AIM To study the genetic alteration in ACF and to define the possibility th
at ACF may be a very early morphological lesion with molecular changes. and
to explore the relationship between ACF and colorectal adenoma even carcin
METHODS DNA from 35 CRC, 15 adenomas, 34 ACF and 10 normal mucus was isolat
ed by means of microdissection. Direct gene sequencing of Kras gene includi
ng codon 12, 13 and 61 as well as the mutation cluster region (MCR) of APC
gene was performed.
RESULTS K-ras gene mutation frequency in ACF, adenoma and carcinoma was 17.
6% (6/ 34), 13.3% ( 2/ 15), and 14.3% ( 5/ 35) respectively, showing no dif
ference ( P > 0. 05) in K-ras gene mutation among three pathologic procedur
es. The K-ras gene mutation in adenoma. carcinoma and 4 ACF restricted in c
odon 12 (GGT --> GAT), but the other 2 mutations from ACF located in codon
13 (GGC --> GAC). Kras gene mutation was found more frequently in older pat
ients and patients with polypoid cancer. No mutation in codon 61 was found
in the three tissue types. Mutation rate of APC gene in adenoma and carcino
ma was 22.9% (8/ 35) and 26.7% (4/ 15), which was higher than ACF (2.9%) (
P < 0.05). APC gene mutation in carcinoma was not correlated with age of pa
tients. location, size and differentiation of tumor.
CONCLUSION ACF might be a very early morphological lesion in the tumorogene
sis of colorectal tumor. The morphological feature and gene mutation status
was different in ACF and adenoma. ACF is possibly putative ". microadenoma
" that might be the precursor of adenoma. In addition, the development of a
subgroup of colorectal carcinomas might undergo a way of "normal epitheliu
m --> ACF --> carcinomas".