Karyotypic abnormalities in benign adrenocortical tumors producing aldosterone.
Because familial hyperaldosteronism type II (FH-II) includes tumor formation, we examined the karyotypes of benign adrenocortical aldosterone-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 from a patient with FH-II) had abnormal karyotypes. All were from male patients, and loss of the Y chromosome was observed in each. One showed loss of chromosome 19, and another showed an unbalanced t(6;7) producing partial trisomy 7q. Oncogenes are present at these breakpoints, and loss of the Y chromosome and monosomy 19 have previously been reported in neoplasia. This is the first report of cytogenetic abnormalities in benign adrenocortical tumors.
Gordon
R D
RD
Endocrine-Hypertension Research Unit, Greenslopes Hospital, Brisbane, Australia.
Stowasser
M
M
Martin
N
N
Epping
A
A
Conic
S
S
Klemm
S A
SA
Tunny
T J
TJ
Rutherford
J C
JC
D000310:Adrenal Gland Neoplasms / Q000235:genetics* / Q000378:metabolism; D000328:Adult; D000450:Aldosterone / Q000378:metabolism*; D002869:Chromosome Aberrations; D002872:Chromosome Deletion; D025063:Chromosome Disorders; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000235:genetics*; D007621:Karyotyping; D008297:Male; D008875:Middle Aged; D014314:Trisomy; D014407:Tumor Cells, Cultured; D014998:Y Chromosome
D000450:Aldosterone