Polyclonal expansion of cells with trisomy 7 in synovia from patients withosteoarthritis

Trisomy 7 as the single chromosome aberration has been found in a variety o f neoplasms and in normal tissue in the proximity of tumors, as well as in non-neoplastic lesions. Recently, we described a nonrandom pattern of chrom osome aberrations, in particular, a gain of chromosome 7, in synovia, carti lage, and osteophytes from patients with osteoarthritis. To study the clona l origin of trisomy 7 in osteoarthritis, multiple synovial samples were col lected from five women, all of whom were informative heterozygotes with reg ard to the X-linked human androgen receptor gene (AR). From each case, thre e to four independent cell cultures were initiated. Trisomic cell populatio ns were subcloned from the individual cultures, and it was established whet her or not the same allele of AR was inactivated in trisomic cells from dif ferent parts of the same joint. The finding of a polyclonal X-inactivation pattern in two of the cases provides strong evidence that gain of an extra copy of chromosome 7 occurs independently in multiple cells.