This study evaluates the potential contribution of the nm23-H1 gene to malignant transformation in patients with
renal cell carcinoma. Using specific
oligonucleotide primers for the nm23-H1 microsatellite repetitive sequence, gene instability was followed by polymerase chain reaction/loss of heterozygosity assay on 54
tumor specimens and the corresponding normal tissue samples. We also determined, immunohistochemically, the relative concentration and localization of the nm23-H1
protein product. From 77.7% informative cases,
DNA from 6
tumors exhibited loss of heterozygosity, regardless of the
tumor stage (TNM). Out of 39 samples analyzed, 30 were negative for Nm23-H1
protein, while the others were only slightly positive. No correlation with
tumor stage was found. Normal renal tissue was also negative for this
protein. Our results provide the evidence for loss of heterozygosity, followed by means of microsatellite tandem-repeat polymorphism, at the nm23-H1 locus in
renal cell carcinoma. However, since no correlation was found between the
tumor stage or metastatic potential on the one hand, and allelic loss and specific
protein expression on the other, it seems that nm23-H1 does not play a key role in the invasiveness of this
tumor type.