Absence of frequent involvement of modifier of Min(APC) in sporadic colorectal cancer.
BACKGROUND
Mutations in the multiple intestinal neoplasia (Min) gene, the mouse homologue of the APC gene, result in the development of intestinal tumors. The degree of tumor expression is suppressed by the modifier of Min (MOM). Alterations in the MOM gene result in markedly increased tumor expression in the mouse. The human homologue of the MOM gene has been mapped to a locus on chromosome 1p35-36, but the role of the MOM gene in the development of human sporadic colorectal cancers has not been defined.


METHODS
The microsatellite marker D1S199 has been previously mapped to the region of the MOM gene and was used as a primer for PCR amplification. The PCR products were subjected to denaturing electrophoresis and analyzed for loss of heterozygosity (LOH) and the mismatch repair phenomenon (RER) of each tumor compared to its mucosal control.


RESULTS
48 consecutive sporadic colorectal cancers and normal adjacent mucosa were analyzed. LOH was noted in 2 of 48 tumors and the RER phenomenon was noted in 6 of 48 tumors. Thus, 8 of 48 tumors (16.7%) showed alterations in the region of the locus of the MOM gene. There was no association between alterations in this region and TNM stage, disease-free survival, overall survival, or p53 mutation.


CONCLUSIONS
Although mutation of the APC gene is an integral component of sporadic colorectal carcinogenesis, alteration in the region including the MOM gene does not appear to play a significant role in the development or clinicopathologic behavior of human sporadic colorectal tumors.
Kahlenberg
M S
MS
Department of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, New York 14263, USA.
Stoler
D L
DL
Petrelli
N J
NJ
Rodriguez-Bigas
M
M
Weber
T K
TK
Anderson
G R
GR
D000483:Alleles; D000818:Animals; D002874:Chromosome Mapping; D002878:Chromosomes, Human, Pair 1 / Q000235:genetics; D003110:Colonic Neoplasms / Q000235:genetics*; D004247:DNA / Q000235:genetics; D017931:DNA Primers; D004260:DNA Repair; D018572:Disease-Free Survival; D004586:Electrophoresis; D005784:Gene Amplification; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics; D017491:Genes, APC / Q000235:genetics*; D016147:Genes, Tumor Suppressor / Q000235:genetics; D016158:Genes, p53 / Q000235:genetics; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism; D019656:Loss of Heterozygosity / Q000235:genetics; D051379:Mice; D018895:Microsatellite Repeats / Q000235:genetics; D009154:Mutation / Q000235:genetics; D009367:Neoplasm Staging; D016133:Polymerase Chain Reaction; D012004:Rectal Neoplasms / Q000235:genetics*; D015996:Survival Rate
D017931:DNA Primers; D004247:DNA