(Cawkwell et al., 1994;Fearon, 1994). Accumulation of these and other unknown genetic changes is considered to be necessary for tumorigenesis, but none of the known changes can foretell metastatic potential (Fearon, 1994).It was not long ago that the new human potential metastasis-suppressor gene family, 'non-metastatic' nm23, was identified (Steeg et al., 1988). nm23-H1 has been mapped to human chromosome locus 17q21.3-22, and the gene encodes a Mr 17 000 protein of unknown function (Backer et al., 1993;. Potential roles for the nm23 protein have been suggested, such as in the formation of a basement membrane, in tumour differentiation and cell proliferation (Caligo et al., 1995;Howlett et al., 1994;Lombardi et al., 1995).A down-regulated expression of nm23-H 1, on either mRNA and/or protein level, has been reported in various human cancers (some with highly metastatic activities), such as malignant melanoma (Florenes et al., 1992;Xerri et al., 1994) (Nakayama et al., 1993). Similar findings have been reported for breast cancer (Bevilacqua et al., 1989;Hennessy et al., 1991;Hirayama et al., 1991;Royds et al., 1993;Stahl et al., 1991; Tokunaga et al., 1993), although this was not the case in a study by SastreGarau et al. (1992). Mutations and deletions of the nm23 gene have been shown in a number of primary tumours, such as neuroblastomas, lung, breast and renal cancer (Leone et al., , 1993, but not in prostatic cancer (Brewster et al., 1994). Taken together, these results suggest that the nm23 gene may have an important role in the mechanism of metastasis in many solid tumour forms.However, the role of the nm23-H 1 gene in tumour progression and for metastatic potential of colorectal cancer, is not clear. Conflicting observations have been reported on the protein level (Ayhan et al., 1993;Haut et al., 1991;Lacombe et al., 1991;Royds et al., 1994;Tannapfel et al., 1995; Yamaguchi et al., 1993;Zeng et al., 1994); on the mRNA level (Haut et al., 1991;Myeroff and Markowitz, 1993; Yamaguchi et al., 1993;Zeng et al., 1994); and on the DNA-level (Bafico et al., 1993; Campo et al., 1994; Cawkwell et al., 1994;Cohn et al., 1991;Heide et al., 1994; lacopetta et al., 1994;Okada et al., 1994;Steeg et al., 1991;Wang et al., 1993;Whitelaw and Northover, 1994).We have previously explored DNA ploidy, cell proliferative index (Lindmark et al., 1991) and p53 status (Kressner et al., 1996) in colorectal cancer, without being able to detect any substantial correlation to common clinicopathological characteristics and to patient survival time. Nevertheless, continued search for prognostic predictors in colorectal cancer is essential. Thus far, no factors have been identified capable of discriminating between patients truly cured by surgery and patients having subclinical micrometastases in Dukes' stages B and C (Dukes and Bussey, 1958). If such factors were to be available, additional therapy could be offered to selected patients running a high risk for tumour relapse. Furthermore, selected patients could be included in survei...