Cancer Research Landon Prizes for Basic and Translational Cancer Research  Tumor Immunology: New Perspectives
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online

[Cancer Research 48, 3405-3410, June 15, 1988]
© 1988 American Association for Cancer Research

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by la Rivière, G.
Right arrow Articles by Roos, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by la Rivière, G.
Right arrow Articles by Roos, E.

Invasiveness in Hepatocyte and Fibroblast Monolayers and Metastatic Potential of T-Cell Hybridomas in Mice

Geertje la Rivière1, Cor A. Schipper1, John G. Collard and Ed Roos2

Division of Cell Biology, The Netherlands Cancer Institute (Antoni van Leeuwenhoek Huis), 121 Plesmanlaan, 1066 CX Amsterdam, The Netherlands

Fusion of noninvasive, nonmetastatic BW5147 T-lymphoma cells with normal T-lymphocytes usually resulted in highly invasive and metastatic T-cell hybridomas, apparently due to properties derived from the normal T-cell. Occasionally hybrids arose that were non- or low invasive, probably by loss of relevant genes upon chromosome segregation, since these cells contained much less DNA than highly invasive hybrids.

The metastatic potential of 20 representative T-cell hybridomas was tested by tail vein injection in syngeneic mice and cells were found to be either nonmetastatic (NM), low metastatic (LM), or high metastatic (HM). NM hybrids were tumorigenic but did not form metastases and HM hybridomas caused wide-spread metastasis. LM cells formed metastases in a limited number of mice and predominantly in lymphoid tissues. In hepatocyte cultures, NM cell lines were found to be the least invasive, HM cells the most, whereas LM hybrids exhibited intermediate levels.

Invasiveness was not only measured in rat hepatocyte cultures but also in rat embryo fibroblast monolayers, and the relative invasive capacity in both model systems correlated well. Pertussis toxin inhibited invasion in both systems to 20–30% of control values. This suggests that the mechanisms of invasion into hepatocyte and fibroblast cultures are at least partially similar and that the fibroblast invasion assay is a relevant model to study aspects of lymphoma metastasis.

We conclude that invasive potential is a prerequisite for T-cell hybridomas to colonize tissues from the bloodstream and that a minimum level of invasiveness is necessary for extensive and wide-spread metastasis formation.

1 Supported by Grant NKI-86-8 from the Koningin Wilhelmina Fonds/Netherlands Cancer Research Foundation.

2 To whom requests for reprints should be addressed.

Received 11/25/87. Revised 3/10/88. Accepted 3/14/88.




This article has been cited by other articles:


Home page
J. Cell Sci.Home page
A. Masztalerz, I. S. Zeelenberg, Y. M. Wijnands, R. de Bruijn, A. M. Drager, H. Janssen, and E. Roos
Synaptotagmin 3 deficiency in T cells impairs recycling of the chemokine receptor CXCR4 and thereby inhibits CXCL12 chemokine-induced migration
J. Cell Sci., January 15, 2007; 120(2): 219 - 228.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
R. D. M. Soede, I. S. Zeelenberg, Y. M. Wijnands, M. Kamp, and E. Roos
Stromal Cell-Derived Factor-1-Induced LFA-1 Activation During In Vivo Migration of T Cell Hybridoma Cells Requires Gq/11, RhoA, and Myosin, as well as Gi and Cdc42
J. Immunol., April 1, 2001; 166(7): 4293 - 4301.
[Abstract] [Full Text] [PDF]


Home page
BloodHome page
R. D. M. Soede, Y. M. Wijnands, M. Kamp, M. A. van der Valk, and E. Roos
Gi and Gq/11 proteins are involved in dissemination of myeloid leukemia cells to the liver and spleen, whereas bone marrow colonization involves Gq/11 but not Gi
Blood, July 15, 2000; 96(2): 691 - 698.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
R. D. M. Soede, M. H. E. Driessens, L. Ruuls-Van Stalle, P. E. M. Van Hulten, A. Brink, and E. Roos
LFA-1 to LFA-1 Signals Involve {zeta}-Associated Protein-70 (ZAP-70) Tyrosine Kinase: Relevance for Invasion and Migration of a T Cell Hybridoma
J. Immunol., October 15, 1999; 163(8): 4253 - 4261.
[Abstract] [Full Text] [PDF]


Home page
J. Cell Biol.Home page
R. D.M. Soede, Y. M. Wijnands, I. Van Kouteren-Cobzaru, and E. Roos
ZAP-70 Tyrosine Kinase Is Required for LFA-1-dependent T Cell Migration
J. Cell Biol., September 7, 1998; 142(5): 1371 - 1379.
[Abstract] [Full Text] [PDF]


Home page
J. Cell Sci.Home page
A. Meijne, M. Driessens, G La Riviere, D Casey, C. Feltkamp, and E Roos
LFA-1 integrin redistribution during T-cell hybridoma invasion of hepatocyte cultures and manganese-induced adhesion to ICAM-1
J. Cell Sci., January 9, 1994; 107(9): 2557 - 2566.
[Abstract] [PDF]


Home page
J. Cell Sci.Home page
G La Riviere, J. Klein Gebbinck, M. Driessens, and E Roos
Pertussis toxin inhibition of T-cell hybridoma invasion is reversed by manganese-induced activation of LFA-1
J. Cell Sci., January 3, 1994; 107(3): 551 - 559.
[Abstract] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1988 by the American Association for Cancer Research.