Increasing genome instability in adrenocortical carcinoma progression with involvement of chromosomes 3, 9 and X at the adenoma stage

The investigation of chromosomal aberrations in adrenocortical tumours has been limited by the difficulties of applying classical cytogenetics to tumours with low levels of proliferation. We have therefore applied the technique of interphase cytogenetics to paraffin-embedded archival specimens of 14...

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Bibliographic Details
Published in:British Journal of Cancer 1999-10, Vol.81 (4), p.684-689
Main Authors: Russell, A J, Sibbald, J, Haak, H, Keith, W N, McNicol, A M
Format: Article
Language:English
Subjects:
Adenoma - genetics
Adrenal Cortex Neoplasms - genetics
Adrenals. Adrenal axis. Renin-angiotensin system (diseases)
Biological and medical sciences
Biomedical and Life Sciences
Biomedicine
Cancer Research
Chromosome Aberrations
Chromosomes, Human, Pair 3
Chromosomes, Human, Pair 9
Drug Resistance
Endocrinopathies
Epidemiology
Humans
Malignant tumors
Medical sciences
Molecular Medicine
Oncology
Regular
regular-article
X Chromosome
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Summary:The investigation of chromosomal aberrations in adrenocortical tumours has been limited by the difficulties of applying classical cytogenetics to tumours with low levels of proliferation. We have therefore applied the technique of interphase cytogenetics to paraffin-embedded archival specimens of 14 adrenocortical adenomas and 13 carcinomas. Hybridizations were performed using centromere-specific probes to chromosomes 3, 4, 9, 17, 18 and X, which have been shown to be altered in other types of tumours. Chromosomal imbalance was defined on the basis of changes in both chromosome index (CI) and signal distribution (SD). Where only one of these was altered, this was classified as a tendency to gain or loss. On the basis of the analysis of optimal hybridizations, carcinomas showed gains in all chromosomes studied, five of nine showing gains in multiple chromosomes. Gains were most common in chromosomes 3, 9 and, in particular X, eight of 11 showing gain, and one a tendency to gain. Chromosomal gain was seen less commonly in adenomas, but again chromosomes 3, 9 and X were involved. Losses were infrequent, only one carcinoma showing loss of chromosome 18, and adenomas showing a tendency to loss of chromosomes 4 (two cases), 17 (one case) and 18 (two cases). Our data suggest that changes in chromosomes 3, 9 and X are early events in adrenocortical tumorigenesis, and that there is increasing chromosomal instability with tumour progression.
ISSN:0007-0920
1476-5381
1532-1827
DOI:10.1038/sj.bjc.6690748