Death and Metastatic Distribution of Tumor Cells in Mice Monitored With &lt;sup&gt;125&lt;/sup&gt;I-Iododeoxyuridine&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;

Hofer, Kurt G.; Prensky, Wolf; Hughes, Walter L.

doi:10.1093/jnci/43.4.763

Cited by 52 publications

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Enhanced Lysis of [125l]5-lodo-2′- Deoxyuridine-Labeled Target Cells in the Presence of Normal Macrophages: Possible Mechanisms of Action

Evans

Eidlen

1985

Journal of Leukocyte Biology

View full text Add to dashboard Cite

The potential mechanisms involved during the faster release of [125I]-iodo-2'-deoxyuridine (125IdUrd)-labeled target sarcoma cells in the presence of normal C57BL/6J peritoneal macrophages were investigated. Maximum (= 90%) "spontaneous" release of 125I from target cells cultured alone occurred over a period of about 10 days. However, after about 3 days, confluent sheets of target cells developed. In the presence of normal macrophages, 90% of the 125I was released between 3 and 7 days, again with the formation of confluent sheets of target cells. This enhanced 125I release was not influenced by increasing the relative concentration of IdUrd using the nonradioactive isotope 127IdUrd. Established mechanisms of target cell destruction were investigated but no evidence was found for the involvement of superoxide anion, hydrogen peroxide, or regulation by prostaglandin synthesis. The macrophage-mediated effect was abrogated by incorporating hydrocortisone-acetate (10(-7) to 10(-4) M) into the culture medium but this did not affect target cell proliferation. The use of serum-free culture medium suggested that macrophages secreted a soluble mediator that was not derived from or dependent on the presence of fetal bovine serum. In addition, macrophage-conditioned medium was able to induce the faster 125I release. The failure to precipitate with 20% trichloroacetic acid the 125I released from target cells cultured in the presence of macrophages indicated that the radioactive component had been separated from the precipitable DNA. The data are discussed in light of two possible hypotheses: that macrophages recognized subtle changes in IdUrd-labeled cells and exacerbate radiotoxicity, and that the faster release reflected proliferative death caused by stimulated growth.

show abstract

Enhanced Lysis of [125l]5-lodo-2′- Deoxyuridine-Labeled Target Cells in the Presence of Normal Macrophages: Possible Mechanisms of Action

Evans

Eidlen

1985

Journal of Leukocyte Biology

View full text Add to dashboard Cite

show abstract

Targeted Radionuclide Tumor Therapy

Stigbrand¹,

Carlsson²,

Adams³

2008

View full text Add to dashboard Cite

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

Kawaguchi

Nakamura

1986

Cancer Metast Rev

View full text Add to dashboard Cite

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.

show abstract

Death and Metastatic Distribution of Tumor Cells in Mice Monitored With <sup>125</sup>I-Iododeoxyuridine<xref ref-type="fn" rid="FN2">2</xref>

Cited by 52 publications

References 15 publications

Enhanced Lysis of [125l]5-lodo-2′- Deoxyuridine-Labeled Target Cells in the Presence of Normal Macrophages: Possible Mechanisms of Action

Enhanced Lysis of [125l]5-lodo-2′- Deoxyuridine-Labeled Target Cells in the Presence of Normal Macrophages: Possible Mechanisms of Action

Targeted Radionuclide Tumor Therapy

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

Contact Info

Product

Resources

About