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. Author manuscript; available in PMC: 2017 Feb 5.
Published in final edited form as: Mol Cell Endocrinol. 2015 Jun 27;421:18–27. doi: 10.1016/j.mce.2015.06.029

TABLE 1.

Single gene models for non-medullary thyroid cancer in the mouse*

Gene Mutation Human phenotype Mouse phenotype Alleles**
BRAF V600E PTC (usually cPTC or fvPTC) PTC TX
KI
KI-I
TX-I
RET-PTC1 Fusion gene PTC PTC (non-invasive) TX
RET-PTC3 Fusion gene PTC PTC (non-invasive) TX
TRK-T1 Fusion gene PTC PTC (non-invasive) TX
H-RAS G12D/G12V PTC or FTC hyperplasia TX/KI
K-RAS G12D PTC or FTC hyperplasia TX/KI
N-RAS Q61K PTC or FTC PTC/FTC TX
Rap1b G12V ND hyperplasia KI-I
PAX8-PPARG Fusion gene FTC hyperplasia TX
PTEN Knockout FTC or PTC FTC (likely strain dependent) Het
KO
Prkar1a Knockout FTC or PTC FTC Het
KO
THRBPV/PV PV (fs443) RTH (het)*** FTC KI (homo)
PIK3CA H1047R FTC (?) Minimal hyperplasia KI-I
SV40 T-ag Viral gene -- ATC TX
*

References for each of the models can be found in the text

**

TX: Transgenic, KI: Knock-in, KI-I: Inducible Knock-in, TX-I: Inducible transgenic, Het: Conventional heterozygote, KO: Knockout (tissue-specific)

***

RTH: Resistance to thyroid hormone.

Note that patients are heterozygous for the mutation. The phenotype is observed in homozygous mice