1.The genomic alterations for benign thyroid nodule, especially adenomatoid nodule, one of the most common types of hyperplasia lesion, are ill-studied.
2. Somatic mutation of BRAF (22/32) is only detected in PTC.
3. Mutations in SPOP (4/38), ZNF148 (6/38) and EZH1 (3/38) are found enriched in adenomatoid nodule.
4.In an expanded cohort of adenomatoid nodule (n=259)mutually exclusive SPOPP94R, EZH1Q571R and ZNF148
mutations are identified in 24.3% of them.
5.Adenomatoid nodules show very few overlapped mutations and distinct gene expression patterns with their coincidental PTC.
6.PTCs evolved independently from their matched benign nodules.
7. Benign nodules possess a unique molecular signature that differs from PTC.
8.Molecular marker evidence that Papillary thyroid cancer and benign nodules have independent origin.
9. This means that in the near future the molecular markers status of a given nodule can be used to assign a nodule to benign and result in no surgery and if there are symptoms or cosmetic reasons the use of ethanol and or radiofrequency ablation methods could be used.
10.The Cancer Genome Atlas (TCGA) project and other studies tumorigenesis related genetic events have been uncovered in 96.5% of PTC (for example, BRAF mutation, RAS mutation and so on)
11. Novel genetic alterations are associated with follicular adenoma, the benign neoplastic thyroid nodule.
12.While the genetic alterations for benign hyperplasia thyroid nodule, especially adenomatoid nodule, one of the most common hyperplasia lesions and undistinguished from follicular thyroid carcinoma in fine need aspiration.
13. Benign hyperplastic thyroid nodules have a distinct molecular pattern all their own. SPOPP94R, EZH1Q571R and ZNF148 mutations,