KARYOTYPIC ABNORMALITIES IN BENIGN ADRENOCORTICAL TUMORS PRODUCING ALDOSTERONE

Because familial hyperaldosteronism type II (FH-II) includes tumor for mation, we examined the karyotypes of benign adrenocortical aldosteron e-producing adenomas (APAs), including those from patients with FH-II. Cell culture was successful in 12 of 14 tumors removed, two of which were from patients with FH-II. Five of the 12 tumors cultured (one fro m a patient with FH-II) had abnormal karyotypes. All were from male pa tients, and loss of the Y chromosome was observed in each. One showed loss of chromosome 19, and another showed an unbalanced t(6;7) produci ng partial trisomy 7q. Oncogenes are present at these breakpoints, and loss of the Y chromosome and monosomy 19 have previously been reporte d in neoplasia. This is the first report of cytogenetic abnormalities in benign adrenocortical tumors.