'
ARID1A mutations are highly prevalent in theses human cancers.
To evaluate the expression levels of
ARID1A and PTEN genes and proteins in mice ovaries, western blot was carried out according to our previous report (19).
ARID1A los correlates with missmatch reparir defiency and intact p53 expression in high grade endometrial carcinomas.
These data suggest that MTUS1 is a target of
ARID1A and PGR in the uterus at GD 3.5.
There were no significant differences between the expression levels of EED, CBX3, MTA1,
ARID1A, ING5, and CBX7 gene between patients with AG and those with GC, although the expression level (fold change level) of these genes was higher in patients with GC than in those with AG (Table 4, 5) (Figure 4).
Loss of
ARID1A expression sensitizes cancer cells to PI3K- and AKT-inhibition.
Shan et al., "Promoter hypermethylation of
ARID1A gene is responsible for its low mRNA expression in many invasive breast cancers," PLoS One, vol.
Sixteen significantly mutated genes were discerned in this molecular subgroup (Table 1): 9 genes previously implicated in endometrial cancer (PTEN, PIK3CA, CTNNB1,
ARID1A, PIK3R1, KRAS, FGFR2, CHD4, SPOP) by us and others [(17, 18); reviewed in (24)], and 7 genes (BCOR, CSMD3, CTCF, MECOM, METTL14, SGK1, SOX17) not previously recognized to have a role in endometrial tumorigenesis.
In a separate study another team of researchers found an association between mutations in
ARID1A and the development of ovarian clear cell and endometrioid carcinomas.
Loss of
ARID1A protein expression occurs as an early event in ovarian clear-cell carcinoma development and frequently coexists with PIK3CA mutations.
In agreement, The Cancer Genome Atlas (TCGA), based on the high number of viral copies and high levels of viral gene expression, proposed the EBV-positive GC (also known as EBVaGC) as a particular GC entity characterized by DNA hypermethylation, increased frequency of PIK3CA,
ARID1A, and BCOR mutations but wild-type p53, and high expression of T cell inhibitory molecules CD274 (PD-L1), PDCD1LG2 (PD-L2), and indoleamine 2,3-dioxygenase 1 (IDO 1) [10, 11].