Thyroid cancer
| PAG Title | Thyroid cancer |
| PAG ID | WIG000630 |
| Type | P |
| Source Link |  MSigDB |
| Publication Reference | NA |
| PAG Description | Papillary thyroid carcinoma (PTC), the most frequent neoplasia originating from the thyroid epithelium, accounts for about 80% of all thyroid cancers. Chimeric oncogenes, created by chromosomal rearrangements involving prevalently RET and, to a less extent, NTRK1 loci, are implicated in the development of papillary carcinoma.These are inappropriately expressed and stimulate constitutive signaling, bypassing the need for receptor activation by growth factors. Alternatively, mutant RAS directly stimulates BRAF, whereas mutant BRAF directly stimulates MEK. Of all thyroid cancers, 15-20% are follicular thyroid carcinoma (FTC). The most distinctive molecular features of follicular carcinoma are the prominence of aneuploidy and the high prevalence of RAS mutations and PAX8-PPAR-gamma rearrangements. The PPAR-gamma rearrangement functions through a dominant-negative effect on the transcriptional activity of wild-type PPAR-gamma. The fusion oncoprotein contributes to malignant transformation by targeting several cellular pathways, some of which are normally engaged by PPAR-gamma. Most poorly differentiated and undifferentiated thyroid carcinomas are considered to derive from pre-existing well-differentiated thyroid carcinoma through additional genetic events, including beta-catenin nuclear accumulation and p53 inactivation, but de novo occurrence might also occur. |
| Species | Homo sapiens |
| nCoCo Score | 1,352 |
| Base PAG ID | WIG000630 |
| Human Phenotyte Annotation | |
| Curator | PAGER curation team |
| Curator Contact | PAGER-contact@googlegroups.com |
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