Expression of the ras oncogene product p21 and Jack fruit lectin (JFL) bind
ing were analyzed in 12 samples of normal rectal tissue, 18 adenomas and 45
carcinomas. Mild expression of ras p21 was observed in 6 of the 12 normal
rectal tissue, Three of the six samples expressed N-ras p21, tao expressed
K-ras p21 and the remaining one H-ras p21, In adenoma, expression of 3 ras
proteins ranged from mild to moderate, The expression of N-ras p21 was maxi
mum in the carcinoma cases, with 91% of samples showing inmunoreactivity, K
-ras p21 was seen in 58% of the cases while H-ras p21 expression was seen i
n 53% of cases. Correlation analysis revealed significant association betwe
en positive p21 immunoreactivity and increasing histological abnormality (r
= 0.74; p < 0.000 for N-ras; r = 0.53; p < 0.05 for H-ras and I = 0.62; p
= 0.03 for K-ras), JFL binding on the other hand, was found to be reduced w
ith increasing histologic abnormality. Normal rectal epithelium showed inte
nse binding with over 60% cells showing a positive reaction. Adenomas were
seen to have moderate to intense staining with a range of 30-60% positive c
ells, Lowest levels of JFL binding was associated with invasive tumors, A s
ignificant negative association was thus extent between JFL binding and his
tological abnormality (r = -0.64, p <0.000). A negative correlation was als
o evident between expression of N-ras and K-ras oncoproteins and JFL bindin
g (r =-0.64, p <0.000 and r =-0.63, p < 0.001 respectively). These results
suggest that ras oncoprotein expression during rectal tumorigenesis is acco
mpanied by cell surface glycoprotein alterations.