Treatment of Thyroid Cancer with Histone Deacetylase Inhibitors and Peroxisome Proliferator-Activated Receptor–γ Agonists

Thyroid ◽  
2005 ◽  
Vol 15 (6) ◽  
pp. 594-599 ◽  
Author(s):  
Wen T. Shen ◽  
Woong-Youn Chung
2005 ◽  
Vol 280 (17) ◽  
pp. 16934-16941 ◽  
Author(s):  
Maofu Fu ◽  
Mahadev Rao ◽  
Toula Bouras ◽  
Chenguang Wang ◽  
Kongming Wu ◽  
...  

2016 ◽  
Vol 36 (10) ◽  
pp. 5019-5024 ◽  
Author(s):  
CHRISTOS DAMASKOS ◽  
SERENA VALSAMI ◽  
ELEFTHERIOS SPARTALIS ◽  
EFSTATHIOS A ANTONIOU ◽  
PERIKLIS TOMOS ◽  
...  

2020 ◽  
Vol 26 ◽  
Author(s):  
Eleftherios Spartalis ◽  
Konstantinos Kotrotsios ◽  
Dimosthenis Chrysikos ◽  
Michael Spartalis ◽  
Stavroula A. Paschou ◽  
...  

Background/Aim: Papillary Thyroid Cancer (PTC) is the most common type of endocrine malignancy. Although PTC has an excellent prognosis, recurrent or metastatic disease could affect patients survival. Recent studies show that Histone Deacetylase Inhibitors (HDACIs) might be promising anticancer agents against PTC. The aim of this review is to evaluate the role of HDACIs as an additional modality in PTC treatment and to depict the latest trends of current research on this field. Materials and Methods: This literature review was performed using the MEDLINE database. The search strategy included terms: “thyroid cancer”, “papillary”, “HDAC”, “histone”, and “deacetylase”. Results: Agents, such as Suberoyl Anilide Hydroxamic Acid, Trichostatin A, Valproic Acid, Sodium butyrate, Panobinostat, Belinostat, Romidepsin, CUDC907 and N-Hydroxy-7-(2-naphthylthio)-Hepanomide have shown promising anti-cancer effects on PTC cell lines but fail to trigger major response in clinical trials. Conclusion: HDACIs have no significant effect as monotherapy against PTC but further research needs to be conducted in order to investigate their potential effect when used as an additional modality.


2004 ◽  
Vol 32 (5) ◽  
pp. 840-842 ◽  
Author(s):  
V.C. Emmans ◽  
H.A. Rodway ◽  
A.N. Hunt ◽  
K.A. Lillycrop

Neuroblastoma is a childhood cancer, which spontaneously regresses. This has led to a search for agents that mimic this process. We show that both natural and synthetic ligands of PPARγ (peroxisome-proliferator-activated receptor γ) inhibit the growth of neuroblastoma cells in vitro. The degree of PPAR activation was attenuated however in the presence of the retinoblastoma protein. Addition of trichostatin A, a histone deacetylase inhibitor, abolished retinoblastoma protein repression of PPAR activity. Moreover, enhanced growth inhibition was observed when neuroblastoma cells were treated with a PPARγ ligand and a histone deacetylase inhibitor, suggesting a combination therapy to treat neuroblastoma might prove more effective than using either agent alone.


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