The Analysis of Malignancy by Cell Fusion

1971 ◽  
Vol 8 (3) ◽  
pp. 673-680
Author(s):  
U. BREGULA ◽  
G. KLEIN ◽  
H. HARRIS
Keyword(s):  
Cell Fusion ◽  
Chromosomal Analysis ◽  
Cell Populations ◽  
Hybrid Cells ◽  
Parental Chromosome ◽  
Chromosomal Constitution ◽  
Diploid Fibroblasts ◽  
Ehrlich Ascites ◽  
Ehrlich Ascites Cells

When Ehrlich ascites cells were fused with diploid fibroblasts, isolated directly from the animal, the resulting hybrid cells regularly produced progressive tumours. However, an analysis of a range of clonal populations of these hybrid cells, each derived from a separate primary fusion, revealed that the chromosomal constitution of these cells was highly unstable; all cell populations were found to have already undergone substantial chromosome losses by the time enough cells were available to permit chromosomal analysis. Thus, although these hybrid cells were highly tumorigenic, the tumours arising from them were not composed of cells with complete parental chromosome sets, but of cells from which some chromosomes had been eliminated.

The Analysis of Malignancy by Cell Fusion

1974 ◽  
Vol 16 (1) ◽  
pp. 189-198
Author(s):  
F. WIENER ◽  
G. KLEIN ◽  
H. HARRIS
Keyword(s):  
Cell Fusion ◽  
Tumour Cells ◽  
Complementation Analysis ◽  
Malignant Cells ◽  
Hybrid Cells ◽  
Malignant Phenotype ◽  
Recessive Character ◽  
Parental Chromosome ◽  
Wide Range

Previous studies with a variety of transplantable mouse tumours showed that in hybrids between malignant and non-malignant cells, malignancy behaved as a recessive character: the hybrid cells, so long as they retained something close to the complete parental chromosome sets, had little or no ability to grow progressively in vivo. In the experiments we now describe the heritable lesions determining the malignant phenotype were further explored by complementation analysis in which the various tumour cells were fused with each other. Forty-two clonal populations derived from twelve crosses between different kinds of tumour cells were examined. Only one cross generated hybrid cells with reduced tumorigenicity: in all other cases the hybrid cells formed were highly malignant. It thus appears that, in a wide range of different tumours, the lesions determining the malignant phenotype, although recessive, fail to complement each other.

An Ultrastructural Study of Interspecific Cell Fusion Induced by Inactivated Sendai Virus

1966 ◽  
Vol 1 (4) ◽  
pp. 401-406
Author(s):  
E. E. SCHNEEBERGER ◽  
H. HARRIS
Keyword(s):  
Cell Fusion ◽  
Hela Cells ◽  
Sendai Virus ◽  
Electron Microscopic Examination ◽  
Electron Microscopic ◽  
Virus Particles ◽  
Large Numbers ◽  
Ehrlich Ascites ◽  
Ehrlich Ascites Cells ◽  
Cytoplasmic Bridges

An electron-microscopic examination was made of the process of cell fusion induced by Sendai virus inactivated by ultraviolet light. Ehrlich ascites cells, HeLa cells, rabbit macrophages, rat lymphocytes and nucleated hen erythrocytes were chosen for study because it had previously been shown that these cells could be fused together, with varying degrees of facility, to form artificial heterokaryons. Cells which had large numbers of microvilli on their surfaces fused together more readily than those which had not, but the presence of microvilli was not essential for fusion to occur. Fusion appeared in all cases to be initiated by the formation of small cytoplasmic bridges between the cells; but virus particles, although present elsewhere on the surface of the cells, were not detected at or near the cytoplasmic bridges. HeLa-hen erythrocyte heterokaryons were formed by the fusion of HeLa cells with red cell ghosts.

scholarly journals Spontaneous fusion of MSC with breast cancer cells can generate tumor dormancy

2021 ◽  
Author(s):  
Catharina Melzer ◽  
Juliane von der Ohe ◽  
Tianjiao Luo ◽  
Ralf Hass
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Fusion ◽  
Cancer Cell ◽  
Tumor Heterogeneity ◽  
Breast Cancer Cells ◽  
Tumor Development ◽  
Cell Populations ◽  
Hybrid Cells

Abstract Background: A variety of different tumors including breast cancer cells can closely interact with mesenchymal stroma/stem-like cells (MSC) in the tumor microenvironment eventually resulting in cell fusion and formation of new hybrid cancer cell populations displaying altered properties. Methods: Lentiviral-transduced MDA-MB-231 cherry breast cancer cells and MSC GFP were co-cultured and a resulting hybrid cancer cell population (MDA-MSC-hyb5) was isolated. Characterization was performed for marker expression and short tandem repeat (STR) fragment analysis compared to the parental cells. Moreover, in vivo tumor development and metastatic capacity of MDA-MSC-hyb5 was studied and unique properties were analyzed by RNA microarray expression analyses compared to other breast cancer hybrid populations. Potential chemotherapeutic sensitivity was carried out in tumor explant cultures of MDA-MSC-hyb5 cells. Results: Direct cellular interactions of MDA-MB-231 cherry breast cancer cells with human MSC GFP in a co-culture model resulted in spontaneous cell fusion by generation of MDA-MSC-hyb5 cherry GFP breast cancer hybrid cells. Proliferative capacity of MDA-MSC-hyb5 cells was about 1.8-fold enhanced when compared to the parental MDA-MB-231 cherry breast cancer cells. In contrast to a spontaneous MDA-MB-231 cherry -induced tumor development in vivo within 18.8 days MDA-MSC-hyb5 cells initially remained quiescent in a dormancy-like state. At distinct time points up to about a half year later after injection NODscid mice started to develop MDA-MSC-hyb5 cell-induced tumors. Following tumor initiation, formation of metastases in various different organs occurred rapidly within about 10.5 days. Changes in gene expression levels were evaluated by RNA-microarray analysis and revealed certain increase in dormancy-associated transcripts in MDA-MSC-hyb5. Chemotherapeutic responsiveness of MDA-MSC-hyb5 cells was partially enhanced as compared to MDA-MB-231 cells, however, some resistance e.g. for taxol was detectable in cancer hybrid cells. Moreover, drug response partially changed during tumor development of MDA-MSC-hyb5 cells suggesting unstable in vivo phenotypes of MDA-hyb5 cells with increased tumor heterogeneity. Conclusions: The spontaneous formation of cancer hybrid cell populations like MDA-MSC-hyb5 by cell fusion contributes to tumorigenic diversification by acquisition of new properties such as altered chemotherapeutic responsiveness. The unique tumor dormancy of MDA-MSC-hyb5 cells not observed in other breast cancer hybrid cells so far markedly increases tumor heterogeneity.

The Analysis of Malignancy by Cell Fusion

1971 ◽  
Vol 8 (3) ◽  
pp. 681-692
Author(s):  
F. WIENER ◽  
G. KLEIN ◽  
H. HARRIS
Keyword(s):  
Tumour Cells ◽  
Hybrid Cells ◽  
Recessive Character ◽  
Parental Chromosome ◽  
Diploid Fibroblasts ◽  
Progressive Loss ◽  
L Cell ◽  
Very High

Diploid fibroblasts were fused with cells of two highly malignant near euploid tumours, a sarcoma induced by polyoma virus and a spontaneous carcinoma; the resulting hybrid cells were tested for their ability to grow progressively in vivo. In the case of the sarcoma/fibroblast hybrids, 15 clonal populations, each derived from a separate primary fusion, were examined. Most of these populations already showed substantial losses of chromosomes by the time enough cells had been generated to permit chromosomal analysis; but a few clones were isolated with chromosomal constitutions approximating to the sum of the 2 parental chromosome sets. Those clones that had undergone substantial chromosomal losses were highly tumorigenic, but some of the clones that contained the complete, or almost complete, chromosome sets of both parent cells, showed a greatly reduced take incidence. Initially these clones produced very few tumours, but the take incidence rose as continued cultivation of the cells in vitro resulted in progressive loss of chromosomes. In the case of the carcinoma/fibroblast hybrids, clonal populations with very high chromosome numbers were selected for special study. These were also found to have a very low take incidence, comparable to that of the hybrids formed by the fusion of the tumour cells with L cell derivatives. None of the tumours produced by the injection of either the sarcoma/fibroblast or carcinoma/fibroblast hybrids were composed of cells containing chromosome complements corresponding to the sum of the 2 parental chromosome sets; all the tumours were formed by selective overgrowth of cells from which some chromosomes had been eliminated. These results indicate that the malignancy of the tumour cells can be suppressed by diploid fibroblasts as well as by the L cell derivatives, but that the rapid chromosome losses characteristic of hybrids between these tumour cells and diploid fibroblasts generate malignant segregants with much greater frequency. In the range of material examined in the present experiments malignancy thus behaves as if it were a recessive character.

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