Histone Deacetylase Inhibitors: A Promising Therapeutic Alternative for Endometrial Carcinoma

Table 1

Genetic alternations in ECs associated with histone-mediated epigenetics.

Genetic alternations in ECs	Impact on EC development and progression	Reference
Silencing of hMLH1/MSH2, PTEN, and PR	Early carcinogenesis, more aggressive carcinomas, resistance to hormonal treatment	[15]
Silencing of hMLH1 and/or MSH2	Microsatellite instability, invasive growth, acquired resistance to cisplatin	[24]
Overexpression of class I HDACs	Significantly more often in high-grade serous subtypes	[25]
Overexpression of HDAC2	Acquisition of aggressive behavior	[26]
Impaired HDAC1 protein expression	Impaired epigenetic status of epithelial and stromal cells	[27]
miR-206 modulation of HDAC6	Progression through the PTEN/AKT/mTOR pathway	[28]
Overexpression of EZH2, FAK, and pFAK	Worse prognosis, decreased overall survival	[29]
Low FOXA1 protein expression	High-grade carcinomas, loss of ERα and PR, poor survival	[30]
ATAD2 expression	Aggressive carcinomas	[31]
Low MIG6 mRNA levels	High-grade carcinomas, failure of PR-mediated growth suppression	[32]
Aberrant expression of miRNAs	Tumorigenesis, metastasis	[33]