Chromosomal aberrations in two adrenocortical tumors, one with a rearrangement at 11p15.
Adrenocortical tumors are detected with increasing frequency, but symptomatic cases with excessive hormone production are rare. We investigated cytogenetically one benign aldosterone-producing tumor (Conn Syndrome)(case 1) and one malignant cortisol-producing tumor (Cushing Syndrome)(case 2). Radioimmunoassay of cell culture supernatant of case 2 detected cortisol secretion during 2 months in culture. Flow cytometry of spill-out cells from case 2 showed a bimodal pattern (DNA Index 1.0, 1.4). Case 1 revealed a marker chromosome in 4/25 cells analyzed; the marker was a long acrocentric partially derived from chromosome 2,der(2q). In case 2, a cytogenetic harvest was achieved after prolonged culture time (6 weeks) and a marker chromosome, add(11)(p15), was detected in 16/22 cells. A breakpoint of 11p13, as well as loss of heterozygosity of alleles on 11p15, has been reported in the literature for other malignant adrenocortical cancers.
Herrmann
M E
ME
Center for Molecular Biology, Wayne State University, Detroit, Michigan.
Rydstedt
L L
LL
Talpos
G B
GB
Ratner
S
S
Wolman
S R
SR
Lalley
P A
PA
D000306:Adrenal Cortex Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D000368:Aged; D002869:Chromosome Aberrations; D002880:Chromosomes, Human, Pair 11; D003480:Cushing Syndrome / Q000235:genetics*; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000235:genetics*; D007621:Karyotyping; D008875:Middle Aged; D009384:Paraneoplastic Endocrine Syndromes / Q000235:genetics*