Mechanisms of organ selective tumour growth by bloodborne cancer cells.

@article{Murphy1988MechanismsOO,
  title={Mechanisms of organ selective tumour growth by bloodborne cancer cells.},
  author={Paul Murphy and Peter Alexander and P. V. Senior and John Fleming and Nigel Kirkham and Irving Taylor},
  journal={British Journal of Cancer},
  year={1988},
  volume={57},
  pages={19 - 31},
  url={https://api.semanticscholar.org/CorpusID:16679642}
}
The sites of tumour development for 6 rat tumours injected into syngeneic rats via different vascular routes was determined and the possibility that the macrophage component of the inflammatory response promoted tumour growth was suggested.
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94 Citations
Background Citations
11
Methods Citations
1
Results Citations
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94 Citations

Preferential growth of bloodborne cancer cells in colonic anastomoses.

Intracardiac injection, in hooded Lister rats, of syngeneic MC28 sarcoma cells never induced tumour growth in normal bowel and the enhancing effect was largely over by the time the healing had progressed 14 days.

Preferential growth of blood-borne cancer cells at sites of trauma--a growth promoting role of macrophages.

Traumatising tissues by procedures such as surgical incision of the abdomen, gut anastomosis, placing a stitch in the kidney or chemical or surgical partial hepatectomy, greatly enhances the likelihood that a cancer cell trapped in the tissues develops into a metastasis.

Differential influence of organ site on three subpopulations of a single mouse mammary tumor at two distinct steps in metastasis

3 tumor subpopulations (seeds) derived from a single tumor were differentially affected by host organ factors (soil) at 2 distinct stages in the metastatic process.

Patterning of B16 melanoma metastasis and colonization generally relates to tumor cell growth-stimulating or growth-inhibiting effects of organs and tissues

Soluble growth-promoting activity enhanced clonogenic growth of isolated tumor cells stimulated by mouse serum, suggesting that metastasis or colony formation might be stimulated in favorable sites by those factors together with blood-borne growth factors.

Contribution of host-derived growth factors to in vivo growth of a transplantable murine mammary carcinoma.

Host-derived EGF contributes to establishment of microcolonies of MT1 carcinoma within the peritoneal cavity by providing growth factors to supplement those produced by the tumour until it reaches a certain critical mass to sustain autocrine growth, or indirectly by affecting the production of other growth-stimulatory factors or cytokines.

A small mammal model of tumour implantation, dissemination and growth factor expression after partial hepatectomy.

Facilitation by partial hepatectomy of tumor growth within the rat liver following intraportal injection of syngeneic tumor cells

L Liver extracts showed that epidermal growth factor-like activity was unaltered by PH, while heparin-binding growth factor activity peaked at 2 days post-PH, before the incidence of tumor growth in the parenchyma increased.

Enhanced growth of tumour cells in healing colonie anastomoses and laparotomy wounds

The same phenomenon of tumours growth enhancement in colonic anastomoses and laparotomy wounds reported after intracardiac injection of tumour cells may well be enhancing tumour growth after intraperitoneal and intraluminal injection.

Tissue procoagulant activity may be important in sustaining metastatic tumour growth

There is a broad correlation between tissue PCA and the ability of a tissue to support metastatic tumour growth, and organs which are preferred sites for metastasis had significantly higher PCA than non-preferred organs.

A murine model of bone marrow micrometastasis in breast cancer

This model is a clinically relevant tool for the analysis of organ specificity of metastasis for women with newly diagnosed stage I, II or III breast cancer.
...

76 References

Pattern of spread of bloodborne tumour

The pattern of bloodborne tumour spread has been studied experimentally in syngeneic rats and a strikingly similar pattern of ‘arterial metastasis’ is seen for all the tumours used despite their very different histological and biological natures.

Target organ patterns of tumors in mice following the arterial dissemination of B16 melanoma cells

The results on a model system suggest that the two major hypotheses used to account for metastatic patterns are not mutually exclusive: the “soil” effect divides the target organs into the twoMajor groups; however, within these groups the incidence of tumors is explicable in terms of the ‘mechanical’ hypothesis.

Changes in anatomical distribution of tumour lesions induced by platelet-active drugs.

It is proposed that thrombocytopenia induced in these experiments is in part a reflection of thrombus formation in the lungs which influences the speed of passage of tumour cells through capillaries.

Organ preferences in metastatic colony formation by spontaneous mammary carcinomas after intra-arterial inoculation.

It is concluded that the distribution of metastatic colonies formed by these spontaneous mammary tumours is influenced by interplay between intrinsic properties of tumour cells, microenvironmental influences in the organs in which the cells arrest, and rheological considerations.

Organ localization and the effect of trauma on the fate of circulating cancer cells.

From these results it is evident that tumor cells lodge not only in the lungs but also in other organs throughout the body, and local trauma apparently is of major importance in the localization and growth of circulating tumor cells.

Analysis of organ-specific effects on metastatic tumor formation by studies in vitro.

The findings are compatible with the hypothesis that normal organs can usually suppress the formation of tumor metastases and that tumors that succeed in establishing metastases have evolved means of escaping the inhibitory effects of organs in which the deposits are found.

Role of immune mechanisms in metastatic patterns of hemopoietic tumors in rats.

The conclusion of these experiments was that the selective organ distribution of tumor metastases was solely dependent on intrinsic cellular properties.

Organ specificity of metastatic tumor colonization is related to organ‐selective growth properties of malignant cells

The present results suggest that metastasis to specific organ sites is also dependent on the survival and growth of B16 cells affected by soluble organ‐derived factors.

Selection and biologic properties of malignant variants of a murine lymphosarcoma.

A syngeneic tumor model system with the RAW117 lymphosarcoma cell line was developed for use in investigations of host and tumor cell properties associated with an enhanced state of malignancy and yielded stable cell lines with preferential tumor colonization at specific sites.

Influence of microenvironment and vascular anatomy on "metastatic" colonization potential of mammary tumors.

Evidence is reported that the microenvironment of an organ can inhibit or permit expression of this intrinsic potential of a given tumor and that the degree and sites of colonization are thus the results of interaction between tumor and organ-specific factors.
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