Abstract
The effect of the Walker 256 rat carcinoma, growing at a site remote from the liver, on liver glycogen synthesis has been determined. Although the mechanism has not been defined it has been shown that the deposition of liver glycogen in response to a glucose load is inhibited in tumour bearing rats. It has been further demonstrated that, by comparison with the normal liver, the liver depleted of glycogen is more susceptible to the development of metases from circulating cancer cells.
Highlights
CLINICAL experience shows that the incidence of liver metastases in patients with gastro-intestinal tract cancer is variable
No difference in liver glycogen concentration was apparent between the control rats and the rats bearing Walker tumours up to 8 days old when the liver sections stained with Best's carmine stain were examined under the microscope
The results of the first two experiments show that the Walker 256 carcinoma, growing at a site remote from the liver, has an inhibiting effect on liver glycogen synthesis after about 8 days of tumour growth
Summary
CLINICAL experience shows that the incidence of liver metastases in patients with gastro-intestinal tract cancer is variable. The possibility that the variable incidence of liver metastases in patients with gastrointestinal cancer might, in part at least, be due to the ability of certain of these tumours to condition the liver to accept and retain cancer cells from the circulation deserves consideration. This communication sets out the results of a series of observations into the effect of an experimental cancer growing at a site remote from the liver on liver glycogen synthesis and demonstrates how alterations in liver glycogen concentration may influence the development of liver metastases from circulating cancer cells
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