If. Pryme et al., THE INDUCTION OF GUT HYPERPLASIA BY PHYTOHEMAGGLUTININ IN THE DIET AND LIMITATION OF TUMOR-GROWTH, Histology and histopathology, 13(2), 1998, pp. 575-583
The growth of a transplantable murine non-Hodgkin lymphoma tumour, dev
eloping either intraperitoneally as an ascites tumour or subcutaneousl
y as a solid tumour, has been shown to be markedly diminished by inclu
ding phytohaemagglutinin (PHA), a lectin present in raw kidney bean (P
haseolus vulgaris) in the diet. In NMRI mice fed PHA within the range
0.45-7.0 mg/g diet, tumours which developed during a 10 day period aft
er subcutaneous injection of cells were about 35% of the dry weight of
those in lactalbumin-fed (control) animals. The reduced rate of growt
h occurred in a dose-dependent manner within the range 0.45-3.5 mg/g d
iet. Based on these observations it has been suggested that a competit
ion between the gut epithelium undergoing hyperplasia and the developi
ng tumour may occur for nutrients from a common body pool, and this ma
y be an important factor with regard to the observed initial low level
of tumour growth following the feeding of a PHA-containing diet. Obse
rvations which showed that the lever of hyperplasia of the small bowel
in response to feeding the PHA diets was higher in noninjected mice c
ompared to those which had been injected with tumour cells substantiat
ed the concept of competition between gut and tumour for nutrients etc
. required for growth. Experiments with a second murine tumour cell li
ne (a plasmacytoma) in Balb/c mice gave similar results indicating tha
t the effect of PHA was not restricted to a single tumour system.