The human carcinomas of gastrointestinal tract (GIT) are developed via "suppressor" (pJJ-dependent) or "mutator" (with deficiency in DNA mismatch repair) pathways. These pathways are known to be accompanies by variations in both clinicopathological and therapeutic characteristics. The mutator pathway manifests in genome microsatellite instability (MSI). All GIT carcinomas can be subdivided in three classes, with high (MSI-H), low (MSI-L) and zero (MSS) level of MSI. 34 DNA samples from GIT carcinomas were analyzed with 9 microsatellites and 5 exones of p53 gene in searching for correlation between the level of MSI and mutations inp53. The MSI-H carcinomas appeared to be of mutator type whereas both MSI-L and MSS were of suppressor type