Anaplastic Thyroid Cancer: A Review of Epidemiology, Pathogenesis, and Treatment

Table 3

Preclinical agents.

Mechanism	Agents	Studies
Loss of p53 or abnormal p53 is expressed in anaplastic thyroid cancer [83]	Adenovirus with wild type p53	Blagosklonny et al. showed that anaplastic thyroid cancer cell lines infected with the p53 adenovirus became more sensitive to doxorubicin.
Unknown [84]	Bovine seminal ribonuclease	In vivo tumor regression of anaplastic thyroid cancer.
Inhibition of cyclin-dependent kinase activity [85]	Bone morphogenic protein	Inhibition of 4 of 6 anaplastic thyroid cancer cell lines.
EGFR Tyrosine-kinase inhibitor [86]	ZD1839 (gefitinib)	EGFR is overexpressed in anaplastic thyroid cancer in vitro/vivo and gefitinib induces apoptosis in vitro and inhibits subcutaneous mouse models of anaplastic thyroid cancer.
EGFR Monoclonal antibody [87]	Cetuximab	As single agent cetuximab had no activity, but with irinotecan it inhibited orthotopic anaplastic thyroid cancer xenografts more than doxorubicin.
EGRF/VEGF Receptor blocker [88]	AEE788	In vitro inhibition and nude-mouse inhibition with pacitaxel.
Histone Deacetylase Inhibitors [77, 89–91]	Valproic acid and other novel agents	Restored radio iodide uptake and restoration of p53 or pseudo- p53 activity.
Inhibition of gelatinase class of matrix metalloproteinases (MMP) that are activated in ATC [92]	MMP-activated LeTx	Reduced endothelial cell recruitment and subsequent tumor vascularization