Table 3.
Literature review summary
| Authors (year) | Probe | Results | Authors’ conclusion |
|---|---|---|---|
| Sugg et al. (1998) [12] | RET/PTC rearrangement | Different rearrangement in 15/17 cases Same rearrangement in 2/17 cases | Most multiple PTCs arise independently |
| Moniz et al. (2002) [13] | X chromosome inactivation (HUMARA assay) | Concordant inactivation in 5/8 cases Discordant inactivation in 3/8 cases | Multiple PTCs may arise from intrathyroid spread or independently, with a slight predominance of the former |
| Shattuck et al. (2005) [11] | X chromosome inactivation (HUMARA assay) | Concordant inactivation in 5/10 cases Discordant inactivation in 5/10 cases | Multiple PTCs may arise from intrathyroid spread or independently |
| Park et al. (2006) [14] | BRAFV600E mutation | 24/61 of the cases showed mutation in some of the nodules but not in others | Multiple PTCs may arise from intrathyroid spread or independently, with a slight predominance of the latter |
| McCarthy et al. (2006) [15] | 1. LOH for 3 microsatellite polymorphic markers 2. X chromosome inactivation (HUMARA assay) |
1. Concordant allelic loss pattern in 20/23 cases 2. Concordant X chromosome inactivation in 13/13 informative cases |
Nearly all multiple PTCs arise from the same clone and are the result of intrathyroid spread |
| Wang et al. (2010) [16] | 1. BRAFV600E mutation 2. X chromosome inactivation (HUMARA assay) |
1. Concordant BRAF status in 18/21 cases 2. Concordant X chromosome inactivation in 9/11 informative cases |
Nearly all multiple PTCs arise from the same clone and are the result of intrathyroid spread |