Malignant properties and DNA content of daughter clones from a mouse fibrosarcoma: differentiation between malignant properties

Suzuki, Norio; Williams, Marcia; Hunter, Nancy

doi:10.1038/bjc.1980.310

Cited by 11 publications

(9 citation statements)

References 25 publications

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“…Thus the observed differences in the decay curves produced by the RIF-1 clones, most likely reflect the different capacities of the RIF-1 clones to become arrested in the lungs, to extravasate capillary endothelia and to survive in the surrounding lung tissue. In contrast to other findings (Suzuki et al, 1980), our observations that both cell retention in the lung and lung colonizing ability are independent of ploidy and of cell size, indicates that mechanical factors alone are not responsible for the metastatic ability of individual RIF-1 clones.…”

Section: Metastatic Ability Of Rif-j Clonescontrasting

confidence: 99%

Clonal variation in the arrest, survival and growth of RIF-1 mouse sarcoma cells in the lungs of C3H mice

Reeve¹,

Twentyman²

1983

Br J Cancer

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The relationship between the long term retention of 125IUdR-labelled tumour cells in the lungs and the formation of pulmonary lesions, has been examined for six in vitro isolated RIF-1 clones. Following i.v. injection, the initial number of cells trapped in the lungs was close to 100% in all cases. However, the rates at which individual clones were subsequently cleared from the lungs and the fraction of persistently retained cells varied considerably. Whilst clones also differed markedly in their lung colony formation efficiency (L.C.F.E.) there was no clear correlation between the long term retention of tumour cells in the lungs and subsequent metastasis formation, even when the retention of one clone was artificially increased in the lungs by admixture with microspheres. The fate after injection of clone 16 which is retained well in the lungs but which is of low L.C.F.E. has been compared with that of clone 19 which is retained poorly in the lung but which is of high L.C.F.E., using in vitro clonogenic capacity as a measure of cell viability in the lungs. Our findings show that clone 16 cells arrested in the lungs are in a viable, albeit "dormant", state some 26 days post i.v. injection. In contrast, arrested clone 19 cells proliferate rapidly in the lungs. These data may indicate varying significance of tumour cell and host properties in the metastatic success or failure of individual RIF-1 clones.

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Section: Metastatic Ability Of Rif-j Clonescontrasting

confidence: 99%

Clonal variation in the arrest, survival and growth of RIF-1 mouse sarcoma cells in the lungs of C3H mice

Reeve¹,

Twentyman²

1983

Br J Cancer

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“…Thus, in the FSA cell clone system, selection processes for cells with higher lung colonizing potential clearly exist for "artificial" metastasis, but such selection processes cannot be demonstrated in spontaneous metastasis from leg tumours. In previous studies (Suzuki et al, 1980), more efficient dissemination of FSA1231 compared with FSA1233 was observed by measuring SLME at different times after i.m. inoculation of these tumour cells in the leg.…”

Section: Testfor Variant Selectionmentioning

confidence: 93%

“…The cell clones have been characterized regarding their malignant and related properties 1979;Suzuki et al, , 1980 Spontaneous lung metastasis efficiency (SLME) determination For determination of SLME, 106 cells were inoculated i.m. into the hind leg of each syngeneic C3H/HeJ mouse (male, 9-11 weeks old; purchased from The Jackson Laboratories, Bar Harbor, Maine).…”

Section: Methodsmentioning

confidence: 99%

“…The tumour cell colonies were large and thick compared to the background normal cells (thin colony-like growth but not reproductive one), which did not disturb counting of tumour cell colonies. The tumour cell colonies were identifiable by specific DNA content (Figure 2) (Suzuki et al, , 1980. As a routine procedure, the cells from culture were always monitored for cell number and modal peak position of the cell volume distribution.…”

Section: Testfor Variant Selectionmentioning

confidence: 99%

“…injection than FSA1231 cells (Suzuki et al, 1980). Therefore, the FSA1231-1233 cell system discriminates artificial and spontaneous lung metastatic processes.…”

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confidence: 91%

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Variant selection and blood-borne “clonogenic” tumour cells in metastasis of FSA cell clones

Suzuki¹

1983

Br J Cancer

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Summary Our studies of the metastatic behaviour of FSA1231 and FSA1233 show that the role of selection processes of metastatic variants at the secondary sites is minimal in the spontaneous metastasis of these systems. In contrast, tumour-cell release efficiency (number of blood-borne clonogenic tumour-cells) correlates well with the difference in spontaneous lung metastasis efficiencies of the cell clones FSA1231 and FSA1233. Also, the different tumour-cell release efficiencies could explain the discrepancy between artificial and spontaneous metastasis of these cell clones.Metastasis involves multiple complex steps, from tumour-cell release into the systemic circulation to deposition and new growth at the secondary sites.

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Experimental systems for analysis of the malignant phenotype

Poste

1982

Cancer Metast Rev

109

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Identification of the cellular and subcellular alterations responsible for the metastatic behavior of malignant tumor cells and development of reliable screening programs for detecting new therapeutic agents for improved treatment of metastatic disease both depend crucially on the availability of experimental systems that can serve as relevant models of human cancer. Recent advances in our understanding of the pathogenesis of cancer metastasis have raised serious doubts about the usefulness of many of the experimental approaches that have long been used in the study of metastasis. Recent findings showing that metastases are caused by specific subpopulations of metastatic tumor cells, and that not all cells in a malignant primary tumor possess metastatic properties, are of profound importance for experimental efforts to understand the mechanism of metastatic phenotype among cells from the same tumor means that the traditional, and widely used, approach of analyzing primary tumors and cultured cell lines containing multiple, phenotypically heterogeneous, subpopulations of cells may provide little or no insight into the properties of the metastatic subpopulations, particularly if they represent only a minor fraction of the entire population. Similarly, the practice of screening potential therapeutic modalities for their ability to reduce the mass and/or growth rate of a primary tumor may be inadequate in predicting the responsiveness of metastatic lesions. Solution of these problems requires that new methods must be devised to isolate and characterize the specific subpopulations of tumor cells endowed with metastatic potential. In addition, knowledge of how the extraordinary phenotypic diversity found in tumor cell subpopulations from the same tumor is generated and how subpopulation diversity is regulated during progressive growth of both the primary tumor and its metastases are of fundamental importance if we are to design meaningful experimental systems for studying the metastatic process. This article reviews our current understanding of these complex issues and their implications for the experimental analysis of the malignant phenotype. The merits and shortcomings of different experimental systems are discussed in detail together with the identification of areas in which new experimental strategies and models are now needed.'

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Malignant properties and DNA content of daughter clones from a mouse fibrosarcoma: differentiation between malignant properties

Cited by 11 publications

References 25 publications

Clonal variation in the arrest, survival and growth of RIF-1 mouse sarcoma cells in the lungs of C3H mice

Clonal variation in the arrest, survival and growth of RIF-1 mouse sarcoma cells in the lungs of C3H mice

Variant selection and blood-borne “clonogenic” tumour cells in metastasis of FSA cell clones

Experimental systems for analysis of the malignant phenotype

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