained round on F110. Responses for KiMSV and tumor cells varied on different heparin-binding proteins; cells remained rounded or detached on F38 derived from pFN or on PF4 but spread effectively with long linear process extension on cellular FN-derived fragments F44 + 47 harboring the extra domaina sequence. That F44 + 47 may contain a new cell-binding site for v-Ki-ras+ cells was also indicated by resistance to bacterial heparitanase in cell responses on F44 + 47 but not on PF4 and extensive catabolism of proteoglycans in the substratum-attached material of these cells. v-Ki-ras- revertant cells, nontumorigenic in nude mice, have reacquired 3T3-like responses to proteolytic fragments, including much more effective spreading on PF4 or on F38 substrata, and have reverted in generating microfilament stress fibers on pFN, a competence lacking in all v-Ki-ras+ cells. These results indicate that (a) v-Ki-ras+ primary and metastatic tumor cells respond similarly to most proteolytic fragments of FNs harboring known binding domains, with a few exceptions; (b) v-Ki-ras gene expression correlates with a new cell surface receptor activity recognized by extra domaina-containing fragments from cellular FNs; and (c) loss of the viral oncogene to generate v-Ki-ras- revertant cells reverts their FN-mediated adhesion responses.
Cancer Res 1990 Jul 15
PMID:Adhesion of Kirsten-ras+ tumor-progressing and Kirsten-ras- revertant 3T3 cells on fibronectin proteolytic fragments. 216 49

Small cell lung cancer (SCLC) is a fatal malignancy due to its propensity to metastasize widely and to reoccur after chemotherapy in a drug-resistant form. While most SCLC cell lines are anchorage independent for growth, laminin induced the attachment of five of six SCLC cell lines tested (NCI-N417, NCI-H345, NCI-H146, NCI-H187, NCI-H510, and NCI-H209). NCI-N417 SCLC cells adopted a flattened morphology on laminin, and a classic SCLC cell line (NCI-H345) demonstrated a neuron-like appearance while the other SCLC cell lines except NCI-H187 cells, attached but did not spread. Adhesion to laminin was associated with increased resistance to several cytotoxic drugs. Matrigel, an extract of basement membrane proteins, greatly accelerated tumor growth when coinjected with SCLC cells in athymic mice. A synthetic peptide from the B1 chain of laminin, cyclic-YIGSR (Tyr-Ile-Gly-Ser-Arg), inhibited laminin-induced SCLC cell adhesion and migration in vitro and reduced the size of the tumors they formed when coinjected with matrigel and YIGSR. These results suggest that the interaction of SCLC cells with laminin and possibly with other basement membrane proteins can enhance their tumorigenicity and drug resistance.
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PMID:Reconstituted basement membrane (matrigel) and laminin can enhance the tumorigenicity and the drug resistance of small cell lung cancer cell lines. 216 54

We present a retrospective analysis of 105 instances of small bowel obstruction (SBO) in 80 patients admitted to our hospital over a ten year period. Adhesions accounted for 73% of the cases and secondary involvement by malignancy for 13%. Appendectomy, colorectal and other pelvic procedures were the most frequent surgical antecedents responsible for the adhesions. In the 86% of cases with a temperature over 100 degrees F there was significant morbidity, mortality and/or strangulation, and this sign also foretold a prolonged hospital stay. Leukocytosis, when present along with abdominal tenderness also predicted a prolonged hospital stay. Strangulation occurred in 4.7% of the instances and was accompanied by at least one of the "classical symptoms". Fourty-five percent of the instances were successfully managed by conservative measures alone, whereas 55% had had surgical treatment. The mean hospital stay for all cases was 15.3 days. The morbidity rate for this series was 21% with a mortality of 3.8%. The largest single cause of death was related to malignant disease (three of four cases). When post-operative adhesions were the etiology, the hospital stay was 8.5 +/- 1.3 days for those treated with conservative measures compared with 16.5 +/- 1.8 days for those in whom a surgical procedure was performed (p less than 0.0001). This latter group also has a higher morbidity (32% compared to 5% for the non-operative group).
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PMID:Small bowel obstruction and its management. 265 44

Human carcinomas of the pancreas are aggressive tumors which traverse basement membrane barriers during invasion and metastasis. In order to examine the relationship of pancreatic tumor cells to basement membranes, we analyzed and compared the capabilities of four biologically different human pancreatic adenocarcinoma lines to adhere to substrate coated with purified basement membrane constituents. Each of the four cell lines adhered readily to purified laminin in a dose-dependent manner, although differences were noted in the time required for optimum attachment. Significant variations in the abilities of the cell lines to attach to purified fibronectin were evident both in concentration dependence and in the time required for attachment and spreading. Adhesion to type IV collagen was negligible for two of the four tumor lines but addition of soluble laminin or fibronectin augmented attachment. The other two cell lines attached only moderately to type IV collagen and this attachment was not enhanced by soluble laminin or fibronectin. When laminin or fibronectin was coated directly over type IV collagen, attachment of all four cell lines was comparable to that for the glycoproteins alone. Although the tumor lines were all established from human neoplasms of similar histological origin and retained the ability to adhere to intact basement membranes prepared from human amnion, they exhibited various patterns of attachment to laminin, fibronectin, and type IV collagen.
Cancer Res 1985 Nov
PMID:Diversity of adhesion to basement membrane components of human pancreatic adenocarcinomas. 293 15

Adhesion variants can be isolated from suspension growing highly metastatic murine ESb tumor cells under reproducible conditions from uncloned as well as from cloned ESb tumor cells. One such variant, ESb-MP, has been analyzed in detail. In vitro it had similar growth properties and high invasive capacity as the parental ESb cells. In vivo, ESb-MP cells showed a reduced growth capacity as compared to ESb cells. This was seen at the site of tumor cell transplantation (increased latency period) as well as at the site of secondary tumor growth in internal organs. ESb-MP tumor cells disseminated much later than ESb cells from the primary tumor into the blood stream. Both tumor lines metastasized to the liver but they affected liver functions in a different way: ESb cells infiltrated the liver diffusely and exerted toxic effects on liver parenchyma very quickly. This resulted in early increase of liver enzyme activity in the blood. In contrast, liver infiltrated by ESb-MP cells showed a more focal type of colonization and the organs seemed to be functioning for much longer periods. In fact, animals inoculated with ESb-MP cells subcutaneously or intravenously had an increased life expectancy compared to ESb-tumor-bearing animals of about 300%. The organotropism of both tumor lines remained similar although there were kinetic and quantitative differences, especially with regard to the kidney. In late stages of tumor growth, ESb-MP-tumor-bearing animals developed a high percentage of metastases in the kidney and around and within the spinal cord, thereby causing a syndrome of hind-leg paralysis. This syndrome was remarkable in its reproducibility, especially after intravenous tumor cell inoculation. The changed adhesiveness thus seemed to have affected the tumor latency period, the speed of dissemination into blood and internal organs, the mode of organ infiltration (focal vs. diffuse) and of metastatic growth, parameters which all might contribute to the greatly reduced overall malignancy.
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PMID:Changes in tumor cell adhesiveness affecting speed of dissemination and mode of metastatic growth. 325 67

Clinical and experimental observations suggest that tumor-induced endothelial cell (EC) injury may be one of several initial events in the establishment of tumor metastases. This work investigates tumor-induced EC injury and the interaction between tumor-damaged EC and platelets. We used cultured bovine EC and extracts of four cultured human malignancies. EC injury was assessed by 51Cr and lactic dehydrogenase (LDH) release. Incubation of EC with melanoma, breast carcinoma or lung carcinoma caused significant LDH and 51Cr release, whereas colon cancer seemed ineffective. Increased adhesion of platelets to tumor-injured EC was noted. These observations indicate that certain varieties of tumor cause EC injury. Adhesion of platelets to tumor-injured EC results in the formation of platelet-tumor thrombi at the endothelial surface, an event that may initiate tumor invasion of the vessel wall.
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PMID:Tumor interaction with vascular endothelium. 366 82


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