Cytogenetics Morphological | Only a few karyotyping studies has been performed. Chromosomal analysis revealed a modal number of 61 with consistent structural abnormalities of add(3)(q11), add(9)(p11), and add(16)(ql1) in one case of adult carcinoma and the karyotype 46, XX, t(4;11)(q35;p13) in the another one. Karyotyping of short-term cultured cells from an 11-cm adrenocortical carcinoma in a 3.5-year-old girl revealed the very complex karyotype 46,XX, inv(9)(p11q12)c/[2]/56-57,XX, +2, +4, +5, +7, +8, inv(9)c, +10, +add (13)(p11), +14, +15, +19, +20, +20, +mar[cp19]. |
Cytogenetics Molecular | Fluorescent in situ hybridization (FISH) studies of carcinomas showed increasing genome instability in carcinoma progression. Loss of heterozygosity (LOH) studies identified allelic losses on chromosomes 11p, 11q, 13q, and 17p. The LOH on 2p16 is strongly associated with the malignant phenotype. Several studies were reported in carcinomas with comparative genomic hybridization (CGH). DNA sequence copy number gains were identified on chromosomes 4, 5, 9q, and 12q and losses on chromosomes 17p, 1p, 2q, 11q, and 9p. All studies showed that the number of genomic changes is closely correlated with tumor behavior. In adenomas, small tumors contain a small or zero number of chromosomal imbalances, and a number of changes increases in larger adenomas and then considerably increases in carcinomas. Of adenomas, the most common alterations were gains of 4q, 17p, 17q and 9q32-qter. Two CGH studies of childhood adrenal tumors showed extensive genetic alterations both in benign and malignant tumors. The copy number changes are distinctly different to those seen in adult tumors thus possibly reflecting different genetic background for these tumors. High-level amplification of 9q34 was very common. |
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