Nondisjunction reduplication of chromosome 3 is not a common mechanism in the development of human renal cell tumors.

Because of the recurrent loss of regions of the chromosome 3 short arm in renal cell carcinomas, a chromosomal mechanism for the expression of recessive cancer genes has been implicated in the development of this type of tumor. Nondisjunction and subsequent reduplication of a mutant chromosome is one of the presumed mitotic mechanisms leading to the expression of recessive cancer genes. Using variant fluorescence at the centromeric region of chromosome 3 and a restriction fragment length polymorphism on chromosome 3p, we found chromosome 3 heteromorphism in the constitutional cells of 14 of 15 patients with renal tumors showing two normal chromosomes 3. This heteromorphism was maintained in each tumor. Therefore, the mechanism of nondisjunction and reduplication in the development of homozygosity for a mutant chromosome 3 in renal tumors remains questionable.