Ultrastructure of the Adhesion of HeLa Cells to Human Vein Wall

Warren, Bruce A.; Güldner, F.-H.

doi:10.1159/000157776

Cited by 5 publications

(4 citation statements)

References 18 publications

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“…The adhesion of circulating tumor cells to vascular endothelial cells as an active process has been proposed by Warren et al (71,72), Cotmore and Carter (73) and Sindelar et al (74). In our observations with rat ascites hepatoma cell lines, the initial interactions occur by the formation of cell-to-cell contacts in which the plasma membranes of the interacting cells are separated by a gap of about 100k (Fig.…”

Section: The Lodgement and Arrest Of Tumor Cellssupporting

confidence: 68%

Analysis of the lodgement and extravasation of tumor cells in experimental models of hematogenous metastasis

Kawaguchi

Nakamura

1986

Cancer Metast Rev

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This review summarizes our experiments on the metastatic distribution patterns of Yoshida sarcoma and several strains of rat ascites hepatomas. These dissemination patterns cannot be explained entirely by either anatomical-mechanical considerations or by the seed-and-soil hypotheses for metastatic localization. In some experimental situations, anatomical-mechanical factors seem more important, but in others the seed-and-soil hypothesis offers a more compelling interpretation. Lodgement of tumor cells in the microcirculation of different organ vascular beds can occur by three non-exclusive mechanisms: direct attachment to vascular endothelial cells; direct adhesion to exposed vascular basement membrane components or by entrapment in thrombi. Similarly, extravasation can also occur via several mechanisms. The first, involves infiltration of tumor cells into perivascular tissues via their own movement. A second mechanism involves sequestration of tumor cells beneath vascular endothelial cells where they are separated from the blood stream. The third option for extravasation involves 'explosive' displacement in which the blood vessel wall swells as a result of intracapillary growth of tumor emboli causing the vessel to rupture.

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Section: The Lodgement and Arrest Of Tumor Cellssupporting

confidence: 68%

Analysis of the lodgement and extravasation of tumor cells in experimental models of hematogenous metastasis

Kawaguchi

Nakamura

1986

Cancer Metast Rev

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“…Binding of tumor cells to the subendothelial matrix could occur via mechanical trauma (Warren and Vales, 1972;Warren, 1973;Warren and Guldner, 1969;Fisher et al, 1967), endothelial cell ischemia secondary to tumor-platelet thrombin embolization (Warren, 1984) or endothelial cell retraction (Nicolson and Custead, 1985;Kramer et al, 1980;Kramer and Nicolson, 1979;Vlodavsky et al, 1983;Zamora et al, 1980). Kramer and Nicolson (1979) have proposed the existence of an adhesion gradient between the endothelium and the subendothelial matrix.…”

Section: Discussionmentioning

confidence: 99%

“…It is well recognized that subendothelial matrix is a more efficient surface for tumor-cell adhesion than the intact endothelial surface (Warren and Vales, 1972;Warren, 1973;Nicolson and Custead, 1985) and that binding of tumor cells to subendothelial matrix is more efficient for penetration of tumor cells into the extravascular environment (Warren and Vales, 1972;Warren, 1973). Binding of tumor cells to the subendothelial matrix could occur via mechanical trauma (Warren and Vales, 1972;Warren, 1973;Warren and Guldner, 1969;Fisher et al, 1967), endothelial cell ischemia secondary to tumor-platelet thrombin embolization (Warren, 1984) or endothelial cell retraction (Nicolson and Custead, 1985;Kramer et al, 1980;Kramer and Nicolson, 1979;Vlodavsky et al, 1983;Zamora et al, 1980). Kramer and Nicolson (1979) have proposed the existence of an adhesion gradient between the endothelium and the subendothelial matrix.…”

Section: Discussionmentioning

confidence: 99%

Thrombin stimulates melanoma tumor‐cell binding to endothelial cells and subendothelial matrix

Klepfish

Greco

Karpatkin

1993

Intl Journal of Cancer

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Thrombin has been shown to activate tumor-cell adhesion to platelets, fibronectin and von Willebrand factor 2-to 3-fold in vitro, and enhance metastasis 10-to 156-fold in vivo. We therefore elected to determine whether thrombin binds to tumor cells and whether thrombin-treated tumor cells enhance their adhesion to endothelial cells, the first barrier to tumor invasion and metastasis. Thrombin-treated human and hamster melanoma cells enhanced their adhesion to bovine aortic endothelial cells 2. I -to 2.3-fold, respectively. Similar results were obtained with bovine capillary endothelial cells. Thrombin activation of tumor cells was rapid, reaching its peak 15 rnin after thrombin activation: and transient, declining to baseline levels by 60 min. '"1-thrombin bound to both SK-Mel-28 and HM-29 cells in a saturation-dependent manner, was inhibitable by unlabelled thrombin, and could be 90% washed away with buffer following 30 min of incubation. Electron microscopy of tumor cells bound to fibronectin-coated millipore filters revealed adhesion of naive as well as thrombin- We have recently reported that thrombin-treated tumor cells enhance their adhesion to naive platelets, fibronectin and von Willebrand factor 2-to 3-fold in vitro; and enhance experimental pulmonary metastasis 10-to 156-fold in vivo (Nierodzik et al., 1992). Similar results were obtained with thrombin-activated platelets in vitro and thrombin injected intravenously with tumor cells (Nierodzik et al., 1991). Because the effect of thrombin on in vivo metastasis was considerably greater than its effect on tumor-cell adhesion to platelets and adhesive ligands, we considered the possibility that thrombintreated tumor cells might also enhance their adhesiveness to endothelial cells, an important host barrier against tumor-cell invasion. This proved to be indeed the case.The present report documents saturation binding of thrombin to tumor cells, enhanced adhesion of cells from 2 different thrombin-treated melanoma lines (HM29 and SK Me1 28) to bovine aortic and capillary endothelial cells, as well as the transient adhesive effect of thrombin treatment (peaking at 15 min and disappearing at 60 min). MATERIAL AND METHODS Tumor-cell linesSK Me1 28 is a human melanoma cell line obtained from the ATCC (Rockville, MD). HM-29 is a hamster melanoma, kindly supplied by Dr. J-C. Bystryn of New York University Medical School. Both were grown in RPMI (GTBCO, Grand Island, NY) supplemented with 1% penicillin-streptomycin, 2% glutamine, 1% non-essential amino acids and 10% FCS (GIBCO) in 50-ml plastic tissue-culture flasks. Cells were harvested at subconfluence with Trypsin-EDTA or EDTA alone. Monoclonal antibodiesAnti-pl (AIAS) was a gift from Dr. M. Hemler, DanaFarber Cancer Institute, Boston, MA. Anti-a3P1 (PB15) was a gift from Dr. W.G. Carter. Anti-qP, (LM609) was a gift from Dr. Cheresh, Scripps Clinic, La Jolla, CA. Anti433 (LK-2 against platelet GPIIIa) was prepared in our laboratory. Rat anti-a5 (PlE5) was a gift from Dr. C. Damsky, UCSF, San Francisco, CA, and a...

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“…The HeLa cells were seen to adhere to the Tegions of damaged vessel wall where the endothelial cells had been abraded off by the previous trauma. The tumour cells stuck to the exposed } layer of the vein wall -the basement membrane of the endothelial cell by means of multiple Microvilli and the cells eventually flattened them-Selves against the basement membrane ( Warren and Guldner, 1969).…”

Section: Investigation Of the Process Of Tumour Metastasismentioning

confidence: 99%

[Presidential Address, 1982] Understanding the cancer process: some aspects of the spread of cancer in man and experimental animals.

Warren¹

1982

Journal and Proceedings of the Royal Society of New South Wales

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The course of the illness in an untreated patient with cancer depends upon the cell of origin of the cancer and the organ in which the cancer arose.Although there are certain general principles concerning spread, malignant tumours comprise a large number of separate diseases rather than a single entity.Removal of the primary tumour (i.e. the tumour in the organ where it first appeared) can usually be achieved and it is the secondary deposits that prove resistant to removal by surgery or treatment by other means.The way these secondary deposits develop is therefore basic to the understanding of the cancer process as a whole and is needed for a rational approach to therapy.Many malignant tumours. spread via the blood stream by way of the release of tumour cells into the circulation and the primary malignant tumour must reach a certain stage in development and size before tumour 'cells are released in significant quantities. Warren, B A. 1982. "[Presidential Address, 1982 Understanding the cancer process: some aspects of the spread of cancer in man and experimental animals." Journal and proceedings of the Royal Society of New South Wales 115(3-4), 95-100.

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Ultrastructure of the Adhesion of HeLa Cells to Human Vein Wall

Cited by 5 publications

References 18 publications

Analysis of the lodgement and extravasation of tumor cells in experimental models of hematogenous metastasis

Analysis of the lodgement and extravasation of tumor cells in experimental models of hematogenous metastasis

Thrombin stimulates melanoma tumor‐cell binding to endothelial cells and subendothelial matrix

[Presidential Address, 1982] Understanding the cancer process: some aspects of the spread of cancer in man and experimental animals.

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