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 .
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) .
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.