Comparative Genomic Hybridization in Thyroid Neoplasms

Daishu Miura, MD ■ Nobuyuki Wada, MD ■ Laurent Brunaud, MD

Thyroid tumors of follicular cell origin serve as a good model for studying possible genetic events in tumor initiation, transformation, and progression. Fagin1 and Wynford-Thomas23 proposed the multistep model of genetic alterations for thyroid tumors that arise from follicular cells (Fig. 36-1). They proposed a model with two main pathways: from follicular adenoma to follicular carcinoma and from low-risk papillary carcinoma to high-risk papillary carcinoma. Subsequently, these differentiated thyroid carcinomas may transform to anaplastic thyroid carcinoma. The latter change, from differentiated to anaplastic, is associated with p53 mutations.3 5

Comparative genomic hybridization (CGH) is a genome scanning technique that allows identification of changes in a relative copy number of DNA sequences (gains or losses), using DNA extracted from clinical tumor samples or cell lines (Fig. 36-2).6 The fluorescence in situ hybridization (FISH) reaction can also be used to detect gains and losses. FISH, however, is restricted to the analysis of metaphase nuclei only, whereas CGH is able to analyze interphase nuclei from cells that are not actively proliferating.

In cancer cells, gains and losses of oncogenes and tumor suppressor genes can be mirrored by chromosomal abnormalities such as chromosomal deletions, monosomies, duplication, polysomies, and gene amplifications such as homogenously staining regions or double-minute chromosomes.7

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