Antigen-activated T lymphocytes infiltrate hepatocyte cultures in a manner comparable to liver-colonizing lymphosarcoma cells

Roos, E.; Pavert, I. V. van de

doi:10.1007/bf00121496

Cited by 26 publications

(10 citation statements)

References 9 publications

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“…as a consequence, metastatic hybrids (Collard et al, 1987a). Activated normal T-lymphocytes exhibit properties considered to be relevant for metastasis formation such as the potential to invade into cultured monolayers of endothelial cells (Savion et al, 1984), hepatocytes (Roos and van Pavert, 1983), and fibroblasts (Collard et al. .…”

Section: Discussionmentioning

confidence: 99%

Sublocalization of an invasion-inducing locus and other genes on human chromosome 7

Habets

Kammen

Willemsen

et al. 1992

Cytogenet Genome Res

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By somatic cell fusion studies between noninvasive mouse T-lymphoma cells and invasive human activated normal T-cells we have previously shown that the genetic information responsible for the induction of invasive and metastatic potential in interspecies T-cell hybrids is located on human chromosome 7. Apparently, genes derived from normal activated T-cells are dominantly expressed in the hybrids and control the invasive and, as a consequence, metastatic potential of these T-lymphoma cells. To sublocalize the invasion-inducing locus on chromosome 7 we have generated hybrids that harbor only specific regions of human chromosome 7 with or without a small fragment of human chromosome 21. Analysis of these hybrids revealed that the invasion-inducing locus maps to 7p12→cen. The human DNA complement of the hybrids was confirmed by Southern blot analysis using a large panel of chromosome 7-specific DNA probes. Several of these genes could be further sublocalized. These included: ARAF2 to 7p12→cen, D7S21 to 7pter→p12, ACTB to 7p15→p12, EGFR to 7p12, MDH2 to 7cen→q22, and PDGFA to 7pter→p15.

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Section: Discussionmentioning

confidence: 99%

Sublocalization of an invasion-inducing locus and other genes on human chromosome 7

Habets

Kammen

Willemsen

et al. 1992

Cytogenet Genome Res

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“…For example, metastatic lymphoma and lymphosarcoma cells often massively invade the liver ad hepatocyte cultures (Table 3) [49,53,230,262], and normal, activated T lymphocytes invade hepatocyte cultures similar to metastatic lymphosarcoma cells [263]. In addition, fusion of normal murine T-lymphocytes with noninvasive, nonmetastatic murine lymphoma cells can yield hybridomas that are highly invasive and metastatic to liver in mice [264,265].…”

Section: Tumor Cell Invasionmentioning

confidence: 99%

Organ specificity of tumor metastasis: role of preferential adhesion, invasion and growth of malignant cells at specific secondary sites

1988

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The locations of distant secondary tumors in many clinical cancers and animal tumors are nonrandom, and their distributions cannot be explained by simple anatomical or mechanical hypotheses based on the simple lodgment or trapping of tumor cell cmboli in the first capillary bed encountered. Evidence from certain experimental tumor systems supports Paget's 'seed and soil' hypothesis on the nonrandom distributions of metastases, in which the unique properties of particular tumor ceils ('seeds') and the different characteristics of each organ microenvironment ('soil') collectively determine the organ preference of metastasis. Experimentally, differential tumor cell adhesion to organ-derived microvessel endothelial cells and organ parenchymal cells, differential invasion of basement membranes and organ tissues, and differential responses to organ-derived growth-stimulatory and -inhibitory factors all appear to be important determinants in explaining the organ preference of metastasis. Each tumor system may achieve organ specificity because of its own unique set of multiple metastasis-associated properties and responses to host microenvironments. As neoplasms progress to more highly malignant states multisite metastases are more likely and organ-specific metastases may be masked or circumvented owing to stochastic events, tumor cell diversification, host selection processes, and increased production of tumor autocrine molecules that may modulate adhesion, invasion, growth, and other properties important in metastasis. The importance of each of these properties, however, appears to vary considerably among different metastatic tumor systems. These and other tumor cell and host properties may eventually be used to predict and explain the unique metastastic distributions of certain human malignancies.

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“…Previously, we and others had found that activated T-cells are very highly invasive [20][21][22], in contrast to non-activated spleen T-cells. We showed that the metastatic hybrid was in fact highly invasive, whereas the parental BW5147 cells were not [9].…”

Section: Hybridomasmentioning

confidence: 99%

Adhesion molecules in lymphoma metastasis

Roos

1991

Cancer Metast Rev

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Recently, many surface proteins of lymphoid cells that mediate adhesion to other cells and extracellular matrix have been identified. Several of these cellular adhesion molecules (CAM) are also expressed by metastatic lymphoma cells and may mediate adhesion to tissue components during the metastatic process. Correlations observed between expression of certain CAM, like MEL-14 and CD44, and particular patterns of spread, support this notion, but conclusive evidence is scarce. We have used T-cell hybridomas to study the mechanisms of wide-spread lymphoid metastasis. The results obtained with this model are reviewed here. The advantages are that a large number of genetically similar cell lines can be generated, which can be grouped in large panels of highly invasive and non-invasive cells. Invasiveness of these cells in hepatocyte and fibroblast monolayers correlates with experimental metastasis. Lymphoid CAM that are potentially involved in metastasis are reviewed. Several of these CAM are not, or not consistently, expressed by the invasive T-cell hybridomas, indicating that they are not indispensable. Notably, some of the CAM involved in the onset of an immune response or in migration into inflamed tissues, like ICAM-1 and VLA-4, and the 'homing receptors' MEL-14 and LPAM-1 do not seem to be involved. CAM that are consistently expressed by the T-cell hybrids include LFA-1, the beta-1 integrin subunit CD29, CD31 (PECAM-1) and CD44 ('Hermes homing receptor'). We have generated considerable evidence that LFA-1 is required for efficient metastasis of T-cell hybrids, based on the behavior of LFA-1-deficient mutants and revertants. High levels of LFA-1 are required. The relevant counterstructure is probably ICAM-2 rather than ICAM-1. Preliminary results suggest that also a beta-1 integrin, possibly VLA-5, plays a role. Finally, we summarize evidence indicating that CD31 and CD44 are primary candidates for involvement in metastatic spread of T-cell hybridomas.

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Antigen-activated T lymphocytes infiltrate hepatocyte cultures in a manner comparable to liver-colonizing lymphosarcoma cells

Cited by 26 publications

References 9 publications

Sublocalization of an invasion-inducing locus and other genes on human chromosome 7

Sublocalization of an invasion-inducing locus and other genes on human chromosome 7

Organ specificity of tumor metastasis: role of preferential adhesion, invasion and growth of malignant cells at specific secondary sites

Adhesion molecules in lymphoma metastasis

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