Abstract
ONE of the main problems of formation of ascites tumours is the mechanism by which fluid accumulates in the peritoneal cavity. Klein1 believed that the tumour cells were capable of eliciting fluid by some sort of irritant property. Goldie et al.2 considered that tumour cell implantation into the serosal membranes was necessary. Siegler and Koprowska3 have recently put forward further evidence for Warner's hypothesis4,5 that solid tumour infiltration is necessary with subsequent host and tumour cell necrosis. Fluid then leaks into the peritoneal cavity from the ruptured tissues. Straube6 attempted to show that both fluid inflow and outflow are altered, the inflow being increased by greater vascular permeability and outflow being decreased by lymphatic blockage. The experiment described here was designed to investigate the effects of various pharmacological and other treatments on ascites production.
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References
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Siegler, R., and Koprowska, I., Cancer Res., 22, 1273 (1962).
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Wheatley, D. N., and Ambrose, E. J., Brit. J. Cancer (in the press).
Wheatley, D. N., Ambrose, E. J., and Easty, G. C., Nature, 199, 188 (1963).
Goldie, H., Walker, M., Biscoe, B., Powell, G. J., and Howse, R. J., Proc. Soc. Exp. Biol. N.Y., 107, 838 (1961).
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WHEATLEY, D. Influence of Various Substances on Production of Ascites Tumour. Nature 202, 1348–1349 (1964). https://doi.org/10.1038/2021348a0
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DOI: https://doi.org/10.1038/2021348a0
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