Short Communication Genome-Wide Appraisal of Thyroid Cancer Progression

Several lines of evidence suggest that follicular cell-derived thyroid cancers represent a continuum of disease that progresses from the highly curable well-differentiated thyroid cancers to the universally fatal anaplastic cancers. However, the genetic mechanisms underlying thyroid cancer progression remain ill defined. We compared the molecular-cytogenetic profiles derived from comparative genomic hybridization (CGH) analysis of major histological variants of thyroid cancer to define genetic variables associated with progression. Overall, a sequential increase in chromosomal complexity was observed from well-differentiated papillary thyroid cancer to poorly differentiated and anaplastic carcinomas, both in terms of the presence of CGH detectable abnormalities ( P (cid:1) 0.003) and the median number of abnormalities per case ( P < 0.001). The presence of multiple abnormalities common to all thyroid cancer variants, including gains of 5p15, 5q11–13, 19p, and 19q and loss of 8p, suggests that these tumors are derived from a common genetic pathway. Gains of 1p34–36, 6p21, 9q34, 17q25, and 20q and losses of 1p11-p31, 2q32–33, 4q11–13, 6q21, and 13q21–31 may represent second-ary events in progression, as they were only detected in poorly differentiated and anaplastic carcinomas.

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