A subset of genetic alterations distinguishes two groups of colon canc
ers. In the first group instability of micro-satellite loci due to a d
efective DNA mismatch repair system is observed. The second group is c
haracterized by recurrent losses of chromosome regions, frequently ass
ociated with hyperploidization. We have developed a technique which en
ables a fine description of allelic losses in this second group of tum
ours. The typing of 278 loci in 47 hyperploid colon cancers has provid
ed information for an average of 160 loci per tumour. The high frequen
cy of allelic losses on chromosomes 17, 18 and 5 was confirmed thus va
lidating our methodological approach. Several additional chromosome se
gments were observed lost in over 40% of the cases, suggesting that tu
mour suppressor genes may map within these regions. Further technical
development should contribute to the identification of these genes.