Previous research shows that
ARID1A mutations that prevent cellular production of
ARID1A are found in about 50% of ovarian clear cell carcinomas, 35% of uterine endometrioid endometrial adenocarcinomas and 30% of ovarian endometrioid carcinomas.
Western blots of
ARID1A and PTEN, and FSHR proteins in mouse ovaries
In conclusion, we basically investigated loss of
ARID1A expression, and molecular groups, and based on chi-square test results, any statistically significant difference was not found between these groups (p=0.110).
PGR and
ARID1A have a critical role in modulating epithelial proliferation at the pre-implantation stage which is a critical requisite for uterine receptivity [11].
The expression of
ARID1A, ING5, and CBX7 genes was significantly lower in the AG than in the control group (fold change<0.5 and fold regulation<-2).
An integrated genomic approach identifies
ARID1A as a candidate tumor-suppressor gene in breast cancer.
Lawrenson et al., "Down-regulation of
ARID1A is sufficient to initiate neoplastic transformation along with epigenetic reprogramming in non-tumorigenic endometriotic cells," Cancer Letters, vol.
Most of the remaining significantly mutated genes (PTEN, PIK3CA, PIK3R1,
ARID1A, RPL22, KRAS, CTNNB1, ATR, FGFR2, CCND1) have well-documented roles in the endometrioid subtype, as discussed earlier in this review and elsewhere (24, 65).
However, investigators also found several mutations that are unique to uterine serous carcinomas (eg, PIK3CA, FBXW7, PPP2R1A, and
ARID1A), providing potential opportunities for targeted pharmacotherapy.
Moreover, recent mutational profiling studies indicate that whereas some carcinosarcomas share mutations with type 1 tumors (PTEN and
ARID1A), others share mutations with uterine papillary serous carcinomas (notably p53 and PPP2R1A) [4].
Mutations in two genes,
ARID1A and PPP2R1A, appear to be linked to ovarian clear cell carcinoma, one of the most aggressive forms of ovarian cancer, investigators reported.
(49-52) More recently, endometriosis with cytologic atypia has been proposed to be a precursor lesion, based on identical molecular and immunohistochemical alterations, loss of
ARID1A and PIK3CA mutations, between clear cell carcinoma and the immediately adjacent foci of atypical endometriosis.